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Theses & Dissertations: Cancer Research

Theses/dissertations from 2024 2024.

Therapeutic Effects of BET Protein Inhibition in B-cell Malignancies and Beyond , Audrey L. Smith

Identification of Mitotic Phosphatases and Cyclin K as Novel Molecular Targets in Pancreatic Cancer , Yi Xiao

Theses/Dissertations from 2023 2023

Development of Combination Therapy Strategies to Treat Cancer Using Dihydroorotate Dehydrogenase Inhibitors , Nicholas Mullen

Overcoming Resistance Mechanisms to CDK4/6 Inhibitor Treatment Using CDK6-Selective PROTAC , Sarah Truong

Theses/Dissertations from 2022 2022

Omics Analysis in Cancer and Development , Emalie J. Clement

Investigating the Role of Splenic Macrophages in Pancreatic Cancer , Daisy V. Gonzalez

Polymeric Chloroquine in Metastatic Pancreatic Cancer Therapy , Rubayat Islam Khan

Evaluating Targets and Therapeutics for the Treatment of Pancreatic Cancer , Shelby M. Knoche

Characterization of 1,1-Diarylethylene FOXM1 Inhibitors Against High-Grade Serous Ovarian Carcinoma Cells , Cassie Liu

Novel Mechanisms of Protein Kinase C α Regulation and Function , Xinyue Li

SOX2 Dosage Governs Tumor Cell Identity and Proliferation , Ethan P. Metz

Post-Transcriptional Control of the Epithelial-to-Mesenchymal Transition (EMT) in Ras-Driven Colorectal Cancers , Chaitra Rao

Use of Machine Learning Algorithms and Highly Multiplexed Immunohistochemistry to Perform In-Depth Characterization of Primary Pancreatic Tumors and Metastatic Sites , Krysten Vance

Characterization of Metastatic Cutaneous Squamous Cell Carcinoma in the Immunosuppressed Patient , Megan E. Wackel

Visceral adipose tissue remodeling in pancreatic ductal adenocarcinoma cachexia: the role of activin A signaling , Pauline Xu

Phos-Tag-Based Screens Identify Novel Therapeutic Targets in Ovarian Cancer and Pancreatic Cancer , Renya Zeng

Theses/Dissertations from 2021 2021

Functional Characterization of Cancer-Associated DNA Polymerase ε Variants , Stephanie R. Barbari

Pancreatic Cancer: Novel Therapy, Research Tools, and Educational Outreach , Ayrianne J. Crawford

Apixaban to Prevent Thrombosis in Adult Patients Treated With Asparaginase , Krishna Gundabolu

Molecular Investigation into the Biologic and Prognostic Elements of Peripheral T-cell Lymphoma with Regulators of Tumor Microenvironment Signaling Explored in Model Systems , Tyler Herek

Utilizing Proteolysis-Targeting Chimeras to Target the Transcriptional Cyclin-Dependent Kinases 9 and 12 , Hannah King

Insights into Cutaneous Squamous Cell Carcinoma Pathogenesis and Metastasis Using a Bedside-to-Bench Approach , Marissa Lobl

Development of a MUC16-Targeted Near-Infrared Antibody Probe for Fluorescence-Guided Surgery of Pancreatic Cancer , Madeline T. Olson

FGFR4 glycosylation and processing in cholangiocarcinoma promote cancer signaling , Andrew J. Phillips

Theses/Dissertations from 2020 2020

Cooperativity of CCNE1 and FOXM1 in High-Grade Serous Ovarian Cancer , Lucy Elge

Characterizing the critical role of metabolic and redox homeostasis in colorectal cancer , Danielle Frodyma

Genomic and Transcriptomic Alterations in Metabolic Regulators and Implications for Anti-tumoral Immune Response , Ryan J. King

Dimers of Isatin Derived Spirocyclic NF-κB Inhibitor Exhibit Potent Anticancer Activity by Inducing UPR Mediated Apoptosis , Smit Kour

From Development to Therapy: A Panoramic Approach to Further Our Understanding of Cancer , Brittany Poelaert

The Cellular Origin and Molecular Drivers of Claudin-Low Mammary Cancer , Patrick D. Raedler

Mitochondrial Metabolism as a Therapeutic Target for Pancreatic Cancer , Simon Shin

Development of Fluorescent Hyaluronic Acid Nanoparticles for Intraoperative Tumor Detection , Nicholas E. Wojtynek

Theses/Dissertations from 2019 2019

The role of E3 ubiquitin ligase FBXO9 in normal and malignant hematopoiesis , R. Willow Hynes-Smith

BRCA1 & CTDP1 BRCT Domainomics in the DNA Damage Response , Kimiko L. Krieger

Targeted Inhibition of Histone Deacetyltransferases for Pancreatic Cancer Therapy , Richard Laschanzky

Human Leukocyte Antigen (HLA) Class I Molecule Components and Amyloid Precursor-Like Protein 2 (APLP2): Roles in Pancreatic Cancer Cell Migration , Bailee Sliker

Theses/Dissertations from 2018 2018

FOXM1 Expression and Contribution to Genomic Instability and Chemoresistance in High-Grade Serous Ovarian Cancer , Carter J. Barger

Overcoming TCF4-Driven BCR Signaling in Diffuse Large B-Cell Lymphoma , Keenan Hartert

Functional Role of Protein Kinase C Alpha in Endometrial Carcinogenesis , Alice Hsu

Functional Signature Ontology-Based Identification and Validation of Novel Therapeutic Targets and Natural Products for the Treatment of Cancer , Beth Neilsen

Elucidating the Roles of Lunatic Fringe in Pancreatic Ductal Adenocarcinoma , Prathamesh Patil

Theses/Dissertations from 2017 2017

Metabolic Reprogramming of Pancreatic Ductal Adenocarcinoma Cells in Response to Chronic Low pH Stress , Jaime Abrego

Understanding the Relationship between TGF-Beta and IGF-1R Signaling in Colorectal Cancer , Katie L. Bailey

The Role of EHD2 in Triple-Negative Breast Cancer Tumorigenesis and Progression , Timothy A. Bielecki

Perturbing anti-apoptotic proteins to develop novel cancer therapies , Jacob Contreras

Role of Ezrin in Colorectal Cancer Cell Survival Regulation , Premila Leiphrakpam

Evaluation of Aminopyrazole Analogs as Cyclin-Dependent Kinase Inhibitors for Colorectal Cancer Therapy , Caroline Robb

Identifying the Role of Janus Kinase 1 in Mammary Gland Development and Breast Cancer , Barbara Swenson

DNMT3A Haploinsufficiency Provokes Hematologic Malignancy of B-Lymphoid, T-Lymphoid, and Myeloid Lineage in Mice , Garland Michael Upchurch

Theses/Dissertations from 2016 2016

EHD1 As a Positive Regulator of Macrophage Colony-Stimulating Factor-1 Receptor , Luke R. Cypher

Inflammation- and Cancer-Associated Neurolymphatic Remodeling and Cachexia in Pancreatic Ductal Adenocarcinoma , Darci M. Fink

Role of CBL-family Ubiquitin Ligases as Critical Negative Regulators of T Cell Activation and Functions , Benjamin Goetz

Exploration into the Functional Impact of MUC1 on the Formation and Regulation of Transcriptional Complexes Containing AP-1 and p53 , Ryan L. Hanson

DNA Polymerase Zeta-Dependent Mutagenesis: Molecular Specificity, Extent of Error-Prone Synthesis, and the Role of dNTP Pools , Olga V. Kochenova

Defining the Role of Phosphorylation and Dephosphorylation in the Regulation of Gap Junction Proteins , Hanjun Li

Molecular Mechanisms Regulating MYC and PGC1β Expression in Colon Cancer , Jamie L. McCall

Pancreatic Cancer Invasion of the Lymphatic Vasculature and Contributions of the Tumor Microenvironment: Roles for E-selectin and CXCR4 , Maria M. Steele

Altered Levels of SOX2, and Its Associated Protein Musashi2, Disrupt Critical Cell Functions in Cancer and Embryonic Stem Cells , Erin L. Wuebben

Theses/Dissertations from 2015 2015

Characterization and target identification of non-toxic IKKβ inhibitors for anticancer therapy , Elizabeth Blowers

Effectors of Ras and KSR1 dependent colon tumorigenesis , Binita Das

Characterization of cancer-associated DNA polymerase delta variants , Tony M. Mertz

A Role for EHD Family Endocytic Regulators in Endothelial Biology , Alexandra E. J. Moffitt

Biochemical pathways regulating mammary epithelial cell homeostasis and differentiation , Chandrani Mukhopadhyay

EPACs: epigenetic regulators that affect cell survival in cancer. , Catherine Murari

Role of the C-terminus of the Catalytic Subunit of Translesion Synthesis Polymerase ζ (Zeta) in UV-induced Mutagensis , Hollie M. Siebler

LGR5 Activates TGFbeta Signaling and Suppresses Metastasis in Colon Cancer , Xiaolin Zhou

LGR5 Activates TGFβ Signaling and Suppresses Metastasis in Colon Cancer , Xiaolin Zhou

Theses/Dissertations from 2014 2014

Genetic dissection of the role of CBL-family ubiquitin ligases and their associated adapters in epidermal growth factor receptor endocytosis , Gulzar Ahmad

Strategies for the identification of chemical probes to study signaling pathways , Jamie Leigh Arnst

Defining the mechanism of signaling through the C-terminus of MUC1 , Roger B. Brown

Targeting telomerase in human pancreatic cancer cells , Katrina Burchett

The identification of KSR1-like molecules in ras-addicted colorectal cancer cells , Drew Gehring

Mechanisms of regulation of AID APOBEC deaminases activity and protection of the genome from promiscuous deamination , Artem Georgievich Lada

Characterization of the DNA-biding properties of human telomeric proteins , Amanda Lakamp-Hawley

Studies on MUC1, p120-catenin, Kaiso: coordinate role of mucins, cell adhesion molecules and cell cycle players in pancreatic cancer , Xiang Liu

Epac interaction with the TGFbeta PKA pathway to regulate cell survival in colon cancer , Meghan Lynn Mendick

Theses/Dissertations from 2013 2013

Deconvolution of the phosphorylation patterns of replication protein A by the DNA damage response to breaks , Kerry D. Brader

Modeling malignant breast cancer occurrence and survival in black and white women , Michael Gleason

The role of dna methyltransferases in myc-induced lymphomagenesis , Ryan A. Hlady

Design and development of inhibitors of CBL (TKB)-protein interactions , Eric A. Kumar

Pancreatic cancer-associated miRNAs : expression, regulation and function , Ashley M. Mohr

Mechanistic studies of mitochondrial outer membrane permeabilization (MOMP) , Xiaming Pang

Novel roles for JAK2/STAT5 signaling in mammary gland development, cancer, and immune dysregulation , Jeffrey Wayne Schmidt

Optimization of therapeutics against lethal pancreatic cancer , Joshua J. Souchek

Theses/Dissertations from 2012 2012

Immune-based novel diagnostic mechanisms for pancreatic cancer , Michael J. Baine

Sox2 associated proteins are essential for cell fate , Jesse Lee Cox

KSR2 regulates cellular proliferation, transformation, and metabolism , Mario R. Fernandez

Discovery of a novel signaling cross-talk between TPX2 and the aurora kinases during mitosis , Jyoti Iyer

Regulation of metabolism by KSR proteins , Paula Jean Klutho

The role of ERK 1/2 signaling in the dna damage-induced G2 , Ryan Kolb

Regulation of the Bcl-2 family network during apoptosis induced by different stimuli , Hernando Lopez

Studies on the role of cullin3 in mitosis , Saili Moghe

Characteristics of amyloid precursor-like protein 2 (APLP2) in pancreatic cancer and Ewing's sarcoma , Haley Louise Capek Peters

Structural and biophysical analysis of a human inosine triphosphate pyrophosphatase polymorphism , Peter David Simone

Functions and regulation of Ron receptor tyrosine kinase in human pancreatic cancer and its therapeutic applications , Yi Zou

Theses/Dissertations from 2011 2011

Coordinate detection of new targets and small molecules for cancer therapy , Kurt Fisher

The role of c-Myc in pancreatic cancer initiation and progression , Wan-Chi Lin

The role of inosine triphosphate pyrophosphatase (ITPA) in maintanence [sic] of genomic stability in human cells , Miriam-Rose Menezes

Molecular insights into major histocompatibility complex class I folding and assembly , Laura Christina Simone

The role of bcl-2 in colon cancer metastatic progression , Wang Wang

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Student theses

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A biologically-inspired artificial lateral line: observations of collective behaviour in fish lead to the development of a novel design of simple and low-cost artificial lateral line sensor.

Supervisor: Hauert, S. (Supervisor), Ioannou, C. (Supervisor) & Genner, M. J. (Supervisor)

Student thesis : Doctoral Thesis › Doctor of Philosophy (PhD)

A characterisation of mononuclear phagocyte dynamics in the healthy and regenerating zebrafish heart

Supervisor: Richardson, B. (Supervisor) & Martin, P. B. (Supervisor)

A Computational Framework for the Optimisation of Antivenom Pharmacokinetics and Pharmacodynamics

Supervisor: Hauert, S. (Supervisor), Blee, J. A. (Supervisor) & Collinson, I. R. (Supervisor)

An Epigenome-Wide Association Study of Eczema

Supervisor: Paternoster, L. (Supervisor), Elliott, H. (Supervisor) & Relton, C. (Supervisor)

Student thesis : Master's Thesis › Master of Science by Research (MScR)

An Investigation into the Link Between Sleep and Alzheimer’s Disease Using a Multi-Method Approach

Supervisor: Coulthard, E. J. (Supervisor) & Ben-Shlomo, Y. (Supervisor)

Applications of HS-AFM Imaging to Marine Microbial Life and its Environment

Supervisor: Day, J. C. C. (Supervisor), Picco, L. M. (Supervisor), Payton, O. D. (Supervisor) & Allen, M. (Supervisor)

Applying ‘omics to understand and predict juvenile idiopathic arthritis

Supervisor: Relton, C. (Supervisor), Ramanan, A. (Supervisor), Sharp, G. (Supervisor) & Zhou, Y. (External person) (Supervisor)

Appraising the causal relationship between DNA methylation and type 2 diabetes

Supervisor: Elliott, H. (Supervisor), Relton, C. (Supervisor) & Sharp, G. (Supervisor)

A qualitative exploration of recruiters' and patients' perspectives and experiences of the recruitment encounter in randomised controlled trials

Supervisor: Young, B. (Supervisor), Rooshenas, L. (Supervisor), Elliott, D. (Supervisor), Jepson, M. (Supervisor) & Donovan , J. L. (Supervisor)

Arole for IGFBP-2 in DNA repair in breast cancer cells

Supervisor: Perks, C. (Supervisor), Holly, J. (Supervisor) & Biernacka, K. M. (Supervisor)

Assessing the feasibility of dietary restriction, including short-term fasting, at the time of chemotherapy

Supervisor: Atkinson, C. (Supervisor), Herbert, G. (Supervisor), Ness, A. (Supervisor) & Perks, C. (Supervisor)

A study of hyperspectral reflectance and fluorescence imaging as alternative Methods for assessing coral health

Supervisor: Day, J. (Supervisor) & Scott, T. (Supervisor)

Biological and lifestyle predictors of survival in head and neck cancer.

Supervisor: Dos Santos Ferreira, D. (Supervisor), Ingle, S. (Supervisor), Ness, A. (Supervisor), Martin, R. (Supervisor) & May, M. T. (Supervisor)

Biosynthetic Studies on Kalimantacin Antibiotics

Supervisor: Willis, C. L. (Supervisor) & Crump, M. P. (Supervisor)

Capturing complexity, comorbidity and frailty in people with parkinsonism and understanding their impact

Supervisor: Ben-Shlomo, Y. (Supervisor) & Henderson, E. (Supervisor)

Causal implications of common infections and platelet function on cardiovascular disease

Supervisor: Paternoster, L. (Supervisor), Richmond, R. (Supervisor), Davey Smith, G. (Supervisor) & Poole, A. (Supervisor)

Causal pathways from cognitive ability to Alzheimer's disease

Supervisor: Davies, N. M. (Supervisor), Anderson, E. L. (Supervisor), Howe, L. D. (Supervisor) & Ben-Shlomo, Y. (Supervisor)

Characterisation of Ataxia Telangiectasia Mutated in RPE-1 cells and its role in cellular sensitivity to hypo-osmotic stress

Supervisor: Mellor, H. H. (Supervisor) & Wood, W. J. (Supervisor)

Characterisation of the cellular compartments containing inhibitory receptors in CD8 + T cells

Supervisor: Wuelfing, C. (Supervisor) & Morgan, D. (Supervisor)

Characterisation of the HELLS and Irc5 subfamily of chromatin remodellers

Supervisor: Dillingham, M. (Supervisor) & Chambers, A. (Supervisor)

Characterising Red Cell-Derived Vesicles in Sickle Cell Disease and Investigating Potential to Induce Tolerance to Human Red Cell Antigens

Supervisor: Blair, A. (Supervisor) & Anstee, D. J. (Supervisor)

Complex trait architecture through the lens of epigenome-wide association studies

Supervisor: Gaunt, T. (Supervisor), Hemani, G. (Supervisor) & Timpson, N. J. (Supervisor)

Decentralised Algorithms for Area Coverage

Supervisor: Ganesh, A. (Supervisor) & Hauert, S. (Supervisor)

Dental care pathways and parent-reported dental outcomes for 5-year-old children born with a cleft in the UK

Supervisor: Fowler, P. V. (Supervisor), Leary, S. D. (Supervisor), Wren, Y. E. (Supervisor) & Williams, J. (Supervisor)

Student thesis : Doctoral Thesis › Doctor of Dental Surgery (DDS)

Diabetes mellitus causes adiposopathy in bone marrow: investigation of the underpinning cellular and molecular mechanisms

Supervisor: Madeddu, P. (Supervisor) & Mellor, H. H. (Supervisor)

Does the association between later eating rhythm and childhood adiposity differ between the UK and China?

Supervisor: Leary, S. D. (Supervisor) & Northstone, K. (Supervisor)

Does the IGF axis influence EMT to play a role in bladder cancer progression?

Supervisor: Perks, C. (Supervisor) & Holly, J. M. P. (Supervisor)

Elucidating mechanisms of tumour resistance to checkpoint blockade

Supervisor: Wooldridge, L. (Supervisor), Morgan, D. (Supervisor) & Wuelfing, C. (Supervisor)

Enhanced numerical techniques for time domain electromagnetic analysis

Evaluation of a primary care epilepsy specialist nurse service.

Supervisor: Bachmann, M. (Supervisor)

Evaluation of Cardiopulmonary Exercise Testing (CPET) as a Prognostic Tool in Idiopathic Pulmonary Fibrosis (IPF)

Supervisor: Maskell, N. (Supervisor) & Millar, A. (Supervisor)

Evolving Morphological Adaption Methods in Compliant Robots

Supervisor: Hauser, H. (Supervisor) & Hauert, S. (Supervisor)

Examining the Role of Placental-derived MicroRNA Secretions in Response to Gestational Hypoxia on Foetal Neurodevelopment

Supervisor: Case, C. P. (Supervisor), Perks, C. M. (Supervisor), Uney, J. B. (Supervisor) & Fulga, T. A. (External person) (Supervisor)

Expertise during surgical innovation: advancing understanding about non-technical skills and related optimisation factors

Supervisor: Mills, N. (Supervisor), Blencowe, N. (Supervisor) & Blazeby, J. (Supervisor)

Exploring the effect of adiposity on platelet function and related pathways: implications for cardiovascular disease

Supervisor: Timpson, N. (Supervisor) & Hers, I. (Supervisor)

Exploring the in vitro behaviour of endothelial cells in different cell culture models

Supervisor: Mellor, H. (Supervisor) & Gaston, K. (Supervisor)

Exploring the microclot-driven pre-metastatic niche: live imaging studies in zebrafish larvae

Supervisor: Martin, P. B. (Supervisor) & Nobes, C. D. (Supervisor)

Exploring the role of BCL-3 in colorectal cancer cell therapeutic resistance

Supervisor: Martin, P. (Supervisor), Cullen, P. (Supervisor) & Williams, A. (Supervisor)

Extra-pulmonary effects of lung function and lung disease

Supervisor: Davey Smith, G. (Supervisor), Dodd, J. (Supervisor) & Granell, R. (Supervisor)

Fatty acid construction within the biosynthesis of the polyketide antibiotic mupirocin

Supervisor: Crump, M. P. (Supervisor), Willis, C. (External person) (Supervisor) & Race, P. R. (Supervisor)

Feeding and Autoimmunity in Children with Down’s Syndrome Evaluation Study (FADES)

Supervisor: Hamilton-Shield, J. P. (Supervisor), Gillespie, K. M. (Supervisor) & Leary, S. D. (Supervisor)

From peptide oligomers to single-chain proteins

Supervisor: Woolfson, D. (Supervisor) & Crump, M. (Supervisor)

Genetic and Environmental Contributions to Trajectories of Depressive Symptoms

Supervisor: Manley, D. (Supervisor), Timpson, N. J. (Supervisor) & Leckie, G. (Supervisor)

Genetic and epidemiologic approaches to elucidate the role of abnormal hip shape in the development of hip osteoarthritis

Supervisor: Davey Smith, G. (Supervisor) & Tobias, J. (Supervisor)

Genetic and epigenetic data as a tool to augment understanding of oropharyngeal cancer

Supervisor: Relton, C. L. (Supervisor), Thomas, S. J. (Supervisor), Richmond, R. C. (Supervisor) & Elliott, H. R. (Supervisor)

Geographical gene-environment interaction and correlation for mental health in the UK and Sweden

Supervisor: Davis, O. S. (Supervisor) & Davey Smith, G. (Supervisor)

Glial autophagy capability and the control of neuroinflammatory signaling in Parkinson’s disease.

Supervisor: Lane, J. D. (Supervisor) & Carroll, B. M. (Supervisor)

'Hi-Fi Nanoscience' : Exploring the nanoscale with optical pickup units

Supervisor: Payton, O. D. (Supervisor) & Day, J. C. C. (Supervisor)

High-throughput proteomic analysis of the dengue virus secretome and the identification of plasma biomarkers of disease severity

Supervisor: Morgan, D. (Supervisor) & Davidson, A. (Supervisor)

Identification of Protein Disulphide-Isomerase A3 Dependent Proteins from the Secretome of MDA-MB-231 Breast Cancer Cells

Supervisor: Adams, J. (Supervisor)

UKnowledge > College of Medicine > Toxicology and Cancer Biology > Theses & Dissertations

Theses and Dissertations--Toxicology and Cancer Biology

Theses/dissertations from 2024 2024.

Elucidation of Mismatch Repair Regulation by ABL1: Advantages/Disadvantages of Tyrosine Kinase Inhibitor Treatment , Hannah Daniels

ACQUIRED TREATMENT RESISTANCE IN PROSTATE CANCER VIA THE PRODUCTION OF RADIATION DERIVED EXTRACELLULAR VESICLES CONTAINING MITOCHONDRIAL PROTEINS , Caitlin Miller

Theses/Dissertations from 2023 2023

ELUCIDATING THE FUNCTIONAL IMPORTANCE OF PEROXIREDOXIN IV IN PROSTATE CANCER AND ITS SECRETION MECHANISM , Na Ding

Targeting EZH2 to Improve Outcomes of Lung Squamous Cell Carcinoma , Tanner DuCote

UNDERSTANDING AND TARGETING THE TPH1-SEROTONIN-HTR3A AXIS IN SMALL CELL LUNG CANCER , Yanning Hao

CONSERVED NOVEL INTERACTIONS BETWEEN POST-REPLICATIVE REPAIR AND MISMATCH REPAIR PROTEINS HAVE DIFFERENTIAL EFFECTS ON DNA REPAIR PATHWAYS , Anna K. Miller

UNDERSTANDING THE ROLE OF PEROXIREDOXIN IV IN COLORECTAL CANCER DEVELOPMENT , Pratik Thapa

BEYOND MITOSIS, PLK1-MEDIATED PHOSPHORYLATION RE-WIRES CANCER METABOLISM AND PROMOTES CANCER PROGRESSION , Qiongsi Zhang

Theses/Dissertations from 2022 2022

ELUCIDATING THE ROLE OF POLYCOMB REPRESSIVE COMPLEX 2 IN LUNG STEM CELL FATE AND LUNG DISEASE , Aria Byrd

SEX DIMORPHISM IN HEMATOPOIESIS AND BONE MARROW NICHE , xiaojing cui

EXTRACELLULAR VESICLES AND CANCER THERAPY: AN INSIGHT INTO THE ROLE OF OXIDATIVE STRESS , Jenni Ho

OVERCOMING RESISTANCE TO SG-ARIS IN CASTRATION-RESISTANT PROSTATE CANCER , Chaohao Li

Theses/Dissertations from 2021 2021

THE TUMOR SUPPRESSOR PAR-4 REGULATES HYPERTROPHIC OBESITY , Nathalia Araujo

Epigenetic States Regulate Tumor Aggressiveness and Response to Targeted Therapies in Lung Adenocarcinoma , Fan Chen

DELINEATING THE ROLE OF FATTY ACID METABOLISM TO IMPROVE THERAPEUTIC STRATEGIES FOR COLORECTAL CANCER , James Drury

DEVELOPMENT OF TOOLS FOR ATOM-LEVEL INTERPRETATION OF STABLE ISOTOPE-RESOLVED METABOLOMICS DATASETS , Huan Jin

MECHANISMS OF CADMIUM-INDUCED AND EPIDERMAL GROWTH FACTOR RECEPTOR MUTATION-DRIVEN LUNG TUMORIGENESIS , Hsuan-Pei Lin

SCIENCE-BASED REGULATION OF PHARMACOLOGICAL SUBSTANCES IN COMPETITION HORSES , Jacob Machin

A NOVEL ROLE FOR NEUROTENSIN IN REGULATION OF STEM CELL FUNCTION IN THE SMALL INTESTINE , Stephanie Rock

Theses/Dissertations from 2020 2020

NOVEL POST-TRANSLATIONAL MODIFICATION AND FUNCTION OF FUS: THE RELEVANCE TO AMYOTROPHIC LATERAL SCLEROSIS , Alexandra Arenas

Prostate Cancer Resistance to Cabazitaxel Chemotherapy , Diane Begemann

Examining the Role of Metabolic Pathways as Therapeutic Modalities for Triple Negative Breast Cancer , Jeremy Andrew Johnson

THE ROLE OF NEURAL PRECURSOR CELL EXPRESSED DEVELOPMENTALLY DOWN-REGULATED PROTEIN 9 IN ENHANCED AGGRESSIVENESS OF HEXAVALENT CHROMIUM TRANSFORMED BRONCHIAL EPITHELIAL CELLS , Peter Van Wie

Theses/Dissertations from 2019 2019

A COMPROMISED LIVER ALTERS PCB TOXICITY AND NUTRIENT METABOLISM , Jazmyne D. L. Barney

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Identifying prognostic biomarkers for cancer using gene expression data

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Thesis: Surviving Cervical Cancer: A History of Prevention, Early Detection, and Treatment

Editor's note:

Alexis Darby defended her thesis titled “Surviving Cervical Cancer: A History of Prevention, Early Detection, and Treatment,” in May 2019 in front of committee members Jane Maienschein, Carolina Abboud, and Karin Ellison, earning her a Bachelor’s degree from Barrett, the Honors College. https://repository.asu.edu/items/53339

Cervical cancer, which many physicians as of 2019 consider to be a success in terms of establishing widely used forms of early preventative and diagnostic technologies, experienced a reduction in incidence rates in women by over fifty percent between 1975 and 2016. Cervical cancer does not often present in women with symptoms until it has entered a later stage of the disease. Because of this fact, in the early twentieth century, physicians were often only able to diagnose cervical cancer when either the woman reported complaints or there was a visual confirmation of lesions on the cervix. The symptoms women often reported included vague abdominal pain, bleeding after sex, and abnormal amounts of vaginal discharge, all of which are non-specific symptoms, making it even harder for women to be diagnosed with cervical cancer.

This thesis answers the following question: How does the history of cervical cancer show that prevention helps reduce rates of cancer-related deaths among women? By studying the history of cervical cancer, people can understand how a cancer that was once one of the top killers of women in the US has declined to become one of the lowest through the establishment of and effective communication of early prevention and diagnostics, both among the general public and within the medical community itself. This thesis is organized based on key episodes which were pertinent to the history of cervical cancer, primarily within the United States and Europe. The episodes are organized in context of the shifts in thought regarding cervical cancer and include topics such as vaccine technologies like the Gardasil and Cervarix vaccines, social awareness movements that educated women on the importance of early detection, and analyses of the early preventative strategies and attempts at treating cervical cancer.

After analyzing eleven key episodes, the thesis determined that, through the narrative of early attempts to treat cervical cancer, shifting the societal thought on cancer, evolving the importance of early detection, and, finally, obtaining a means of prevention, the history of cervical cancer does demonstrate that the development of preventative strategies has resulted in reducing cancer-related deaths among women. Understanding what it took for physicians to evolve from simply detecting cervical cancer to being able to prevent it entirely matters because it can change the way we think about managing other forms of cancer.

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• Open access
• Published: 26 November 2018

The 150 most important questions in cancer research and clinical oncology series: questions 94–101

Edited by Cancer Communications

Cancer Communications

Cancer Communications volume  38 , Article number:  69 ( 2018 ) Cite this article

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Since the beginning of 2017, Cancer Communications (former title: Chinese Journal of Cancer ) has published a series of important questions regarding cancer research and clinical oncology, to provide an enhanced stimulus for cancer research, and to accelerate collaborations between institutions and investigators. In this edition, the following 8 valuable questions are presented. Question 94. The origin of tumors: time for a new paradigm? Question 95. How can we accelerate the identification of biomarkers for the early detection of pancreatic ductal adenocarcinoma? Question 96. Can we improve the treatment outcomes of metastatic pancreatic ductal adenocarcinoma through precision medicine guided by a combination of the genetic and proteomic information of the tumor? Question 97. What are the parameters that determine a competent immune system that gives a complete response to cancers after immune induction? Question 98. Is high local concentration of metformin essential for its anti-cancer activity? Question 99. How can we monitor the emergence of cancer cells anywhere in the body through plasma testing? Question 100. Can phytochemicals be more specific and efficient at targeting P-glycoproteins to overcome multi-drug resistance in cancer cells? Question 101. Is cell migration a selectable trait in the natural evolution of carcinoma?

Until now, the battle against cancer is still ongoing, but there are also ongoing discoveries being made. Milestones in cancer research and treatments are being achieved every year; at a quicker pace, as compared to decades ago. Likewise, some cancers that were considered incurable are now partly curable, lives that could not be saved are now being saved, and for those with yet little options, they are now having best-supporting care. With an objective to promote worldwide cancer research and even accelerate inter-countries collaborations, since the beginning of 2017, Cancer Communications (former title: Chinese Journal of Cancer ) has launched a program of publishing 150 most important questions in cancer research and clinical oncology [ 1 ]. We are providing a platform for researchers to freely voice-out their novel ideas, and propositions to enhance the communications on how and where our focus should be placed [ 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 ]. In this edition, 8 valuable and inspiring questions, Question 94–101, from highly distinguished professionals from different parts of the world are presented. If you have any novel proposition(s) and Question(s), please feel free to contact Ms. Ji Ruan via email: [email protected].

Question 94: The origin of tumors: time for a new paradigm?

Background and implications.

“There is no worse blind man than the one who doesn’t want to see. There is no worse deaf man than the one who doesn’t want to hear. And there is no worse madman than the one who doesn’t want to understand.” —Ancient Proverb

In the past half-century, cancer biologists have focused on a dogma in which cancer was viewed as a proliferative disease due to mechanisms that activate genes (oncogenes) to promote cell proliferation or inactivate genes (tumor suppressor genes) to suppress tumor growth. In retrospect, these concepts were established based on functional selections, by using tissue culture (largely mouse NIH 3T3 cells) for the selection of transformed foci at the time when we knew virtually nothing about the human genome [ 14 ]. However, it is very difficult to use these genes individually or in combinations to transform primary human cells. Further, the simplified view of uncontrolled proliferation cannot explain the tumor as being a malignant organ or a teratoma, as observed by pathologists over centuries. Recently, the cancer genomic atlas project has revealed a wide variety of genetic alterations ranging from no mutation to multiple chromosomal deletions or fragmentations, which make the identification of cancer driver mutations very challenging in a background of such a massive genomic rearrangement. Paradoxically, this increase the evidences demonstrating that the oncogenic mutations are commonly found in many normal tissues, further challenging the dogma that genetic alteration is the primary driver of this disease.

Logically, the birth of a tumor should undergo an embryonic-like development at the beginning, similar to that of a human. However, the nature of such somatic-derived early embryo has been elusive. Recently, we provided evidence to show that polyploid giant cancer cells (PGCCs), which have been previously considered non-dividing, are actually capable of self-renewal, generating viable daughter cells via amitotic budding, splitting and burst, and capable of acquisition of embryonic-like stemness [ 15 , 16 , 17 ]. The mode of PGCC division is remarkably similar to that of blastomere, a first step in human embryogenesis following fertilization. The blastomere nucleus continuously divides 4–5 times without cytoplasmic division to generate 16–32 cells and then to form compaction/morulae before developing into a blastocyst [ 18 ]. Based on these data and similarity to the earliest stage of human embryogenesis, I propose a new theory that tumor initiation can be achieved via a dualistic origin, similar to the first step of human embryogenesis via the formation of blastomere-like cells, i.e. the activation of blastomere or blastomere-like cells which leads to the dedifferentiation of germ cells or somatic cells, respectively, which is then followed by the differentiation to generate their respective stem cells, and the differentiation arrest at a specific developmental hierarchy leading to tumor initiation [ 19 ]. The somatic-derived blastomere-like cancer stem cell follows its own mode of cell growth and division and is named as the giant cell cycle. This cycle includes four distinct but overlapping phases: the initiation, self-renewal, termination, and stability phases. The giant cell cycle can be tracked in vitro and in vivo due to their salient giant cell morphology (Fig.  1 ).

One mononucleated polyploid giant cancer cell (PGCC) in the background of regular size diploid cancer cells. The PGCC can be seen to be at least 100 times larger than that of regular cancer cells

This new theory challenges the traditional paradigm that cancer is a proliferative disease, and proposes that the initiation of cancer requires blastomere-like division that is similar to that of humans before achieving stable proliferation at specific developmental hierarchy in at least half of all human cancers. This question calls for all investigators in the cancer research community to investigate the role of PGCCs in the initiation, progression, resistance, and metastasis of cancer and to look for novel agents to block the different stages of the giant cell cycle.

The histopathology (phenotype) of cancers has been there all the time. It is just the theory of cancer origin proposed by scientists that changes from time to time. After all, trillions of dollars have been invested in fighting this disease by basing on its genetic origin in the past half-century, yet, little insight has been gained [ 14 ]. Here are two quotes from Einstein: “Insanity: doing the same thing over and over again expecting different results”, and “We cannot solve our problems with the same thinking we used when created them”.

In short, it is time to change our mindset and to start pursuing PGCCs, which we can observe under the microscope. But with very little understanding about these cells, it is time for a shift in paradigm.

Jinsong Liu.

Affiliation

Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030-4095, USA.

Email address

[email protected]

Question 95: How can we accelerate the identification of biomarkers for the early detection of pancreatic ductal adenocarcinoma?

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers in the world with a dismal 5-year overall survival rate of less than 5%; which has not been significantly improved since the past decades. Although surgical resection is the only option for curative treatment of PDAC, only 15%–20% of patients with PDAC have the chance to undergo curative resection, leaving the rest with only palliative options in hope for increasing their quality of life; since they were already at unresectable and non-curative stages at their first diagnosis.

The lack of specific symptoms in the early-stage of PDAC is responsible for rendering an early diagnosis difficult. Therefore, more sensitive and specific screening methodologies for its early detection is urgently needed to improve its diagnosis, starting early treatments, and ameliorating prognoses. The diagnosis so far relies on imaging modalities such as abdominal ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), endoscopic ultrasound (EUS), endoscopic retrograde cholangiopancreatography (ERCP), and positron emission tomography (PET). One may propose to screen for pancreatic cancer in high-risk populations, which is highly recommended, however screening intervention for all the people is not a wise choice; when considering the relatively low prevalence of PDAC, and the difficulty for diagnosing it in its early stage [ 20 ].

Therefore, alternative diagnostic tools for early detection of PDAC are highly expected. Among the biomarkers currently used in clinical practice, carbohydrate antigen 19–9 (CA19–9) is among the most useful one for supporting the diagnosis of PDAC, but it is neither sufficiently sensitive nor specific for its early detection. Yachida et al. reported in 2010 that the initiating mutation in the pancreas occurs approximately two decades before the PDAC to start growing in distant organs [ 21 ], which indicates a broad time of the window of opportunity for the early detection of PDAC. With the advancement in next-generation sequencing technology, the number of reported studies regarding novel potential molecular biomarkers in bodily fluids including the blood, feces, urine, saliva, and pancreatic juice for early detection of PDAC has been increasing. Such biomarkers may be susceptible to detect mutations at the genetic or epigenetic level, identifying important non-coding RNA (especially microRNA and long non-coding RNA), providing insights regarding the metabolic profiles, estimating the tumor level in liquid biopsies (circulating free DNA, circulating tumor cells and exosomes), and so on.

Another approach to identifying biomarkers for the early detection of pancreatic cancer is using animal models. In spontaneous animal models of pancreatic cancer, such as Kras-mutated mouse models, it is expected that by high throughput analyses of the genetic/epigenetic/proteomic alterations, some novel biomarkers might be able to be identified. For instance, Sharma et al. reported in 2017 that the detection of phosphatidylserine-positive exosomes enabled the diagnosis of early-stage malignancies in LSL-Kras G12D , Cdkn2a lox/lox : p48 Cre and LSL-Kras G12d/+ , LSL-Trp R172H/+ , and P48 Cre mice [ 22 ].

These analyses in clinical samples or animal models hold the clues for the early detection of PDAC, however, further studies are required to validate their diagnostic performance. What’s most important, will be the lining-up of these identified prospective biomarkers, to validate their sensitivities and specificities. This will determine their potential for widespread clinical applicability, and hopefully, accelerate the early diagnosis of PDAC.

Mikiya Takao 1,2 , Hirotaka Matsuo 2 , Junji Yamamoto 1 , and Nariyoshi Shinomiya 2 .

1 Department of Surgery, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan; 2 Department of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan.

E-mail address

[email protected]; [email protected]; [email protected]; [email protected]

Question 96: Can we improve the treatment outcomes of metastatic pancreatic ductal adenocarcinoma through precision medicine guided by a combination of the genetic and proteomic information of the tumor?

Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant cancers, and nearly half of the patients had metastatic PDAC when they are initially diagnosed. When they are accompanied by metastatic tumors, unlike most solid cancer, PDAC cannot be cured with primary surgical resection alone [ 23 , 24 ]. Also, since PDAC has poor responses to conventional therapies, improvements in adjunctive treatment approach including chemo- and immuno-therapy are earnestly required. From this standpoint, recent results regarding the differences in the molecular evolution of pancreatic cancer subtypes provide a new insight into its therapeutic development [ 25 ], which may lead to the improvement of the prognosis of not only metastatic PDAC but also of locally advanced or recurrent PDAC.

In fact, new chemotherapeutic regimens such as the combination of gemcitabine with nab-paclitaxel and FOLFIRINOX have been reported to show improved prognosis despite a lack of examples of past successes in the treatment of patients with metastatic PDAC who had undergone R0 resection [ 26 ]. While many mutations including KRAS , CDKN2A , TP53, and SMAD4 are associated with pancreatic carcinogenesis, no effective molecular targeted drug has been introduced in the clinical setting so far. A recent report of a phase I/II study on refametinib, a MEK inhibitor, indicated that KRAS mutation status might affect the overall response rate, disease control rate, progression-free survival, and overall survival of PDAC in combination with gemcitabine [ 27 ].

While immunotherapy is expected to bring a great improvement in cancer treatment, until now, immune checkpoint inhibitors have achieved limited clinical benefit for patients with PDAC. This might be because PDAC creates a uniquely immunosuppressive tumor microenvironment, where tumor-associated immunosuppressive cells and accompanying desmoplastic stroma prevent the tumor cells from T cell infiltration. Recently reported studies have indicated that immunotherapy might be effective when combined with focal adhesion kinase (FAK) inhibitor [ 28 ] or IL-6 inhibitor [ 29 ], but more studies are required to validate their use in clinical practice.

As such, we believe that if the dynamic monitoring of drug sensitivity/resistance in the individual patients is coupled with precision treatment based on individualized genetics/epigenetics/proteomics alterations in the patients’ tumor, this could improve the treatment outcomes of PDAC.

Mikiya Takao 1,2 , Hirotaka Matsuo 2 , Junji Yamamoto 1 , and Nariyoshi Shinomiya 2.

Question 97: What are the parameters that determine a competent immune system that gives a complete response to cancers after immune induction?

Recently, cancer immunotherapy has shown great clinical benefit in multiple types of cancers [ 30 , 31 , 32 ]. It has provided new approaches for cancer treatment. However, it has been observed that only a fraction of patients respond to immunotherapy.

Much effort has been made to identify markers for immunotherapeutic response. Tumor mutation burden (TMB), mismatch repair (MMR) deficiency, PD-L1 expression, and tumor infiltration lymphocyte (TIL) have been found to be associated with an increased response rate in checkpoint blockade therapies. Unfortunately, a precise prediction is still challenging in this field. Moreover, when to stop the treatment of immunotherapy is an urgent question that remains to be elucidated.

In other words, there is no available approach to determine if a patient has generated a good immune response against the cancer after immunotherapy treatments. All of these indicate the complexity and challenges that reside for implementing novel man-induced cancer-effective immune response therapeutics. A variety of immune cells play collaborative roles at different stages to recognize antigens and eventually to generate an effective anti-cancer immune response. Given the high complexity of the immune system, a rational evaluation approach is needed to cover the whole process. Moreover, we need to perfect vaccine immunization and/or in vitro activation of T cells to augment the function of the immune system; particularly the formation of immune memory.

Edison Liu 1 , Penghui Zhou 2 , Jiang Li 2 .

1 The Jackson Laboratory, Bar Harbor, ME 04609, USA; 2 Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, P. R. China.

[email protected]; [email protected]; [email protected]

Question 98: Is high local concentration of metformin essential for its anti-cancer activity?

Metformin was approved as a first line of anti-diabetic drug since decades. Interestingly, the fact that clinical epidemiological studies have shown that metformin can reduce the risk of a variety of cancers stimulates considerable recognition to explore its anticancer activity.

Although the in vitro and in vivo experimental results have demonstrated that metformin can have some potential anti-tumor effects, more than 100 clinical trials did not achieve such desirable results [ 33 ]. We and others believe that the main problem resides in the prescribing doses used. For cancer treatment, a much higher dose may be needed for observing any anti-tumor activities, as compared to the doses prescribed for diabetics [ 34 , 35 , 36 ].

Further, if the traditional local/oral administration approach is favored, the prescribed metformin may not be at the required dose-concentration once it reaches the blood to have the effective anti-cancer activities. We, therefore, propose that intravesical instillation of metformin into the bladder lumen could be a promising way to treat for bladder cancer, at least. We have already obtained encouraging results both in vitro and in vivo experiments, including in an orthotopical bladder cancer model [ 36 , 37 ]. Now, we are waiting to observe its prospective clinical outcome.

Mei Peng 1 , Xiaoping Yang 2 .

1 Department of Pharmacy, Xiangya Hospital, Central South University. Changsha, Hunan 410083, P. R. China; 2 Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha, Hunan 410013, P. R. China.

[email protected]; [email protected]

Question 99: How can we monitor the emergence of cancer cells anywhere in the body through plasma testing?

The early detection of cancer is still a relentless worldwide challenge. The sensitivity and specificity of traditional blood tumor markers and imaging technologies are still to be greatly improved. Hence, novel approaches for the early detection of cancer are urgently needed.

The emergence of liquid biopsy technologies opens a new driveway for solving such issues. According to the definition of the National Cancer Institute of the United States, a liquid biopsy is a test done on a sample of blood to look for tumorigenic cancer cells or pieces of tumor cells’ DNA that are circulating in the blood [ 38 ]. This definition implies two main types of the current liquid biopsy: one that detects circulating tumor cells and the other that detects non-cellular material in the blood, including tumor DNA, RNA, and exosomes.

Circulating tumor cells (CTCs) are referred to as tumor cells that have been shed from the primary tumor location and have found their way to the peripheral blood. CTCs were first described in 1869 by an Australian pathologist, Thomas Ashworth, in a patient with metastatic cancer [ 39 ]. The importance of CTCs in modern cancer research began in the mid-1990s with the demonstration that CTCs exist early in the course of the disease.

It is estimated that there are about 1–10 CTCs per mL in whole blood of patients with metastatic cancer, even fewer in patients with early-stage cancer [ 40 ]. For comparison, 1 mL of blood contains a few million white blood cells and a billion erythrocytes. The identification of CTCs, being in such low frequency, requires some special tumoral markers (e.g., EpCAM and cytokeratins) to capture and isolate them. Unfortunately, the common markers for recognizing the majority of CTCs are not effective enough for clinical application [ 41 ]. Although accumulated evidences have shown that the presence of CTCs is a strong negative prognostic factor in the patients with metastatic breast, lung and colorectal cancers, detecting CTCs might not be an ideal branch to hold on for the hope of early cancer detection [ 42 , 43 , 44 , 45 ].

Circulating tumor DNA (ctDNA) is tumor-derived fragmented DNA in the circulatory system, which is mainly derived from the tumor cell death through necrosis and/or apoptosis [ 46 ]. Given its origin, ctDNA inherently carries cancer-specific genetic and epigenetic aberrations, which can be used as a surrogate source of tumor DNA for cancer diagnosis and prognostic prediction. Ideally, as a noninvasive tumor early screening tool, a liquid biopsy test should be able to detect many types of cancers and provide the information of tumor origin for further specific clinical management. In fact, the somatic mutations of ctDNA in different types of tumor are highly variable, even in the different individuals with the same type of tumor [ 47 ]. Additionally, most tumors do not possess driver mutations, with some notable exceptions, which make the somatic mutations of ctDNA not suitable for early detection of the tumor.

Increased methylation of the promoter regions of tumor suppressor genes is an early event in many types of tumor, suggesting that altered ctDNA methylation patterns could be one of the first detectable neoplastic changes associated with tumorigenesis [ 48 ]. ctDNA methylation profiling provides several advantages over somatic mutation analysis for cancer detection including higher clinical sensitivity and dynamic range, multiple detectable methylation target regions, and multiple altered CpG sites within each targeted genomic region. Further, each methylation marker is present in both cancer tissue and ctDNA, whereas only a fraction of mutations present in cancer tissue could be detected in ctDNA.

In 2017, there were two inspiring studies that revealed the values of using ctDNA methylation analysis for cancer early diagnosis [ 49 , 50 ]. After partitioning the human genome into blocks of tightly coupled CpG methylation sites, namely methylation haplotype blocks (MHBs), Guo and colleagues performed tissue-specific methylation analyses at the MHBs level to accurately determine the tissue origin of the cancer using ctDNA from their enrolled patients [ 49 ]. In another study, Xu and colleagues identified a hepatocellular carcinoma (HCC) enriched methylation marker panel by comparing the HCC tissue and blood leukocytes from normal individuals and showed that methylation profiles of HCC tumor DNA and matched plasma ctDNA were highly correlated. In this study, after quantitative measurement of the methylation level of candidate markers in ctDNA from a large cohort of 1098 HCC patients and 835 normal controls, ten methylation markers were selected to construct a diagnostic prediction model. The proposed model demonstrated a high diagnostic specificity and sensitivity, and was highly correlated with tumor burden, treatment response, and tumor stage [ 50 ].

With the rapid development of highly sensitive detection methods, especially the technologies of massively parallel sequencing or next-generation sequencing (NGS)-based assays and digital PCR (dPCR), we strongly believe that the identification of a broader “pan-cancer” methylation panel applied for ctDNA analyses, probably in combination with detections of somatic mutation and tumor-derived exosomes, would allow more effective screening for common cancers in the near future.

Edison Liu 1 , Hui-Yan Luo 2 .

[email protected]; [email protected]

Question 100: Can phytochemicals be more specific and efficient at targeting P-glycoproteins to overcome multi-drug resistance in cancer cells?

Though several anticancer agents are approved to treat different types of cancers, their full potentials have been limited due to the occurrence of drug resistance. Resistance to anticancer drugs develops by a variety of mechanisms, one of which is increased drug efflux by transporters. The ATP-binding cassette (ABC) family drug efflux transporter P-glycoprotein (P-gp or multi-drug resistance protein 1 [MDRP1]) has been extensively studied and is known to play a major role in the development of multi-drug resistance (MDR) to chemotherapy [ 51 ]. In brief, overexpressed P-gp efflux out a wide variety of anticancer agents (e.g.: vinca alkaloids, doxorubicin, paclitaxel, etc.), leading to a lower concentration of these drugs inside cancer cells, thereby resulting in MDR. Over the past three decades, researchers have developed several synthetic P-gp inhibitors to block the efflux of anticancer drugs and have tested them in clinical trials, in combination with chemotherapeutic drugs. But none were found to be suitable enough in overcoming MDR and to be released for marketing, mainly due to the side effects associated with cross-reactivity towards other ABC transporters (BCRP and MRP-1) and the inhibition of CYP450 drug metabolizing enzymes [ 52 , 53 ].

On the other hand, a number of phytochemicals have been reported to have P-gp inhibitory activity. Moreover, detailed structure–activity studies on these phytochemicals have delineated the functional groups essential for P-gp inhibition [ 53 , 54 ]. Currently, one of the phytochemicals, tetrandrine (CBT-1 ® ; NSC-77037), is being used in a Phase I clinical trial ( http://www.ClinicalTrials.gov ; NCT03002805) in combination with doxorubicin for the treatment of metastatic sarcoma. Before developing phytochemicals or their derivatives as P-gp inhibitors, they need to be investigated thoroughly for their cross-reactivity towards other ABC transporters and CYP450 inhibition, in order to avoid toxicities similar to the older generation P-gp inhibitors that have failed in clinical trials.

Therefore, the selectivity for P-gp over other drug transporters and drug metabolizing enzymes should be considered as important criterias for the development of phytochemicals and their derivatives for overcoming MDR.

Mohane Selvaraj Coumar and Safiulla Basha Syed.

Centre for Bioinformatics, School of Life Sciences, Pondicherry University, Kalapet, Puducherry 605014, India.

[email protected]; [email protected]

Question 101: Is cell migration a selectable trait in the natural evolution of carcinoma?

The propensity of solid tumor malignancy to metastasize remains the main cause of cancer-related death, an extraordinary unmet clinical need, and an unanswered question in basic cancer research. While dissemination has been traditionally viewed as a late process in the progression of malignant tumors, amount of evidence indicates that it can occur early in the natural history of cancer, frequently when the primary lesion is still barely detectable.

A prerequisite for cancer dissemination is the acquisition of migratory/invasive properties. However, whether, and if so, how the migratory phenotype is selected for during the natural evolution of cancer and what advantage, if any, it may provide to the growing malignant cells remains an open issue. The answers to these questions are relevant not only for our understating of cancer biology but also for the strategies we adopt in an attempt of curbing this disease. Frequently, indeed, particularly in pharmaceutical settings, targeting migration has been considered much like trying “to shut the stable door after the horse has bolted” and no serious efforts in pursuing this aim has been done.

We argue, instead, that migration might be an intrinsic cancer trait that much like proliferation or increased survival confers to the growing tumor masses with striking selective advantages. The most compelling evidence in support for this contention stems from studies using mathematical modeling of cancer evolution. Surprisingly, these works highlighted the notion that cell migration is an intrinsic, selectable property of malignant cells, so intimately intertwined with more obvious evolutionarily-driven cancer traits to directly impact not only on the potential of malignant cells to disseminate but also on their growth dynamics, and ultimately provide a selective evolutionary advantage. Whether in real life this holds true remains to be assessed, nevertheless, work of this kind defines a framework where the acquisition of migration can be understood in a term of not just as a way to spread, but also to trigger the emergence of malignant clones with favorable genetic or epigenetic traits.

Alternatively, migratory phenotypes might emerge as a response to unfavorable conditions, including the mechanically challenging environment which tumors, and particularly epithelial-derived carcinoma, invariably experience. Becoming motile, however, may not per se being fixed as phenotypic advantageous traits unless it is accompanied or is causing the emergence of specific traits, including drug resistance, self-renewal, and survival. This might be the case, for example, during the process of epithelial-to-mesenchymal transition (EMT), which is emerging as an overarching mechanism for dissemination. EMT, indeed, may transiently equip individual cancer cells not only with migratory/invasive capacity but also with increased resistance to drug treatment, stemness potential at the expanse of fast proliferation.

Thus, within this framework targeting pro-migratory genes, proteins and processes may become a therapeutically valid alternative or a complementary strategy not only to control carcinoma dissemination but also its progression and development.

Giorgio Scita.

IFOM, The FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy; Department of Oncology and Hemato-Oncology (DIPO), School of Medicine, University of Milan, Via Festa del Perdono 7, 20122, Italy.

[email protected]

Qian CN, Zhang W, Xu RH. Defeating cancer: the 150 most important questions in cancer research and clinical oncology. Chin J Cancer. 2016;35(1):104. https://doi.org/10.1186/s40880-016-0165-4 .

Article   PubMed   PubMed Central   Google Scholar  

Wee JT, Poh SS. The most important questions in cancer research and clinical oncology: question 1. Could the vertical transmission of human papilloma virus (HPV) infection account for the cause, characteristics, and epidemiology of HPV-positive oropharyngeal carcinoma, non-smoking East Asian female lung adenocarcinoma, and/or East Asian triple-negative breast carcinoma? Chin J Cancer. 2017;36(1):13. https://doi.org/10.1186/s40880-016-0168-1 .

Venniyoor A. The most important questions in cancer research and clinical oncology—Question 2–5. Obesity-related cancers: more questions than answers. Chin J Cancer. 2017;36(1):18. https://doi.org/10.1186/s40880-017-0185-8 .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 6–14: Edited by Chinese Journal of Cancer. Chin J Cancer. 2017;36(1):33. https://doi.org/10.1186/s40880-017-0200-0 .

Article   Google Scholar  

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 15–24: Edited by Chinese Journal of Cancer. Chin J Cancer. 2017;36(1):39. https://doi.org/10.1186/s40880-017-0205-8 .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 25–30: Edited by Chinese Journal of Cancer. Chin J Cancer. 2017;36(1):42. https://doi.org/10.1186/s40880-017-0210-y .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 31–39: Edited by Chinese Journal of Cancer. Chin J Cancer. 2017;36(1):48. https://doi.org/10.1186/s40880-017-0215-6 .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 40–49. Chin J Cancer. 2017;36(1):55. https://doi.org/10.1186/s40880-017-0222-7 .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 50–56. Chin J Cancer. 2017;36(1):69. https://doi.org/10.1186/s40880-017-0236-1 .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 57–66: Edited by Chinese Journal of Cancer. Chin J Cancer. 2017;36(1):79. https://doi.org/10.1186/s40880-017-0249-9 .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 67–75: Edited by Chinese Journal of Cancer. Chin J Cancer. 2017;36(1):86. https://doi.org/10.1186/s40880-017-0254-z .

Editorial Office of Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 76–85: Edited by Chinese Journal of Cancer. Chin J Cancer. 2017;36(1):91. https://doi.org/10.1186/s40880-017-0259-7 .

Chinese Journal of C. The 150 most important questions in cancer research and clinical oncology series: questions 86–93: Edited by Chinese Journal of Cancer. Chin J Cancer. 2018;37(1):1. https://doi.org/10.1186/s40880-018-0266-3 .

Weinberg RA. Coming full circle-from endless complexity to simplicity and back again. Cell. 2014;157(1):267–71. https://doi.org/10.1016/j.cell.2014.03.004 .

Article   CAS   PubMed   Google Scholar  

Niu N, Mercado-Uribe I, Liu J. Dedifferentiation into blastomere-like cancer stem cells via formation of polyploid giant cancer cells. Oncogene. 2017;36(34):4887–900. https://doi.org/10.1038/onc.2017.72 .

Article   CAS   PubMed   PubMed Central   Google Scholar  

Niu N, Zhang J, Zhang N, Mercado-Uribe I, Tao F, Han Z, et al. Linking genomic reorganization to tumor initiation via the giant cell cycle. Oncogenesis. 2016;5(12):e281. https://doi.org/10.1038/oncsis.2016.75 .

Zhang S, Mercado-Uribe I, Xing Z, Sun B, Kuang J, Liu J. Generation of cancer stem-like cells through the formation of polyploid giant cancer cells. Oncogene. 2014;33(1):116–28. https://doi.org/10.1038/onc.2013.96 .

Hemberger M, Dean W, Reik W. Epigenetic dynamics of stem cells and cell lineage commitment: digging Waddington’s canal. Nat Rev Mol Cell Biol. 2009;10(8):526–37. https://doi.org/10.1038/nrm2727 .

Liu J. The dualistic origin of human tumors. Semin Cancer Biol. 2018. https://doi.org/10.1016/j.semcancer.2018.07.004 .

Zhou B, Xu JW, Cheng YG, Gao JY, Hu SY, Wang L, et al. Early detection of pancreatic cancer: where are we now and where are we going? Int J Cancer. 2017;141(2):231–41. https://doi.org/10.1002/ijc.30670 .

Yachida S, Jones S, Bozic I, Antal T, Leary R, Fu B, et al. Distant metastasis occurs late during the genetic evolution of pancreatic cancer. Nature. 2010;467(7319):1114–7. https://doi.org/10.1038/nature09515 .

Sharma R, Huang X, Brekken RA, Schroit AJ. Detection of phosphatidylserine-positive exosomes for the diagnosis of early-stage malignancies. Br J Cancer. 2017;117(4):545–52. https://doi.org/10.1038/bjc.2017.183 .

Ryan DP, Hong TS, Bardeesy N. Pancreatic adenocarcinoma. N Engl J Med. 2014;371(11):1039–49. https://doi.org/10.1056/NEJMra1404198 .

Takada T, Yasuda H, Amano H, Yoshida M, Uchida T. Simultaneous hepatic resection with pancreato-duodenectomy for metastatic pancreatic head carcinoma: does it improve survival? Hepatogastroenterology. 1997;44(14):567–73.

CAS   PubMed   Google Scholar  

Bailey P, Chang DK, Nones K, Johns AL, Patch AM, Gingras MC, et al. Genomic analyses identify molecular subtypes of pancreatic cancer. Nature. 2016;531(7592):47–52. https://doi.org/10.1038/nature16965 .

Frigerio I, Regi P, Giardino A, Scopelliti F, Girelli R, Bassi C, et al. Downstaging in stage IV pancreatic cancer: a new population eligible for surgery? Ann Surg Oncol. 2017;24(8):2397–403. https://doi.org/10.1245/s10434-017-5885-4 .

Article   PubMed   Google Scholar  

Van Laethem JL, Riess H, Jassem J, Haas M, Martens UM, Weekes C, et al. Phase I/II study of refametinib (BAY 86-9766) in combination with gemcitabine in advanced pancreatic cancer. Target Oncol. 2017;12(1):97–109. https://doi.org/10.1007/s11523-016-0469-y .

Jiang H, Hegde S, Knolhoff BL, Zhu Y, Herndon JM, Meyer MA, et al. Targeting focal adhesion kinase renders pancreatic cancers responsive to checkpoint immunotherapy. Nat Med. 2016;22(8):851–60. https://doi.org/10.1038/nm.4123 .

Mace TA, Shakya R, Pitarresi JR, Swanson B, McQuinn CW, Loftus S, et al. IL-6 and PD-L1 antibody blockade combination therapy reduces tumour progression in murine models of pancreatic cancer. Gut. 2018;67(2):320–32. https://doi.org/10.1136/gutjnl-2016-311585 .

Immunotherapy Beats Chemo for Bladder Cancer. Cancer Discov. 2017;7(5):OF8. https://doi.org/10.1158/2159-8290.cd-nb2017-035 .

Dummer R, Ascierto PA, Gogas HJ, Arance A, Mandala M, Liszkay G, et al. Encorafenib plus binimetinib versus vemurafenib or encorafenib in patients with BRAF-mutant melanoma (COLUMBUS): a multicentre, open-label, randomised phase 3 trial. Lancet Oncol. 2018;19(5):603–15. https://doi.org/10.1016/S1470-2045(18)30142-6 .

Garassino MC, Cho BC, Kim JH, Mazieres J, Vansteenkiste J, Lena H, et al. Durvalumab as third-line or later treatment for advanced non-small-cell lung cancer (ATLANTIC): an open-label, single-arm, phase 2 study. Lancet Oncol. 2018;19(4):521–36. https://doi.org/10.1016/S1470-2045(18)30144-X .

U.S. National Library of Medicine. ClinicalTrials.gov.

Liu Z, Yokoyama NN, Blair CA, Li X, Avizonis D, Wu XR, et al. High sensitivity of an Ha-RAS transgenic model of superficial bladder cancer to metformin is associated with approximately 240-fold higher drug concentration in urine than serum. Mol Cancer Ther. 2016;15(3):430–8. https://doi.org/10.1158/1535-7163.MCT-15-0714-T .

Menendez JA, Quirantes-Pine R, Rodriguez-Gallego E, Cufi S, Corominas-Faja B, Cuyas E, et al. Oncobiguanides: paracelsus’ law and nonconventional routes for administering diabetobiguanides for cancer treatment. Oncotarget. 2014;5(9):2344–8. https://doi.org/10.18632/oncotarget.1965 .

Peng M, Su Q, Zeng Q, Li L, Liu Z, Xue L, et al. High efficacy of intravesical treatment of metformin on bladder cancer in preclinical model. Oncotarget. 2016;7(8):9102–17. https://doi.org/10.18632/oncotarget.6933 .

Peng M, Huang Y, Tao T, Peng CY, Su Q, Xu W, et al. Metformin and gefitinib cooperate to inhibit bladder cancer growth via both AMPK and EGFR pathways joining at Akt and Erk. Sci Rep. 2016;6:28611. https://doi.org/10.1038/srep28611 .

Definition of liquid biopsy. In: NCI Dictionary of Cancer Terms. National Cancer Institute. https://www.cancer.gov/publications/dictionaries/cancer-terms/def/liquid-biopsy .

Ta A. A case of cancer in which cells similar to those in the tumors were seen in the blood after death. Aust Med J. 1869;14:146–9.

Google Scholar  

Miller MC, Doyle GV, Terstappen LW. Significance of circulating tumor cells detected by the cell search system in patients with metastatic breast colorectal and prostate cancer. J Oncol. 2010;2010:617421. https://doi.org/10.1155/2010/617421 .

Nagrath S, Sequist LV, Maheswaran S, Bell DW, Irimia D, Ulkus L, et al. Isolation of rare circulating tumour cells in cancer patients by microchip technology. Nature. 2007;450(7173):1235–9. https://doi.org/10.1038/nature06385 .

Bidard FC, Proudhon C, Pierga JY. Circulating tumor cells in breast cancer. Mol Oncol. 2016;10(3):418–30. https://doi.org/10.1016/j.molonc.2016.01.001 .

Cohen SJ, Punt CJ, Iannotti N, Saidman BH, Sabbath KD, Gabrail NY, et al. Relationship of circulating tumor cells to tumor response, progression-free survival, and overall survival in patients with metastatic colorectal cancer. J Clin Oncol. 2008;26(19):3213–21. https://doi.org/10.1200/JCO.2007.15.8923 .

Ignatiadis M, Dawson SJ. Circulating tumor cells and circulating tumor DNA for precision medicine: dream or reality? Ann Oncol. 2014;25(12):2304–13. https://doi.org/10.1093/annonc/mdu480 .

Krebs MG, Sloane R, Priest L, Lancashire L, Hou JM, Greystoke A, et al. Evaluation and prognostic significance of circulating tumor cells in patients with non-small-cell lung cancer. J Clin Oncol. 2011;29(12):1556–63. https://doi.org/10.1200/JCO.2010.28.7045 .

Diaz LA Jr, Bardelli A. Liquid biopsies: genotyping circulating tumor DNA. J Clin Oncol. 2014;32(6):579–86. https://doi.org/10.1200/JCO.2012.45.2011 .

Kandoth C, McLellan MD, Vandin F, Ye K, Niu B, Lu C, et al. Mutational landscape and significance across 12 major cancer types. Nature. 2013;502(7471):333–9. https://doi.org/10.1038/nature12634 .

Esteller M. Epigenetics in cancer. N Engl J Med. 2008;358(11):1148–59. https://doi.org/10.1056/NEJMra072067 .

Guo S, Diep D, Plongthongkum N, Fung HL, Zhang K, Zhang K. Identification of methylation haplotype blocks aids in deconvolution of heterogeneous tissue samples and tumor tissue-of-origin mapping from plasma DNA. Nat Genet. 2017;49(4):635–42. https://doi.org/10.1038/ng.3805 .

Xu RH, Wei W, Krawczyk M, Wang W, Luo H, Flagg K, et al. Circulating tumour DNA methylation markers for diagnosis and prognosis of hepatocellular carcinoma. Nat Mater. 2017;16(11):1155–61. https://doi.org/10.1038/nmat4997 .

Robey RW, Pluchino KM, Hall MD, Fojo AT, Bates SE, Gottesman MM. Revisiting the role of ABC transporters in multidrug-resistant cancer. Nat Rev Cancer. 2018. https://doi.org/10.1038/s41568-018-0005-8 .

Chung FS, Santiago JS, Jesus MF, Trinidad CV, See MF. Disrupting P-glycoprotein function in clinical settings: what can we learn from the fundamental aspects of this transporter? Am J Cancer Res. 2016;6(8):1583–98.

CAS   PubMed   PubMed Central   Google Scholar  

Syed SB, Coumar MS. P-Glycoprotein mediated multidrug resistance reversal by phytochemicals: a review of SAR & future perspective for drug design. Curr Top Med Chem. 2016;16(22):2484–508.

Abdallah HM, Al-Abd AM, El-Dine RS, El-Halawany AM. P-Glycoprotein inhibitors of natural origin as potential tumor chemo-sensitizers: a review. J Adv Res. 2015;6(1):45–62. https://doi.org/10.1016/j.jare.2014.11.008 .

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Original research

Impact of social determinants of health on cancer care: a survey of community oncologists, marjorie e zettler.

1 Specialty Solutions, Cardinal Health Inc, Dublin, Ohio, USA

Bruce A Feinberg

Yolaine jeune-smith, ajeet gajra.

2 Department of Medicine, SUNY Upstate Medical University, Syracuse, New York, USA

Associated Data

Data are available on reasonable request.

Cancer survival rates have improved over the past few decades, yet socioeconomic disparities persist. Social determinants of health (SDOH) have consistently been shown to correlate with health outcomes. The objective of this study was to characterise oncologists’ perceptions of the impact of SDOH on their patients, and their opinions on how these effects could be remediated.

Cross-sectional survey of physicians.

Web-based survey completed prior to live meetings held between February and April 2020.

Participants

Oncologists/haematologists from across the USA.

Clinical practice in a community-based or hospital-based setting.

Main outcome and measure

Physician responses regarding how SDOH affected their patients, which factors represented the most significant barriers to optimal health outcomes and how the impact of SDOH could be mitigated through assistance programmes.

Of the 165 physicians who completed the survey, 93% agreed that SDOH had a significant impact on their patients’ health outcomes. Financial security/lack of insurance and access to transportation were identified most often as the greatest barriers for their patients (83% and 58%, respectively). Eighty-one per cent of physicians indicated that they and their staff had limited time to spend assisting patients with social needs, and 76% reported that assistance programmes were not readily accessible. Government organisations, hospitals, non-profit organisations and commercial payers were selected by 50% or more of oncologists surveyed as who should be responsible for delivering assistance programmes to patients with social needs; 42% indicated that pharmaceutical manufacturers should also be responsible.

Our survey found that most oncologists were aware of the impact of SDOH on their patients but were constrained in their time to assist patients with social needs. The physicians in our study identified a need for more accessible assistance programmes and greater involvement from all stakeholders in addressing SDOH to improve health outcomes.

Strengths and limitations of this study

• This study exploring the perspectives of oncologists from community practices across the USA on social determinants of health is the first of its kind.
• The participating physicians represented a large sample with broad geographic distribution, but the results may not be generalisable to all oncology practices within the USA.
• The survey relied on the physicians’ views of the impact of social determinants of health on their patients; however, the physicians may not have had a complete picture of their patients’ circumstances, and views may be subjective.

Introduction

Social determinants of health (SDOH), defined by the WHO as ‘the conditions in which people are born, grow, work, live, and age, and the wider set of forces and systems shaping the conditions of daily life’, have garnered increased attention in recent years as evidence linking SDOH to health outcomes grows. 1 Although there is no universally accepted consensus on the specific factors comprising SDOH, examples include economic stability (eg, poverty, food insufficiency or housing instability), education, social support, health insurance status, and access to transportation. 2 Research indicates that clinical care accounts for less than 20% of health outcomes in the USA, with socioeconomic factors, health behaviours and the physical environment contributing greater influence on outcomes. 3 These findings provide further evidence that most of what impacts health occurs outside the walls of a clinic or hospital and underscore the need for interventions targeting social and economic conditions to meaningfully improve health outcomes. Although healthcare expenditures in the USA surpass those of other developed nations, healthcare outcomes do not reflect the increased investment. 4 Payers and healthcare systems have increasingly looked to addressing SDOH as a means to resolve this discrepancy and reduce healthcare costs. 5 6

The impact of SDOH is particularly relevant to patients with cancer, as cancer is one of the costliest diseases to treat (second only to heart disease). 7 Patients who reside in zip codes with lower socioeconomic status have lower rates of cancer screening and are more often diagnosed with cancer at a later stage of disease. 8 9 Furthermore, patients with cancer living in areas of greater deprivation experience a higher incidence of rehospitalisation and mortality. 10 11 Financial hardship associated with cancer treatment is well documented and disproportionately affects patients with lower educational attainment, lower family income and those who are uninsured. 12 Rising costs of cancer care and therapies, coupled with the prevalence of cancer (in 2020, there are an estimated 18.1 million cancer survivors in the USA, and 1.8 million patients will be diagnosed with cancer this year), put a growing number of cancer patients at risk. 13 14 As value-based care models shift more accountability to healthcare providers with respect to quality of care, cost containment and improvements in outcomes, awareness of the impact of SDOH on patients has emerged as an essential element of care. For example, as a component of the Oncology Care Model’s (OCM) comprehensive, coordinated cancer care, each patient in participating practices must have a documented care plan that includes estimating out-of-pocket costs and addressing health-related social needs. 15 The objective of this study was to gain insight into practising oncologists’ views on SDOH and interventions to alleviate negative effects of SDOH. In this paper, we present the results of surveys completed by oncologists regarding their perceptions of the impact of SDOH on their patients and their opinions on potential solutions to mitigate the SDOH burden.

Physicians in the Cardinal Health Oncology Provider Extended Network (a community of over 7000 medical oncologists or haematologists, practising in a community-based or hospital-based setting in the USA) were invited to participate in a series of live market research meetings held between February and April 2020. Advanced practice providers and other healthcare professionals were not invited to take part in the meetings. To be eligible for an invitation, physicians must have been actively practising, must have represented different practices with a broad geographic distribution across the USA and could not have participated in another live meeting in the preceding 9 months. All physicians who were invited and agreed to take part in the live meeting completed a premeeting survey. Participants received an honorarium for their participation and were unaware that they would be asked about SDOH at the time they agreed to participation. In the survey, the physicians were asked a series of 10 multiple-choice (single select, modified Likert and multiselect) questions regarding their perceptions of the impact of SDOH on their patients, and their opinions on how the effects of SDOH should be mitigated. Participants submitted their responses via a web-based survey. Responses were summarised using descriptive statistics. A χ 2 test was performed to compare responses to individual questions among physicians representing practices participating in the OCM versus those from practices not participating in the OCM. No adjustments were made for multiple comparisons. This study was exempt from institutional review board review.

Patient and public involvement

No patients were involved in this study.

A total of 165 physicians were invited to participate and responded to the survey ( table 1 ). The primary medical specialty reported was medical oncology for 33% of respondents, haematology oncology for 65% and other for 2%. The physicians saw a median of 20 patients per day, and the median number of years in practice for the respondents was 18. The regional location of their primary practice was reported as the south for 44% of respondents, the midwest for 21%, the west for 8% and the northeast for 27%. Of the 165 practices represented, 68 (41%) were participating in the OCM value-based care model.

Characteristics of survey respondents

All participants provided answers to all 10 questions. The majority of oncologists surveyed agreed that SDOH, including financial security, food security, social isolation, housing security, addiction, access to transportation and patient health literacy, had a significant impact on their patients’ ability to achieve an optimal health outcome (51% selected the response strongly agree; 42% agree; 7% neither agree nor disagree; 1% disagree; 0% strongly disagree). As shown in table 2 , most of the participating oncologists said at least half of their patients were negatively impacted by SDOH (4% chose the response all or nearly all; 24% most; 40% about half; 32% few; 0% none).

Responses to the question: in your opinion, what portion of your patients are negatively impacted by social determinants?

The SDOH that were the most significant barriers for the patients of the oncologists surveyed are presented in figure 1 . Financial security/lack of health insurance was the response selected most often (83%), followed by access to transportation (58%), health literacy (53%), social isolation (43%), housing security (18%), addiction (12%) and food security (7%). Accordingly, the top 2 types of assistance oncologists indicated would have the greatest impact on helping their patients achieve better outcomes were assistance with the cost of medicine (79%) and assistance with transportation to clinic/physician office (57%).

Responses to the question: which social determinants are the most significant barriers for your patients? (Please select your top 3). *Includes lack of health insurance.

When asked how often they and their staff talked to patients affected by SDOH about how these factors may be interfering with their care, 18% of oncologists surveyed selected ‘all the time’, while 51% selected ‘often’, 29% ‘occasionally’, 2% ‘rarely’ and 0% ‘never’ ( table 3 ). The majority of oncologists indicated that they and their staff were constrained in the amount of time they could spend assisting patients with social needs, with 34% responding that they strongly agree, 47% agree, 14% neither agree nor disagree, 5% disagree and 0% strongly disagree.

Responses to the question: among patients affected by social determinants, how often do you or your staff talk to them about how these factors may be interfering with their care?

Most oncologists agreed that assistance programmes to help patients with social needs were not readily accessible: 20% chose the response strongly agree, 56% agree, 16% neither agree nor disagree, 7% disagree and 1% strongly disagree. When asked who should have responsibility for delivering assistance programmes to patients, 50% or more of oncologists surveyed indicated that government organisations, hospitals/cancer centres, non-profit organisations and commercial payers/insurance companies all should be responsible; fewer than half (42%) indicated that responsibility should fall to pharmaceutical manufacturers ( figure 2A ). Only 2% of surveyed oncologists believed that pharmaceutical companies should not be involved in the social needs of patients; most agreed that manufacturers can play a role in supporting the social needs of patients by offering more copay assistance programmes, patient assistance programmes/free drug programmes or patient education programmes ( figure 2B ).

(A) Responses to the question: who should have responsibility for delivering assistance programmes to patients? (Please select all that apply. (B) Responses to the statement: I believe pharmaceutical manufacturers can play a role in supporting the social needs of patients by offering more: (Please select all that apply).

To assess the impact of OCM participation, we explored potential differences in the perception of the contributions of SDOH on patient outcomes among oncologists from OCM and non-OCM practices. Only a few differences were noted to be statistically significant: oncologists from non-OCM practices identified food security as a barrier to optimal outcomes more often than those from OCM practices (59% vs 43%, p=0.04). Twice as many oncologists from OCM practices identified housing security as a barrier compared with non-OCM participants (25% vs 12% p=0.04). A greater proportion of OCM participants favoured that hospitals and cancer centres should play a greater role in patient assistance programmes (59% vs 43% p<0.05).

In this survey of 165 practising oncologists in the USA, 93% agreed that SDOH impacted their patients’ ability to achieve optimal health outcomes. Two-thirds of the oncologists in our study estimated that half or more of their patients were impacted by SDOH, with financial security and access to transportation representing the most significant barriers. Nearly 70% of oncologists reported talking to their patients about how SDOH affected their care often or all the time, although most reported that they and their staff had limited time available to help patients with their social needs. Three quarters of oncologists surveyed thought that assistance programmes were not readily accessible. Most of the respondents indicated that the responsibility for providing assistance to patients with social needs fell to government organisations, hospitals, non-profit organisations and commercial payers, although pharmaceutical companies could provide support through copay assistance, free drug programmes or patient education. We did not find dramatic differences in the perceptions of oncologists from OCM and non-OCM practices.

Across the broader medical community, the recognition of the importance of identifying patients at risk for poor outcomes due to SDOH is reflected in the issuance of policy statements related to screening by professional societies such as the American Academy of Family Physicians, the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists. 16–18 Similarly, the American Cancer Society has published a framework for addressing SDOH, which includes recommendations for screening, to further cancer health equity. 19 In addition, the Centers for Medicare & Medicaid Services’ (CMS) Accountable Health Community model implements screening for health-related social needs among Medicare and Medicaid beneficiaries receiving healthcare at participating sites. 20 However, despite these recommendations, how often screening for SDOH occurs in clinical practice has not been well described. A study of 739 hospitals and 2190 physician practices in the USA found that only 24.4% of hospitals and 15.6% of physician practices screened patients for the five specific social needs outlined in the CMS Accountable Health Communities Model (food insecurity, housing instability, utility needs, transportation needs, and interpersonal violence). For those that did not screen for any of the five, the most common barriers cited were lack of time and financial resources. 21

To alleviate the burden of screening, several strategies have been undertaken to better capture SDOH within electronic health records (EHRs). The American Medical Association in collaboration with UnitedHealthcare is working to create 23 new International Classification of Disease (ICD)-10 codes related to SDOH, including access to nutritious food, adequate and safe housing, available transportation, financial ability to pay for medications and utilities, and caregiver needs. 22 The use of artificial intelligence (AI) also figures prominently into efforts to improve identification of SDOH for patients: natural language processing of the unstructured notes in EHRs has been shown to identify greater prevalence of tobacco use, alcohol abuse, drug abuse, depression, housing instability, fall risk and poor social support than could be identified through administrative data. 23 Health systems such as Mount Sinai have adopted AI solutions to pull data from unstructured notes to help identify patients at risk. 24 Other health systems are using AI technology that integrates clinical factors from the EHR with socioeconomic factors to flag patients at risk for readmission. 25 26 Decision models incorporating clinical EHR data and community-level SDOH data have demonstrated the ability to predict the need for social service referrals. 27 Applied machine learning using SDOH data alone has also been shown to accurately predict emergency department visits or hospital admissions. 28 Finally, in a recent pilot study, an AI decision tool that incorporated SDOH helped patients with cancer receive timely palliative care by identifying those who were at risk for short-term mortality. 29

The physicians in our study viewed the responsibility for assisting patients with social needs as belonging to government organisations, non-profit organisations, pharmaceutical companies, hospitals and commercial payers. In the past decade, these entities have made important strides towards mitigating the impact of SDOH on clinical outcomes through policy changes, commitments for community programmes and initiatives to support individual patients that go beyond screening. The Affordable Care Act, enacted in 2010, requires tax-exempt hospitals to conduct community health needs assessments every 3 years and to create an implementation strategy to improve health at the community level. 30 Some states have also established waivers that allow Medicaid dollars to pay for interventions to support social needs of patients. 31 Non-profits such as the Leukemia & Lymphoma Society provide copay assistance, travel assistance, education and community support to patients, 32 and foundations such as the Robert Wood Johnson Foundation provide grants for programmes to address food and housing insecurity, among other SDOH. 33 Patient assistance programmes provided by pharmaceutical companies, 34 as well as patient support and adherence programmes, copay and prior authorisation support provided through hub services, are important resources for patients and providers. In addition, recent years have seen significant funding initiatives by hospitals, health systems and payers to address SDOH. From 2017 to 2019, direct financial investments in programmes addressing SDOH in the USA are estimated at $2.5 billion, involving 57 health systems and 917 hospitals across the USA. 35 The majority of the funds were focused on housing initiatives, followed by employment, education, food security, social and community context and transportation. 35 Commercial payers such as Anthem, Kaiser Permanente and United Healthcare have also invested millions into affordable housing solutions, and Humana introduced their Bold Goal strategy to address food insecurity, loneliness and social isolation, and transportation barriers, recognising that the investment is likely to result in lower healthcare costs. 36–39 There is evidence to support investment in social needs leading to better health outcomes: one study found that US states with a higher ratio of social to health spending (calculated as the sum of social service spending and public health spending divided by the sum of Medicare spending and Medicaid spending) had significantly better subsequent health outcomes across multiple health measures (including mortality rates for lung cancer). 40

At the level of the individual oncology practice, one strategy broadly employed to address the social needs of patients has been the addition of a navigator to the care team. Nurse, social worker or counsellor navigators perform tasks such as making arrangements for patient services or peer support groups, referring patients to resources and assisting patients with low health literacy. 41 Providing patient navigation is another component of the OCM value-based care model, 15 an important point to note as 41% of the physicians in our study represented practices participating in the OCM. By reducing barriers to care and bridging gaps for patients with cancer who have social needs, patient navigation has been shown to improve outcomes and increase patient satisfaction. 42 In addition, the creation of a financial navigator role at some oncology practices, to help patients with copay assistance applications, free drug options and other resources to cover expenses during their care, has proven successful in reducing patient out-of-pocket costs. 43

Limitations of this study include its descriptive nature and its reliance on physicians’ estimates of the impact of SDOH on their patients and the amount of time spent by staff in assisting patients. We did not have access to any patient or practice data to support these estimates. Additionally, while the physicians in our study represented practices with broad geographic distribution across the USA, we have no information on the communities where the practices are located or the representation of patients within the practices. Finally, our sample did not include radiation or surgical oncologists, which may limit the generalisability of our results.

Conclusions

To our knowledge, this is the first peer-reviewed publication to date to assess oncologists’ perceptions of the impact of SDOH on their patients and their thoughts about how SDOH could be addressed. We found that while awareness of SDOH was high (nearly all oncologists surveyed agreed that SDOH influences their patients’ health outcomes), most oncologists did not have the time or resources to assist their patients with social needs and did not consider assistance programmes to be readily accessible. Recognition of the negative consequences of SDOH burden is important, but physicians in our study lacked adequate means to resolve the issues. Borrowing from the concept of a cancer ‘groundshot’, the most effective solutions may be the simplest. 44 For the most immediate impact on cancer morbidity and mortality, we believe that what is needed more urgently than expensive new technology or therapeutics that may only provide modest benefits to a small proportion of cancer patients is to ensure that all patients with cancer are equipped with the basic necessities of life: housing and food security, access to care and affordable treatment. While straightforward in concept, the challenge of addressing SDOH to promote health equity and improve health outcomes is a complex, long-term endeavour. The incorporation of patient navigators into the care team for some oncology practices has shown that interventions targeting patients’ social needs can be effective, but larger scale interventions at the community and national level will ultimately be needed to effect meaningful change. Collaborative action by professional organisations such as the American Society of Clinical Oncology, the Oncology Nursing Association and the Association of Oncology Social Work may be one avenue to drive this change. It remains to be seen if efforts underway to improve screening to identify patients at risk for poor outcomes due to SDOH burden, and increased investment by hospitals, health systems and payers in initiatives targeting SDOH, will translate into improved outcomes for patients with cancer.

Supplementary Material

Contributors: AG and BAF designed the study. YJ-S analysed the data. MEZ, AG and BAF interpreted the results. MEZ drafted the manuscript. All authors critically reviewed and approved the manuscript.

Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: All support for the present manuscript including provision of study materials and article processing charges was provided by Cardinal Health. All authors are employees of Cardinal Health and may own stock in Cardinal Health.

Patient and public involvement: Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

Provenance and peer review: Not commissioned; externally peer reviewed.

Data availability statement

Ethics statements, patient consent for publication.

Not applicable.

Ethics approval

The data used in this study did not include any identifiers that met the standard for ethics board review.

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What is functional precision medicine?

Even though two people with the same cancer might get the same medicine, they can have very different outcomes. Because each patient's tumor is unique, it can be challenging to know which treatment works best.

To solve this problem, doctors analyze DNA mutations in the patient's tumor, blood or saliva to match cancer medicines to patients. This approach is called  precision medicine . However, the relationship between cancer DNA and how effective medicines will be against them is very complex. Matching medications to patients based on a single mutation overlooks other genetic and nongenetic mechanisms that influence how cells respond to drugs.

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How to best match medicines to patients through DNA is still a major challenge. Overall,  only 10% of cancer patients   experience a clinical benefit  from treatments matched to tumor DNA mutations.

Functional precision medicine takes a different approach to personalizing treatments. My team and I take a sample of a patient's cancer cells from a biopsy, grow the cells in the lab and expose them to over 100 drugs approved by the Food and Drug Administration. In this process, called  drug sensitivity testing , we look for the medications that kill the cancer cells.

New clinical trial results

Providing functional precision medicine to cancer patients  in real life  is very challenging. Off-label use of drugs and financial restrictions are key barriers. The health of cancer patients can also deteriorate rapidly, and physicians may be hesitant to try new methods.

But this is starting to change. Two teams in Europe recently showed that functional precision medicine could match effective treatments to  about 55% of   adult patients  with blood cancers such as leukemia and lymphoma that did not respond to standard treatments.

Most recently, my team's clinical trial  focused on childhood cancer patients  whose cancer came back or didn't respond to treatment. We applied our functional precision medicine approach to 25 patients with different types of cancer.

Our trial showed that we could provide treatment options for almost all patients in less than two weeks. My colleague  Arlet Maria Acanda de la Rocha  was instrumental in helping return drug sensitivity data to patients as fast as possible. We were able to provide test results within 10 days of receiving a sample, compared with the roughly 30 days that standard genomic testing results that focus on identifying specific cancer mutations typically take to process.

Most importantly, our study showed that  83% of cancer patients  who received treatments guided by our approach had clinical benefit, including improved response and survival.

Expanding into the real world

Functional precision medicine opens new paths to understanding how cancer drugs can be better matched to patients. Although doctors can read any patient's DNA today, interpreting the results to understand how a patient will respond to cancer treatment is much more challenging. Combining drug sensitivity testing with DNA analysis can help personalize cancer treatments for each patient.

I, along with colleague  Noah E. Berlow , have started to add artificial intelligence to our functional precision medicine program. AI enables us to analyze each patient's data to better match them with tailored treatments and drug combinations. AI also allows us to understand the complex relationships between DNA mutations within tumors and how different treatments will affect them.

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My team and I have  started two   clinical trials  to expand the results of our previous studies on providing treatment recommendations through functional precision medicine. We're recruiting a larger cohort of adults and children with cancers that have come back or are resistant to treatment.

The more data we have, the easier it will become to understand how to best treat cancer and ultimately help more patients access personalized cancer treatments.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article .

Diana Azzam is an Assistant Professor and Research Director of the newly established Center for Advancing Personalized Cancer Treatments (CAPCT) at Florida International University. She has a Masters in Biochemistry from the American University of Beirut, Lebanon and a PhD in Biochemistry & Molecular Biology from the University of Miami, Florida. Her lab focuses on implementing functional precision medicine (FPM) approaches in adult and pediatric cancer patients that have run out of treatment options. Working with local hospitals including Nicklaus Children's Hospital and Cleveland Clinic Florida, her lab delivers individualized treatment plans based on a patient's cancer genomic profile and ex vivo drug response. She is currently engaged in two clinical studies to assess feasibility and clinical utility of FPM in relapsed/refractory patients with childhood cancer (ClinicalTrials.gov registration: NCT05857969) and adult cancer (ClinicalTrials.gov registration: NCT06024603). She is working on setting up the first CLIA-certified lab in the State of Florida dedicated for functional cancer drug testing. Her goal is to launch large-scale prospective multi-center randomized clinical trials to better assess efficacy of FPM approaches in the treatment of refractory/relapsed cancers. In parallel, she is working on utilizing FPM as a tool to reduce health disparities in childhood cancer patients from minority populations. She is also integrating a novel machine learning approach to identify specific biomarkers among minority populations that can be targeted using FDA-approved drugs. Her lab also investigates cancer stem cells and how they may result from chronic environmental exposures to toxic metals such as arsenic.

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