Gad Getz

Harvard University

H-index: 228

North America-United States

Description

Gad Getz, With an exceptional h-index of 228 and a recent h-index of 197 (since 2020), a distinguished researcher at Harvard University, specializes in the field of Cancer Genomics, Computational Biology, Bioinformatics.

His recent articles reflect a diverse array of research interests and contributions to the field:

Histopathologic and proteogenomic heterogeneity reveals features of clear cell renal cell carcinoma aggressiveness

Genomic and transcriptomic analysis of checkpoint blockade response in advanced non-small cell lung cancer

Genetic events associated with venetoclax resistance in CLL identified by whole-exome sequencing of patient samples

Evolutionary history of transformation from chronic lymphocytic leukemia to Richter syndrome

Inferring early genetic progression in cancers with unobtainable premalignant disease

Pan-cancer analysis of post-translational modifications reveals shared patterns of protein regulation

Clonal origin of KMT2A wild-type lineage-switch leukemia following CAR-T cell and blinatumomab therapy

In Vivo Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities

Professor Information

University	Harvard University
Position	Massachusetts General Hospital and Broad Institute of Harvard and MIT
Citations(all)	342986
Citations(since 2020)	208304
Cited By	219935
hIndex(all)	228
hIndex(since 2020)	197
i10Index(all)	387
i10Index(since 2020)	368
Email	Access Email
University Profile Page	Harvard University

Research & Interests List

Cancer Genomics

Computational Biology

Bioinformatics

Top articles of Gad Getz

Histopathologic and proteogenomic heterogeneity reveals features of clear cell renal cell carcinoma aggressiveness

Clear cell renal cell carcinomas (ccRCCs) represent ∼75% of RCC cases and account for most RCC-associated deaths. Inter- and intratumoral heterogeneity (ITH) results in varying prognosis and treatment outcomes. To obtain the most comprehensive profile of ccRCC, we perform integrative histopathologic, proteogenomic, and metabolomic analyses on 305 ccRCC tumor segments and 166 paired adjacent normal tissues from 213 cases. Combining histologic and molecular profiles reveals ITH in 90% of ccRCCs, with 50% demonstrating immune signature heterogeneity. High tumor grade, along with BAP1 mutation, genome instability, increased hypermethylation, and a specific protein glycosylation signature define a high-risk disease subset, where UCHL1 expression displays prognostic value. Single-nuclei RNA sequencing of the adverse sarcomatoid and rhabdoid phenotypes uncover gene signatures and …

Authors

Yize Li,Tung-Shing M Lih,Saravana M Dhanasekaran,Rahul Mannan,Lijun Chen,Marcin Cieslik,Yige Wu,Rita Jiu-Hsien Lu,David J Clark,Iga Kołodziejczak,Runyu Hong,Siqi Chen,Yanyan Zhao,Seema Chugh,Wagma Caravan,Nataly Naser Al Deen,Noshad Hosseini,Chelsea J Newton,Karsten Krug,Yuanwei Xu,Kyung-Cho Cho,Yingwei Hu,Yuping Zhang,Chandan Kumar-Sinha,Weiping Ma,Anna Calinawan,Matthew A Wyczalkowski,Michael C Wendl,Yuefan Wang,Shenghao Guo,Cissy Zhang,Anne Le,Aniket Dagar,Alex Hopkins,Hanbyul Cho,Felipe da Veiga Leprevost,Xiaojun Jing,Guo Ci Teo,Wenke Liu,Melissa A Reimers,Russell Pachynski,Alexander J Lazar,Arul M Chinnaiyan,Brian A Van Tine,Bing Zhang,Karin D Rodland,Gad Getz,DR Mani,Pei Wang,Feng Chen,Galen Hostetter,Mathangi Thiagarajan,W Marston Linehan,David Fenyö,Scott D Jewell,Gilbert S Omenn,Rohit Mehra,Maciej Wiznerowicz,Ana I Robles,Mehdi Mesri,Tara Hiltke,Eunkyung An,Henry Rodriguez,Daniel W Chan,Christopher J Ricketts,Alexey I Nesvizhskii,Hui Zhang,Li Ding,Alicia Francis,Amanda G Paulovich,Andrzej Antczak,Anthony Green,Antonio Colaprico,Ari Hakimi,Barb Pruetz,Barbara Hindenach,Birendra Kumar Yadav,Boris Reva,Brenda Fevrier-Sullivan,Brian J Druker,Cezary Szczylik,Charles A Goldthwaite,Chet Birger,Corbin D Jones,Daniel C Rohrer,Darlene Tansil,David Chesla,David Heiman,Elizabeth Duffy,Eri E Schadt,Francesca Petralia,Gabriel Bromiński,Gabriela M Quiroga-Garza,George D Wilson,Ginny Xiaohe Li,Grace Zhao,Yi Hsiao,James Hsieh,Jan Lubiński,Jasmin Bavarva,Jasmine Huang,Jason Hafron,Jennifer Eschbacher,Jennifer Hon,Jesse Francis,John Freymann,Josh Vo,Joshua Wang,Justin Kirby,Kakhaber Zaalishvili,Karen A Ketchum,Katherine A Hoadley,Ki Sung Um,Liqun Qi,Marcin J Domagalski,Matt Tobin,Maureen Dyer,Meenakshi Anurag,Melissa Borucki,Michael A Gillette,Michael J Birrer,Michael M Ittmann,Michael H Roehrl,Michael Schnaubelt,Michael Smith,Mina Fam,Nancy Roche,Negin Vatanian,Nicollette Maunganidze,Olga Potapova,Oxana V Paklina,Pamela VanderKolk,Patricia Castro,Paweł Kurzawa,Pushpa Hariharan,Qin Li,Qing Kay Li,Rajiv Dhir,Ratna R Thangudu,Rebecca Montgomery,Richard D Smith,Sailaja Mareedu,Samuel H Payne,Sandra Cerda,Sandra Cottingham,Sarah Haynes,Shankha Satpathy,Shannon Richey,Shilpi Singh,Shirley X Tsang

Journal

Cancer Cell

Published Date

2023/1/9

Genomic and transcriptomic analysis of checkpoint blockade response in advanced non-small cell lung cancer

Anti-PD-1/PD-L1 agents have transformed the treatment landscape of advanced non-small cell lung cancer (NSCLC). To expand our understanding of the molecular features underlying response to checkpoint inhibitors in NSCLC, we describe here the first joint analysis of the Stand Up To Cancer-Mark Foundation cohort, a resource of whole exome and/or RNA sequencing from 393 patients with NSCLC treated with anti-PD-(L)1 therapy, along with matched clinical response annotation. We identify a number of associations between molecular features and outcome, including (1) favorable (for example, ATM altered) and unfavorable (for example, TERT amplified) genomic subgroups, (2) a prominent association between expression of inducible components of the immunoproteasome and response and (3) a dedifferentiated tumor-intrinsic subtype with enhanced response to checkpoint blockade. Taken together …

Authors

Arvind Ravi,Matthew D Hellmann,Monica B Arniella,Mark Holton,Samuel S Freeman,Vivek Naranbhai,Chip Stewart,Ignaty Leshchiner,Jaegil Kim,Yo Akiyama,Aaron T Griffin,Natalie I Vokes,Mustafa Sakhi,Vashine Kamesan,Hira Rizvi,Biagio Ricciuti,Patrick M Forde,Valsamo Anagnostou,Jonathan W Riess,Don L Gibbons,Nathan A Pennell,Vamsidhar Velcheti,Subba R Digumarthy,Mari Mino-Kenudson,Andrea Califano,John V Heymach,Roy S Herbst,Julie R Brahmer,Kurt A Schalper,Victor E Velculescu,Brian S Henick,Naiyer Rizvi,Pasi A Jänne,Mark M Awad,Andrew Chow,Benjamin D Greenbaum,Marta Luksza,Alice T Shaw,Jedd Wolchok,Nir Hacohen,Gad Getz,Justin F Gainor

Journal

Nature genetics

Published Date

2023/5

Genetic events associated with venetoclax resistance in CLL identified by whole-exome sequencing of patient samples

Although BCL2 mutations are reported as later occurring events leading to venetoclax resistance, many other mechanisms of progression have been reported though remain poorly understood. Here, we analyze longitudinal tumor samples from 11 patients with disease progression while receiving venetoclax to characterize the clonal evolution of resistance. All patients tested showed increased in vitro resistance to venetoclax at the posttreatment time point. We found the previously described acquired BCL2-G101V mutation in only 4 of 11 patients, with 2 patients showing a very low variant allele fraction (0.03%-4.68%). Whole-exome sequencing revealed acquired loss(8p) in 4 of 11 patients, of which 2 patients also had gain (1q21.2-21.3) in the same cells affecting the MCL1 gene. In vitro experiments showed that CLL cells from the 4 patients with loss(8p) were more resistant to venetoclax than cells from those …

Authors

Jasneet Kaur Khalsa,Justin Cha,Filippo Utro,Aishath Naeem,Ishwarya Murali,Yanan Kuang,Kevin Vasquez,Liang Li,Svitlana Tyekucheva,Stacey M Fernandes,Lauren Veronese,Romain Guieze,Binu Kandathilparambil Sasi,Zixu Wang,John-Hanson Machado,Harrison Bai,Maryam Alasfour,Kahn Rhrissorrakrai,Chaya Levovitz,Brian P Danysh,Kara Slowik,Raquel A Jacobs,Matthew S Davids,Cloud P Paweletz,Ignaty Leshchiner,Laxmi Parida,Gad Getz,Jennifer R Brown

Journal

Blood

Published Date

2023/8/3

Evolutionary history of transformation from chronic lymphocytic leukemia to Richter syndrome

Richter syndrome (RS) arising from chronic lymphocytic leukemia (CLL) exemplifies an aggressive malignancy that develops from an indolent neoplasm. To decipher the genetics underlying this transformation, we computationally deconvoluted admixtures of CLL and RS cells from 52 patients with RS, evaluating paired CLL–RS whole-exome sequencing data. We discovered RS-specific somatic driver mutations (including IRF2BP2, SRSF1, B2M, DNMT3A and CCND3), recurrent copy-number alterations beyond del(9p21)(CDKN2A/B), whole-genome duplication and chromothripsis, which were confirmed in 45 independent RS cases and in an external set of RS whole genomes. Through unsupervised clustering, clonally related RS was largely distinct from diffuse large B cell lymphoma. We distinguished pathways that were dysregulated in RS versus CLL, and detected clonal evolution of transformation at single …

Authors

Erin M Parry,Ignaty Leshchiner,Romain Guièze,Connor Johnson,Eugen Tausch,Sameer A Parikh,Camilla Lemvigh,Julien Broséus,Sébastien Hergalant,Conor Messer,Filippo Utro,Chaya Levovitz,Kahn Rhrissorrakrai,Liang Li,Daniel Rosebrock,Shanye Yin,Stephanie Deng,Kara Slowik,Raquel Jacobs,Teddy Huang,Shuqiang Li,Geoff Fell,Robert Redd,Ziao Lin,Binyamin A Knisbacher,Dimitri Livitz,Christof Schneider,Neil Ruthen,Liudmila Elagina,Amaro Taylor-Weiner,Bria Persaud,Aina Martinez,Stacey M Fernandes,Noelia Purroy,Annabelle J Anandappa,Jialin Ma,Julian Hess,Laura Z Rassenti,Thomas J Kipps,Nitin Jain,William Wierda,Florence Cymbalista,Pierre Feugier,Neil E Kay,Kenneth J Livak,Brian P Danysh,Chip Stewart,Donna Neuberg,Matthew S Davids,Jennifer R Brown,Laxmi Parida,Stephan Stilgenbauer,Gad Getz,Catherine J Wu

Journal

Nature Medicine

Published Date

2023/1/9

Inferring early genetic progression in cancers with unobtainable premalignant disease

Analysis of premalignant tissue has identified the typical order of somatic events leading to invasive tumors in several cancer types. For other cancers, premalignant tissue is unobtainable, leaving genetic progression unknown. Here, we demonstrate how to infer progression from exome sequencing of primary tumors. Our computational method, PhylogicNDT, recapitulated the previous experimentally determined genetic progression of human papillomavirus-negative (HPV–) head and neck squamous cell carcinoma (HNSCC). We then evaluated HPV+ HNSCC, which lacks premalignant tissue, and uncovered its previously unknown progression, identifying early drivers. We converted relative timing estimates of driver mutations and HPV integration to years before diagnosis based on a clock-like mutational signature. We associated the timing of transitions to aneuploidy with increased intratumor genetic …

Authors

Ignaty Leshchiner,Edmund A Mroz,Justin Cha,Daniel Rosebrock,Oliver Spiro,Juliana Bonilla-Velez,William C Faquin,Armida Lefranc-Torres,Derrick T Lin,William A Michaud,Gad Getz,James W Rocco

Journal

Nature Cancer

Published Date

2023/4

Pan-cancer analysis of post-translational modifications reveals shared patterns of protein regulation

Post-translational modifications (PTMs) play key roles in regulating cell signaling and physiology in both normal and cancer cells. Advances in mass spectrometry enable high-throughput, accurate, and sensitive measurement of PTM levels to better understand their role, prevalence, and crosstalk. Here, we analyze the largest collection of proteogenomics data from 1,110 patients with PTM profiles across 11 cancer types (10 from the National Cancer Institute's Clinical Proteomic Tumor Analysis Consortium [CPTAC]). Our study reveals pan-cancer patterns of changes in protein acetylation and phosphorylation involved in hallmark cancer processes. These patterns revealed subsets of tumors, from different cancer types, including those with dysregulated DNA repair driven by phosphorylation, altered metabolic regulation associated with immune response driven by acetylation, affected kinase specificity by crosstalk …

Authors

Yifat Geffen,Shankara Anand,Yo Akiyama,Tomer M Yaron,Yizhe Song,Jared L Johnson,Akshay Govindan,Özgün Babur,Yize Li,Emily Huntsman,Liang-Bo Wang,Chet Birger,David I Heiman,Qing Zhang,Mendy Miller,Yosef E Maruvka,Nicholas J Haradhvala,Anna Calinawan,Saveliy Belkin,Alexander Kerelsky,Karl R Clauser,Karsten Krug,Shankha Satpathy,Samuel H Payne,DR Mani,Michael A Gillette,Saravana M Dhanasekaran,Mathangi Thiagarajan,Mehdi Mesri,Henry Rodriguez,Ana I Robles,Steven A Carr,Alexander J Lazar,François Aguet,Lewis C Cantley,Li Ding,Gad Getz,Eunkyung An,Meenakshi Anurag,Jasmin Bavarva,Michael J Birrer,Song Cao,Michele Ceccarelli,Daniel W Chan,Arul M Chinnaiyan,Hanbyul Cho,Shrabanti Chowdhury,Marcin P Cieslik,Antonio Colaprico,Felipe da Veiga Leprevost,Corbin Day,Marcin J Domagalski,Yongchao Dou,Brian J Druker,Nathan Edwards,Matthew J Ellis,David Fenyo,Steven M Foltz,Alicia Francis,Tania J Gonzalez Robles,Sara JC Gosline,Zeynep H Gümüş,Tara Hiltke,Runyu Hong,Galen Hostetter,Yingwei Hu,Chen Huang,Antonio Iavarone,Eric J Jaehnig,Scott D Jewel,Jiayi Ji,Wen Jiang,Lizabeth Katsnelson,Karen A Ketchum,Iga Kolodziejczak,Chandan Kumar-Sinha,Jonathan T Lei,Wen-Wei Liang,Yuxing Liao,Caleb M Lindgren,Tao Liu,Wenke Liu,Weiping Ma,Wilson McKerrow,Alexey I Nesvizhskii,Chelsea Newton,Robert Oldroyd,Gilbert S Omenn,Amanda G Paulovich,Francesca Petralia,Pietro Pugliese,Boris Reva,Karin D Rodland,Kelly V Ruggles,Dmitry Rykunov,Fernanda Martins Rodrigues,Sara R Savage,Eric E Schadt,Michael Schnaubelt,Tobias Schraink,Zhiao Shi,Richard D Smith,Xiaoyu Song,Vasileios Stathias,Erik P Storrs,Stephan Schürer,Myvizhi Esai Selvan,Jimin Tan,Nadezhda V Terekhanova,Ratna R Thangudu,Nicole Tignor,Joshua M Wang,Pei Wang,Ying Cindy Wang,Bo Wen,Maciej Wiznerowicz,Yige Wu,Matthew A Wyczalkowski,Lijun Yao,Xinpei Yi,Bing Zhang,Hui Zhang,Xu Zhang,Zhen Zhang,Daniel Cui Zhou

Journal

Cell

Published Date

2023/8/31

Clonal origin of KMT2A wild-type lineage-switch leukemia following CAR-T cell and blinatumomab therapy

Children with acute lymphoblastic leukemia (ALL) undergoing anti-CD19 therapy occasionally develop acute myeloid leukemia (AML). The clonal origin of such lineage-switch leukemias, , – remains unresolved. Here, we reconstructed the phylogeny of multiple leukemias in a girl who, following multiply relapsed ALL, received anti-CD19 cellular and antibody treatment and subsequently developed AML. Whole genome sequencing unambiguously revealed the AML derived from the initial ALL, with distinct driver mutations that were detectable before emergence. Extensive prior diversification and subsequent clonal selection underpins this fatal lineage switch. Genomic monitoring of primary leukemias and recurrences may predict therapy resistance, especially regarding anti-CD19 treatment.

Authors

Tim HH Coorens,Grace Collord,Taryn D Treger,Stuart Adams,Emily Mitchell,Barbara Newman,Gad Getz,Anna L Godfrey,Jack Bartram,Sam Behjati

Journal

Nature Cancer

Published Date

2023/8

In Vivo Modeling of CLL Transformation to Richter Syndrome Reveals Convergent Evolutionary Paths and Therapeutic Vulnerabilities

Transformation to aggressive disease histologies generates formidable clinical challenges across cancers, but biological insights remain few. We modeled the genetic heterogeneity of chronic lymphocytic leukemia (CLL) through multiplexed in vivo CRISPR-Cas9 B-cell editing of recurrent CLL loss-of-function drivers in mice and recapitulated the process of transformation from indolent CLL into large cell lymphoma [i.e., Richter syndrome (RS)]. Evolutionary trajectories of 64 mice carrying diverse combinatorial gene assortments revealed coselection of mutations in Trp53, Mga, and Chd2 and the dual impact of clonal Mga/Chd2 mutations on E2F/MYC and interferon signaling dysregulation. Comparative human and murine RS analyses demonstrated tonic PI3K signaling as a key feature of transformed disease, with constitutive activation of the AKT and S6 kinases, downmodulation of the PTEN …

Authors

Elisa Ten Hacken,Tomasz Sewastianik,Shanye Yin,Gabriela Brunsting Hoffmann,Michaela Gruber,Kendell Clement,Livius Penter,Robert A Redd,Neil Ruthen,Sébastien Hergalant,Alanna Sholokhova,Geoffrey Fell,Erin M Parry,Julien Broséus,Romain Guieze,Fabienne Lucas,María Hernández-Sánchez,Kaitlyn Baranowski,Jackson Southard,Heather Joyal,Leah Billington,Fara Faye D Regis,Elizabeth Witten,Mohamed Uduman,Binyamin A Knisbacher,Shuqiang Li,Haoxiang Lyu,Tiziana Vaisitti,Silvia Deaglio,Giorgio Inghirami,Pierre Feugier,Stephan Stilgenbauer,Eugen Tausch,Matthew S Davids,Gad Getz,Kenneth J Livak,Ivana Bozic,Donna S Neuberg,Ruben D Carrasco,Catherine J Wu

Journal

Blood cancer discovery

Published Date

2023/3/1

Professor FAQs

What is Gad Getz's h-index at Harvard University?

The h-index of Gad Getz has been 197 since 2020 and 228 in total.

What are Gad Getz's top articles?

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