David J. McConkey

ORCID: 0000-0003-1971-0638
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About
Contact & Profiles
Research Areas
  • Bladder and Urothelial Cancer Treatments
  • Urinary and Genital Oncology Studies
  • Epigenetics and DNA Methylation
  • Cancer Immunotherapy and Biomarkers
  • Cell death mechanisms and regulation
  • Cancer, Hypoxia, and Metabolism
  • Cancer Research and Treatments
  • Ferroptosis and cancer prognosis
  • Ubiquitin and proteasome pathways
  • Immune cells in cancer
  • Cancer-related Molecular Pathways
  • Pancreatic and Hepatic Oncology Research
  • Signaling Pathways in Disease
  • Cancer, Lipids, and Metabolism
  • Esophageal Cancer Research and Treatment
  • Angiogenesis and VEGF in Cancer
  • RNA modifications and cancer
  • Immune Cell Function and Interaction
  • Peptidase Inhibition and Analysis
  • Cancer Cells and Metastasis
  • Galectins and Cancer Biology
  • NF-κB Signaling Pathways
  • Renal cell carcinoma treatment
  • Cancer Genomics and Diagnostics
  • Lung Cancer Treatments and Mutations

Johns Hopkins University
2016-2025

Sidney Kimmel Comprehensive Cancer Center
2021-2025

Cancer Institute (WIA)
2018-2025

Johns Hopkins Medicine
2017-2025

University of Baltimore
2017-2024

The University of Texas MD Anderson Cancer Center
2011-2024

Bladder Cancer Advocacy Network
2016-2024

Johns Hopkins Hospital
2023-2024

Sidney Kimmel Cancer Center
2024

Rice University
2024

John N. Weinstein Rehan Akbani Bradley M. Broom Wenyi Wang Roeland Verhaak and 95 more David J. McConkey Seth P. Lerner Margaret Morgan Chad J. Creighton C. Smith Andrew D. Cherniack Jaegil Kim Chandra Sekhar Pedamallu Michael S. Noble Hikmat Al‐Ahmadie Victor E. Reuter Jonathan E. Rosenberg Dean F. Bajorin Bernard H. Bochner David B. Solit Theresa M. Koppie Brian D. Robinson Dmitry A. Gordenin David C. Fargo Leszek J. Klimczak Steven A. Roberts Jessie L.‐S. Au Peter W. Laird Toshinori Hinoue Nikolaus Schultz Ricardo Ramírez Donna E. Hansel Katherine A. Hoadley William Y. Kim Jeffrey S. Damrauer Stephen B. Baylin Andrew J. Mungall A. Gordon Robertson Andy Chu David J. Kwiatkowski Carrie Sougnez Kristian Cibulskis Lee Lichtenstein Andrey Sivachenko Chip Stewart Michael S. Lawrence Gad Getz Eric Lander Stacey B. Gabrie Lawrence A. Donehower Scott L. Carter Gordon Saksena Steven E. Schumacher Samuel S. Freeman Joonil Jung Ami S. Bhatt Trevor J. Pugh Rameen Beroukhim Matthew Meyerson Adrian Ally Miruna Balasundaram Yaron S.N. Butterfield Noreen Dhalla Carrie Hirst Robert A. Holt Steven J.M. Jones Darlene Lee Haiyan I. Li Marco A. Marra Michael Mayo Richard A. Moore Jacqueline E. Schein Payal Sipahimalani Angela Tam Nina Thiessen Tina Wong Natasja Wye Reanne Bowlby Eric Chuah Ranabir Guin Hui Shen Arnoud Boot Timothy J. Triche Phillip H. Lai David Van Den Berg Daniel J. Weisenberger Saianand Balu Tom Bodenheimer Alan P. Hoyle Joshua M. Stuart Shaowu Meng Lisle E. Mose Janae V. Simons Mathew G. Soloway Junyuan Wu Joel S. Parker D. Neil Hayes Jeffrey Roach Elizabeth Buda Corbin D. Jones

Urothelial carcinoma of the bladder is a common malignancy that causes approximately 150,000 deaths per year worldwide. So far, no molecularly targeted agents have been approved for treatment disease. As part The Cancer Genome Atlas project, we report here an integrated analysis 131 urothelial carcinomas to provide comprehensive landscape molecular alterations. There were statistically significant recurrent mutations in 32 genes, including multiple genes involved cell-cycle regulation,...

10.1038/nature12965 article EN cc-by-nc-sa Nature 2014-01-28
A. Gordon Robertson Jaegil Kim Hikmat Al‐Ahmadie Joaquim Bellmunt Guangwu Guo and 95 more Andrew D. Cherniack Toshinori Hinoue Peter W. Laird Katherine A. Hoadley Rehan Akbani Mauro A. A. Castro Ewan A. Gibb Rupa S. Kanchi Dmitry A. Gordenin Sachet A. Shukla Francisco Sánchez-Vega Donna E. Hansel Bogdan Czerniak Victor E. Reuter Xiaoping Su Benílton de Sá Carvalho Vinicius S Chagas Karen Mungall Sara Sadeghi Chandra Sekhar Pedamallu Yiling Lu Leszek J. Klimczak Jiexin Zhang Caleb Choo Akinyemi I. Ojesina Susan Bullman Kristen Leraas Tara M. Lichtenberg Catherine J. Wu N. Schultz Gad Getz Matthew Meyerson Gordon B. Mills David J. McConkey John N. Weinstein David J. Kwiatkowski Seth P. Lerner Rehan Akbani Hikmat Al‐Ahmadie Monique Albert Iakovina Alexopoulou Adrian Ally Tatjana Antic Manju Aron Miruna Balasundaram John M.S. Bartlett Stephen B. Baylin Allison Beaver Joaquim Bellmunt İnanç Birol Lori Boice Arnoud Boot Jay Bowen Reanne Bowlby Denise Brooks Bradley M. Broom Wiam Bshara Susan Bullman Eric Burks Flavio Mavignier Cárcano Rebecca Carlsen Benilton S. Carvalho André Lopes Carvalho Eric Castle Mauro A. A. Castro Mauro A. A. Castro James W.F. Catto Vinicius S Chagas Andrew D. Cherniack David Chesla Caleb Choo Eric Chuah Sudha Chudamani Victoria K. Cortessis Sandra Cottingham Daniel Crain Erin Curley Bogdan Czerniak Siamak Daneshmand John A. Demchok Noreen Dhalla Hooman Djaladat John Eckman Sophie Egea Jay Engel Ina Felau Martin L. Ferguson Johanna Gardner Julie M. Gastier‐Foster Mark Gerken Gad Getz Ewan A. Gibb Carmen Gomez‐Fernandez Dmitry A. Gordenin Guangwu Guo

10.1016/j.cell.2017.09.007 article EN publisher-specific-oa Cell 2017-10-01

A better understanding of drug resistance mechanisms is required to improve outcomes in patients with pancreatic cancer. Here, we characterized patterns sensitivity and three conventional chemotherapeutic agents divergent action [gemcitabine, 5-fluorouracil (5-FU), cisplatin] cancer cells. Four (L3.6pl, BxPC-3, CFPAC-1, SU86.86) were sensitive five (PANC-1, Hs766T, AsPC-1, MIAPaCa-2, MPanc96) resistant all based on GI(50) (50% growth inhibition). Gene expression profiling unsupervised...

10.1158/0008-5472.can-08-2819 article EN Cancer Research 2009-07-08

Cytotoxic chemotherapy targets elements common to all nucleated human cells, such as DNA and microtubules, yet it selectively kills tumor cells. Here we show that clinical response these drugs correlates with, may be partially governed by, the pretreatment proximity of cell mitochondria apoptotic threshold, a property called mitochondrial priming. We used BH3 profiling measure priming in cells from patients with multiple myeloma, acute myelogenous lymphoblastic leukemia, ovarian cancer. This...

10.1126/science.1206727 article EN Science 2011-10-28

Glucocorticoid hormones kill immature thymocytes by activating a self-destructive process that involves extensive DNA fragmentation. It has been demonstrated thymocyte suicide is dependent on an early, sustained increase in cytosolic Ca2+ concentration, and new protein synthesis, but the biochemical lesion leads to cell death not established. To determine whether endonuclease activation or of another Ca2+-de-pendent could mediate killing, we treated with glucocorticoid methylprednisolone...

10.1096/fasebj.3.7.2497041 article EN The FASEB Journal 1989-05-01

Suspensions of thymocytes from young rats were incubated with 2,3,7,8- tetrachlorodibenzo- p -dioxin (TCDD), which resulted in a sustained increase cytosolic free Ca 2+ concentration followed by DNA fragmentation and loss cell viability. Both the prevented cells treated inhibitor protein synthesis, cycloheximide, killing not detected when "Ca -free" medium or pretreated high concentrations calcium probe, quin-2 tetraacetoxymethyl ester. These results indicate that TCDD can kill immature...

10.1126/science.3262923 article EN Science 1988-10-14

The epithelial-to-mesenchymal transition (EMT) is a cell development-regulated process in which noncoding RNAs act as crucial modulators. Recent studies have implied that EMT may contribute to resistance epidermal growth factor receptor (EGFR)-directed therapy. aims of this study were determine the potential role microRNAs (miRNA) controlling and inducing sensitivity human bladder cancer cells inhibitory effects anti-EGFR therapy.miRNA array screening real-time reverse transcription-PCR used...

10.1158/1078-0432.ccr-08-2245 article EN Clinical Cancer Research 2009-08-12

Multiple studies in recent years have identified highly tumorigenic populations of cells that drive tumor formation. These cancer stem (CSCs), or tumor-initiating (TICs), exhibit properties normal and are associated with resistance to current therapies. As pancreatic adenocarcinoma is among the most resistant human cancers chemo-radiation therapy, we sought evaluate presence cell capacities tumors. Understanding which possess capabilities critical characterizing understanding biology CSCs...

10.1371/journal.pone.0020636 article EN cc-by PLoS ONE 2011-06-13

The advent of Omics technologies has been key to the molecular subclassification urothelial bladder cancer. Several groups have used different strategies this aim, with partially overlapping findings. meeting at Spanish National Cancer Research Center-CNIO was held discuss such classifications and reach consensus where appropriate. After updated presentations on work performed by teams attending meeting, a reached regarding existence group Basal-Squamous-like tumors - designated BASQ...

10.3233/blc-150037 article EN Bladder Cancer 2016-01-07
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