Ed Reznik
As seen in:
Nature,
Wiley Online Library,
MDPI,
Genome Biology,
Science Magazine,
Cell Press,
EBioMedicine,
medRxiv,
Cancer Discovery
Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile
Articles by Ed Reznik
A health-system-scale, episode-resolved multimodal atlas of cancer cachexia
Abstract Cancer cachexia is a wasting syndrome with outsized impact on morbidity and mortality, yet its drivers and systemic consequences remain poorly defined. In this study, we repurposed longitudinal clinicogenomic data from 52,236 patients with cancer profiled by MSK-IMPACT (2010–2024) at Memorial Sloan Kettering Cancer Center to define episode-resolved trajectories of consensus-defined cachectic weight loss and linked these events to outcomes, serology and tumor genotypes.
Macrophage-supported metabolic adaptation drives tumor survival under nutrient stress
|
Abstract INTRODUCTION RESULTS DISCUSSION MATERIALS AND METHODS Acknowledgments Supplementary Materials REFERENCES Information & Authors Metrics & Citations View Options References Figures Tables Media Share This article has 0 eLetter . Abstract Triple-negative breast cancer (TNBC) develops in hypoxic, nutrient-limited tumors enriched with macrophages and cell death.
By Sherina Malkani, David Roach, Lara Perren, Nancy Santiappillai, Andrew Cho, Georg Verch, Ana C Codo, Achuth Nair, Allie Lipshutz, Celia Martínez de la Torre, Eric Liu, Marjan Berishaj, Alissa Trzeciak, Zhaoquan Wang, Michelle Saoi, Waleska Saitz Rojas, Justin Cross, Ed Reznik, Justin Perry, Kayvan R. Keshari
|
Science Magazine
Verified
Cancer type-specific variation in patterns of driver alterations across 50,000 tumors
|
Main text (Cancer Cell , 1–18, May 11, 2026) Due to a typesetting error, this article was initially published online with an incorrect Received date of March 4, 2025. The manuscript was originally submitted to on April 26, 2024, and subsequently transferred to on January 7, 2026. The Received date should have reflected the original submission date of April 26, 2024. The journal has now corrected the Received date online and apologizes to the authors and readers for the confusion.
By Chaitanya Bandlamudi, Daniel Muldoon, Ino de Bruijn, Mingxuan Zhang, Michael V. Gormally, Emily Harrold, Subhiksha Nandakumar, Shaleigh A. Smith, Mark Jeng, Sydney Woods, Kanika Arora, Walid K. Chatila, Bastien Nguyen, Henry Walch, Jun Woo, Craig M. Bielski, Christopher H Fong, Thinh Tran, Gaofei Zhao, Miika Mehine, Sam E. Tischfield, Allison Richards, Suraj Rajendran, Hongxin Zhang, Christoph K. Kreitzer, Ronak Shah, Risha Huq, Jesse Galle, Tina Alano, Ramyasree Madupuri, Ritika Kundra, Justin Jee, Karl Pichotta, Michele Waters, Richard A. Hickman, Josephine K. Dermawan, Jie-Fu Chen, Anton Safonov, Konrad H. Stopsack, Ritesh R. Kotecha, Hira Rizvi, Claire F. Friedman, Pedram Razavi, Ezra Y Rosen, Yonina R. Murciano-Goroff, Luc G.T. Morris, James A. Fagin, Ingo K. Mellinghoff, Ping Chi, Neerav Shukla, Adam Schoenfeld, Gregory J Riely, Charles M. Rudin, Alexander Drilon, Jake Lee, Hikmat Al-Ahmadie, Gopa Iyer, Anna Varghese, Eileen M. O’Reilly, Zsofia K. Stadler, Mark E. Robson, Ed Reznik, Jianjiong Gao, Diana Mandelker, Irina Ostrovnaya, Satshil Rana, Gowtham Jayakumaran, Anita S. Bowman, Abhinita S Mohanty, Anoop Rema Balakrishnan, Aijazuddin Syed, Ryan N. Ptashkin, Jacklyn Casanova-Murphy, Debyani Chakravarty, Ryma Benayed, Maria E. Arcila, Sarat Chandarlapaty, Helena A. Yu, Neal Rosen, Mark T.A. Donoghue, Christopher A Klebanoff, Rona Yaeger, A. Rose Brannon, Ahmet Zehir, Marc Ladanyi, Nikolaus Schultz, David B. Solit, Michael Berger Verified
|
Cell Press
Verified
Cancer type-specific variation in patterns of driver alterations across 50,000 tumors
|
Refers to: Keywords cancer type-specific tissue-specific driver alterations hotspots precision oncology clinical sequencing age of cancer diagnosis HLA genotype neoantigen-directed TCR therapies HLA loss of heterozygosity Introduction Cancer is a genetic disease defined by the serial acquisition of cell fitness-promoting mutations, referred to as “drivers.”1 Characterization of driver alterations is fundamental to understanding cancer pathogenesis, molecular classification of tumors, and...
By Chaitanya Bandlamudi, Daniel Muldoon, Ino de Bruijn, Mingxuan Zhang, Michael V. Gormally, Emily Harrold, Subhiksha Nandakumar, Shaleigh A. Smith, Mark Jeng, Sydney Woods, Kanika Arora, Walid K. Chatila, Bastien Nguyen, Henry Walch, Jun Woo, Craig M. Bielski, Christopher H Fong, Thinh Tran, Gaofei Zhao, Miika Mehine, Sam E. Tischfield, Allison Richards, Suraj Rajendran, Hongxin Zhang, Christoph K. Kreitzer, Ronak Shah, Risha Huq, Jesse Galle, Tina Alano, Ramyasree Madupuri, Ritika Kundra, Justin Jee, Karl Pichotta, Michele Waters, Richard A. Hickman, Josephine K. Dermawan, Jie-Fu Chen, Anton Safonov, Konrad H. Stopsack, Ritesh R. Kotecha, Hira Rizvi, Claire F. Friedman, Pedram Razavi, Ezra Y Rosen, Yonina R. Murciano-Goroff, Luc G.T. Morris, James A. Fagin, Ingo K. Mellinghoff, Ping Chi, Neerav Shukla, Adam Schoenfeld, Gregory J Riely, Charles M. Rudin, Alexander Drilon, Jake Lee, Hikmat Al-Ahmadie, Gopa Iyer, Anna Varghese, Eileen M. O'Reilly, Zsofia K. Stadler, Mark E. Robson, Ed Reznik, Jianjiong Gao, Diana Mandelker, Irina Ostrovnaya, Satshil Rana, Gowtham Jayakumaran, Anita S. Bowman, Abhinita S Mohanty, Anoop Rema Balakrishnan, Aijazuddin Syed, Ryan N. Ptashkin, Jacklyn Casanova-Murphy, Debyani Chakravarty, Ryma Benayed, Maria E. Arcila, Sarat Chandarlapaty, Helena A. Yu, Neal Rosen, Mark T.A. Donoghue, Christopher A Klebanoff, Rona Yaeger, A. Rose Brannon, Ahmet Zehir, Marc Ladanyi, Nikolaus Schultz, David B. Solit, Michael Berger Verified
|
Cell Press
Verified
Mechanistic insights make cancer cachexia a targetable syndrome - Nature Medicine
Two studies establish a mechanism, biomarker and therapeutic strategy for cancer cachexia, all centered around the HIF-2 pathway. The findings reframe this intractable metabolic syndrome as a pharmacologically treatable condition.
Functionally dominant hotspot mutations of mitochondrial ribosomal RNA genes in cancer - Nature Genetics
Abstract The vast majority of recurrent somatic mutations arising in tumors affect protein-coding genes in the nuclear genome. Here, through population-scale analysis of 14,106 whole tumor genomes, we report the discovery of highly recurrent mutations affecting both the small (12S, MT-RNR1) and large (16S, MT-RNR2) mitochondrial RNA subunits of the mitochondrial ribosome encoded within mitochondrial DNA (mtDNA).
Biomarkers for renal cell carcinoma — a pragmatic approach - Nature Reviews Urology
The management of metastatic renal cell carcinoma (RCC) has undergone a major transformation, with median survival increasing from <1 year to ~5 years. However, biomarker development in RCC has lagged, largely because the most effective therapies, such as immune checkpoint inhibitors and VEGFR tyrosine kinase inhibitors, act on the tumour microenvironment rather than directly on tumour cells.
UnitedMet harnesses RNA–metabolite covariation to impute metabolite levels in clinical samples - Nature Cancer
Abstract Comprehensively studying metabolism requires metabolite measurements. Such measurements, however, are often unavailable in large cohorts of tissue samples. To address this basic barrier, we propose a Bayesian framework (‘UnitedMet’) that leverages RNA–metabolite covariation to impute otherwise unmeasured metabolite levels from widely available transcriptomic data. UnitedMet is equally capable of imputing whole pool sizes and outcomes of isotope tracing experiments.
PAK4-targeted PROTACs in clear cell renal cell carcinoma: a two-for-one targeted and immune therapy?
Clear cell RCC (ccRCC) accounts for around 75% of RCC cases and is characterized by the near-ubiquitous biallelic inactivation of Renal cell carcinoma (RCC) affects approximately 82,000 patients and causes over 15,000 deaths in the United States per year.VHL, which ultimately activates a pseudohypoxia program driven by the hypoxia inducible factor (HIF) family.
UnitedMet harnesses RNA-metabolite covariation to impute metabolite levels in clinical samples
The authors have declared no competing interest. This project was generously supported by the Cycle for Survival, the Marie-Josee and Henry R. Kravis Center for Molecular Oncology and the National Cancer Institute Cancer Center Core (grant P30-CA008748) supporting Memorial Sloan Kettering Cancer Center.
Mitochondrial DNA mutations drive aerobic glycolysis to enhance checkpoint blockade response in melanoma - Nature Cancer
Abstract The mitochondrial genome (mtDNA) encodes essential machinery for oxidative phosphorylation and metabolic homeostasis. Tumor mtDNA is among the most somatically mutated regions of the cancer genome, but whether these mutations impact tumor biology is debated. We engineered truncating mutations of the mtDNA-encoded complex I gene, Mt-Nd5, into several murine models of melanoma.
Career pathways, part 11
Save citation to file Format: Add to My Bibliography Your saved search Name of saved search: Search terms: Frequency: Which day? Which day? Report format: Send at most: Send even when there aren't any new results Optional text in email: Create a file for external citation management software
Advances in Imaging-Based Biomarkers in Renal Cell Carcinoma: A Critical Analysis of the Current Literature
Abstract : Simple Summary Current imaging techniques do not reliably distinguish renal cell carcinoma from other renal diseases. This review summarizes recent advances in other imaging methods for the diagnosis and monitoring of potential kidney tumors.
bims-mibica 2022-09-04 papers
Sci Adv. 2022 Sep 02. 8(35): eabn9550 In mice and humans with cancer, intravenous 13C-glucose infusion results in 13C labeling of tumor tricarboxylic acid (TCA) cycle intermediates, indicating that pyruvate oxidation in the TCA cycle occurs in tumors. The TCA cycle is usually coupled to the electron transport chain (ETC) because NADH generated by the cycle is reoxidized to NAD+ by the ETC.
Chemerin Tips the Scales in ccRCC to Evade Ferroptosis
In the Spotlight Ed Reznik, Hui Jiang and A. Ari Hakimi DOI: 10.1158/2159-8290.CD-21-0610 Published August 2021 This article requires a subscription to view the full text. You may purchase access to this article or login to access your subscription using the links below. Abstract Summary: Obesity is both a risk factor for the development of the most common form of kidney cancer, clear cell renal cell carcinoma (ccRCC), and a prognostically protective factor for clinical outcomes.
A pan-cancer analysis of PBAF complex mutations and their association with immunotherapy response
Abstract There is conflicting data regarding the role of PBAF complex mutations and response to immune checkpoint blockade (ICB) therapy in clear cell renal cell carcinoma (ccRCC) and other solid tumors. We assess the prevalence of PBAF complex mutations from two large cohorts including the pan-cancer TCGA project (n = 10,359) and the MSK-IMPACT pan-cancer immunotherapy cohort (n = 3700). Across both cohorts, PBAF complex mutations, predominantly PBRM1 mutations, are most common in ccRCC.
Publisher Correction: The long tail of oncogenic drivers in prostate cancer
Access provided by Correction to: Nature Genetics https://doi.org/10.1038/s41588-018-0078-z, published online 2 April 2018. In the HTML version of this article, the author group ‘PCF/SU2C International Prostate Cancer Dream Team’ was duplicated and appeared at the end of the author list but should have appeared only once, in the third-to-last position.
The Cancer Genome Atlas Comprehensive Molecular Characterization of Renal Cell Carcinoma
In the originally published version of this article, the author list contained two errors. Specifically, David J. Kwiatkowski was misspelled as David J. Kwaitkowski, and William Y. Kim was inadvertently written as William T. Kim. Both names have been corrected online.
The Cancer Genome Atlas Comprehensive Molecular Characterization of Renal Cell Carcinoma
Gene and Pathway Alteration Associates with Survival in Specific RCC Subtypes mRNA sequence reads were aligned to the human reference genome (hg38) and transcriptome (Ensembl v82, September 2015) using STAR 2.4.2a (Dobin et al., 2013xSTAR: ultrafast universal RNA-seq aligner. Dobin, A., Davis, C.A., Schlesinger, F., Drenkow, J., Zaleski, C., Jha, S., Batut, P., Chaisson, M., and Gingeras, T.R. Bioinformatics.
A Landscape of Metabolic Variation across Tumor Types
Analysis of Metabolic Variation in Tumors and Normal Tissue In spite of the diversity of genetic alterations across cancers, it is possible that the development of cancer may place common demands on cellular metabolism, irrespective of the tissue of origin. In this study, we offer a glimpse into the common patterns and distinguishing features of metabolic reprogramming across cancers.
Genome-Scale Architecture of Small Molecule Regulatory Networks and the Fundamental Trade-Off between Regulation and Enzymatic Activity
Landscape of Interactions in the E. coli SMRN Design Principles in the Regulation of Central Carbon Metabolism How Is a Metabolite’s Role as Regulator and Substrate Balanced? Quantifying the Metabolic Response to Small Molecules across Different Conditions and the Trade-Off between Regulation and Enzymatic Activity The regulatory action of small molecules on enzymes and other proteins ensures robust operation of metabolism upon dynamic changes.
Show More
loading
Actions
Is this you?
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Get in touch with Ed
Contact Ed, search articles and posts on X, monitor coverage, and track replies from one place.
Learn more about Muck Rack