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2. Sex-Biased ZRSR2 Mutations in Myeloid Malignancies Impair Plasmacytoid Dendritic Cell Activation and Apoptosis

Author

Togami, Katsuhiro, Chung, Sun Sook, Madan, Vikas, Booth, Christopher AG, Kenyon, Christopher M, Cabal-Hierro, Lucia, Taylor, Justin, Kim, Sunhee S, Griffin, Gabriel K, Ghandi, Mahmoud, Li, Jia, Li, Yvonne Y, Angelot-Delettre, Fanny, Biichle, Sabeha, Seiler, Michael, Buonamici, Silvia, Lovitch, Scott B, Louissaint, Abner, Morgan, Elizabeth A, Jardin, Fabrice, Piccaluga, Pier Paolo, Weinstock, David M, Hammerman, Peter S, Yang, Henry, Konopleva, Marina, Pemmaraju, Naveen, Garnache-Ottou, Francine, Abdel-Wahab, Omar, Koeffler, H Phillip, and Lane, Andrew A

Subjects
Rare Diseases, Clinical Research, Cancer, Hematology, Genetics, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Apoptosis, Dendritic Cells, Female, Gender Identity, Humans, Male, Mutation, Myeloproliferative Disorders, Ribonucleoproteins, Oncology and Carcinogenesis
Abstract

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an aggressive leukemia of plasmacytoid dendritic cells (pDC). BPDCN occurs at least three times more frequently in men than in women, but the reasons for this sex bias are unknown. Here, studying genomics of primary BPDCN and modeling disease-associated mutations, we link acquired alterations in RNA splicing to abnormal pDC development and inflammatory response through Toll-like receptors. Loss-of-function mutations in ZRSR2, an X chromosome gene encoding a splicing factor, are enriched in BPDCN, and nearly all mutations occur in males. ZRSR2 mutation impairs pDC activation and apoptosis after inflammatory stimuli, associated with intron retention and inability to upregulate the transcription factor IRF7. In vivo, BPDCN-associated mutations promote pDC expansion and signatures of decreased activation. These data support a model in which male-biased mutations in hematopoietic progenitors alter pDC function and confer protection from apoptosis, which may impair immunity and predispose to leukemic transformation. SIGNIFICANCE: Sex bias in cancer is well recognized, but the underlying mechanisms are incompletely defined. We connect X chromosome mutations in ZRSR2 to an extremely male-predominant leukemia. Aberrant RNA splicing induced by ZRSR2 mutation impairs dendritic cell inflammatory signaling, interferon production, and apoptosis, revealing a sex- and lineage-related tumor suppressor pathway.This article is highlighted in the In This Issue feature, p. 275.

Published
2022

3. A Nonlinear Acceleration Method for Iterative Algorithms

Author

Shamsi, Mahdi, Ghandi, Mahmoud, and Marvasti, Farokh

Subjects
Electrical Engineering and Systems Science - Signal Processing, Computer Science - Machine Learning, Electrical Engineering and Systems Science - Image and Video Processing, Mathematics - Numerical Analysis
Abstract

Iterative methods have led to better understanding and solving problems such as missing sampling, deconvolution, inverse systems, impulsive and Salt and Pepper noise removal problems. However, the challenges such as the speed of convergence and or the accuracy of the answer still remain. In order to improve the existing iterative algorithms, a non-linear method is discussed in this paper. The mentioned method is analyzed from different aspects, including its convergence and its ability to accelerate recursive algorithms. We show that this method is capable of improving Iterative Method (IM) as a non-uniform sampling reconstruction algorithm and some iterative sparse recovery algorithms such as Iterative Reweighted Least Squares (IRLS), Iterative Method with Adaptive Thresholding (IMAT), Smoothed l0 (SL0) and Alternating Direction Method of Multipliers (ADMM) for solving LASSO problems family (including Lasso itself, Lasso-LSQR and group-Lasso). It is also capable of both accelerating and stabilizing the well-known Chebyshev Acceleration (CA) method. Furthermore, the proposed algorithm can extend the stability range by reducing the sensitivity of iterative algorithms to the changes of adaptation rate.

Published
2019

5. Next-generation characterization of the Cancer Cell Line Encyclopedia

Author

Ghandi, Mahmoud, Huang, Franklin W, Jané-Valbuena, Judit, Kryukov, Gregory V, Lo, Christopher C, McDonald, E Robert, Barretina, Jordi, Gelfand, Ellen T, Bielski, Craig M, Li, Haoxin, Hu, Kevin, Andreev-Drakhlin, Alexander Y, Kim, Jaegil, Hess, Julian M, Haas, Brian J, Aguet, François, Weir, Barbara A, Rothberg, Michael V, Paolella, Brenton R, Lawrence, Michael S, Akbani, Rehan, Lu, Yiling, Tiv, Hong L, Gokhale, Prafulla C, de Weck, Antoine, Mansour, Ali Amin, Oh, Coyin, Shih, Juliann, Hadi, Kevin, Rosen, Yanay, Bistline, Jonathan, Venkatesan, Kavitha, Reddy, Anupama, Sonkin, Dmitriy, Liu, Manway, Lehar, Joseph, Korn, Joshua M, Porter, Dale A, Jones, Michael D, Golji, Javad, Caponigro, Giordano, Taylor, Jordan E, Dunning, Caitlin M, Creech, Amanda L, Warren, Allison C, McFarland, James M, Zamanighomi, Mahdi, Kauffmann, Audrey, Stransky, Nicolas, Imielinski, Marcin, Maruvka, Yosef E, Cherniack, Andrew D, Tsherniak, Aviad, Vazquez, Francisca, Jaffe, Jacob D, Lane, Andrew A, Weinstock, David M, Johannessen, Cory M, Morrissey, Michael P, Stegmeier, Frank, Schlegel, Robert, Hahn, William C, Getz, Gad, Mills, Gordon B, Boehm, Jesse S, Golub, Todd R, Garraway, Levi A, and Sellers, William R

Subjects
Genetics, Human Genome, Lung, Cancer, Biotechnology, Lung Cancer, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Antineoplastic Agents, Biomarkers, Tumor, Cell Line, Tumor, DNA Methylation, Drug Resistance, Neoplasm, Ethnicity, Gene Editing, Histones, Humans, MicroRNAs, Molecular Targeted Therapy, Neoplasms, Protein Array Analysis, RNA Splicing, General Science & Technology
Abstract

Large panels of comprehensively characterized human cancer models, including the Cancer Cell Line Encyclopedia (CCLE), have provided a rigorous framework with which to study genetic variants, candidate targets, and small-molecule and biological therapeutics and to identify new marker-driven cancer dependencies. To improve our understanding of the molecular features that contribute to cancer phenotypes, including drug responses, here we have expanded the characterizations of cancer cell lines to include genetic, RNA splicing, DNA methylation, histone H3 modification, microRNA expression and reverse-phase protein array data for 1,072 cell lines from individuals of various lineages and ethnicities. Integration of these data with functional characterizations such as drug-sensitivity, short hairpin RNA knockdown and CRISPR-Cas9 knockout data reveals potential targets for cancer drugs and associated biomarkers. Together, this dataset and an accompanying public data portal provide a resource for the acceleration of cancer research using model cancer cell lines.

Published
2019

6. Decomposing Oncogenic Transcriptional Signatures to Generate Maps of Divergent Cellular States

Author

Kim, Jong Wook, Abudayyeh, Omar O, Yeerna, Huwate, Yeang, Chen-Hsiang, Stewart, Michelle, Jenkins, Russell W, Kitajima, Shunsuke, Konieczkowski, David J, Medetgul-Ernar, Kate, Cavazos, Taylor, Mah, Clarence, Ting, Stephanie, Van Allen, Eliezer M, Cohen, Ofir, Mcdermott, John, Damato, Emily, Aguirre, Andrew J, Liang, Jonathan, Liberzon, Arthur, Alexe, Gabriella, Doench, John, Ghandi, Mahmoud, Vazquez, Francisca, Weir, Barbara A, Tsherniak, Aviad, Subramanian, Aravind, Meneses-Cime, Karina, Park, Jason, Clemons, Paul, Garraway, Levi A, Thomas, David, Boehm, Jesse S, Barbie, David A, Hahn, William C, Mesirov, Jill P, and Tamayo, Pablo

Subjects
Biological Sciences, Genetics, Biotechnology, Human Genome, Cancer, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Biomarkers, Tumor, Cell Line, Tumor, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genes, ras, Genome, Humans, MAP Kinase Signaling System, Neoplasms, Precision Medicine, Bayesian nomogram, cellular states, drug sensitivity, genetic dependency, inferential model, matrix factorization, oncoGPS, oncogenic pathway, precision medicine, transcriptional signatures, Biochemistry and Cell Biology, Biochemistry and cell biology
Abstract

The systematic sequencing of the cancer genome has led to the identification of numerous genetic alterations in cancer. However, a deeper understanding of the functional consequences of these alterations is necessary to guide appropriate therapeutic strategies. Here, we describe Onco-GPS (OncoGenic Positioning System), a data-driven analysis framework to organize individual tumor samples with shared oncogenic alterations onto a reference map defined by their underlying cellular states. We applied the methodology to the RAS pathway and identified nine distinct components that reflect transcriptional activities downstream of RAS and defined several functional states associated with patterns of transcriptional component activation that associates with genomic hallmarks and response to genetic and pharmacological perturbations. These results show that the Onco-GPS is an effective approach to explore the complex landscape of oncogenic cellular states across cancers, and an analytic framework to summarize knowledge, establish relationships, and generate more effective disease models for research or as part of individualized precision medicine paradigms.

Published
2017

7. Distinct Classes of Complex Structural Variation Uncovered across Thousands of Cancer Genome Graphs

Author

Hadi, Kevin, Yao, Xiaotong, Behr, Julie M., Deshpande, Aditya, Xanthopoulakis, Charalampos, Tian, Huasong, Kudman, Sarah, Rosiene, Joel, Darmofal, Madison, DeRose, Joseph, Mortensen, Rick, Adney, Emily M., Shaiber, Alon, Gajic, Zoran, Sigouros, Michael, Eng, Kenneth, Wala, Jeremiah A., Wrzeszczyński, Kazimierz O., Arora, Kanika, Shah, Minita, Emde, Anne-Katrin, Felice, Vanessa, Frank, Mayu O., Darnell, Robert B., Ghandi, Mahmoud, Huang, Franklin, Dewhurst, Sally, Maciejowski, John, de Lange, Titia, Setton, Jeremy, Riaz, Nadeem, Reis-Filho, Jorge S., Powell, Simon, Knowles, David A., Reznik, Ed, Mishra, Bud, Beroukhim, Rameen, Zody, Michael C., Robine, Nicolas, Oman, Kenji M., Sanchez, Carissa A., Kuhner, Mary K., Smith, Lucian P., Galipeau, Patricia C., Paulson, Thomas G., Reid, Brian J., Li, Xiaohong, Wilkes, David, Sboner, Andrea, Mosquera, Juan Miguel, Elemento, Olivier, and Imielinski, Marcin

Published
2020
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9. Characterizing genomic alterations in cancer by complementary functional associations

Author

Kim, Jong Wook, Botvinnik, Olga B, Abudayyeh, Omar, Birger, Chet, Rosenbluh, Joseph, Shrestha, Yashaswi, Abazeed, Mohamed E, Hammerman, Peter S, DiCara, Daniel, Konieczkowski, David J, Johannessen, Cory M, Liberzon, Arthur, Alizad-Rahvar, Amir Reza, Alexe, Gabriela, Aguirre, Andrew, Ghandi, Mahmoud, Greulich, Heidi, Vazquez, Francisca, Weir, Barbara A, Van Allen, Eliezer M, Tsherniak, Aviad, Shao, Diane D, Zack, Travis I, Noble, Michael, Getz, Gad, Beroukhim, Rameen, Garraway, Levi A, Ardakani, Masoud, Romualdi, Chiara, Sales, Gabriele, Barbie, David A, Boehm, Jesse S, Hahn, William C, Mesirov, Jill P, and Tamayo, Pablo

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Cancer, Human Genome, Biotechnology, 2.1 Biological and endogenous factors, Good Health and Well Being, Biomarkers, Tumor, Chromosome Mapping, Drug Resistance, Neoplasm, Genes, Neoplasm, Genetic Predisposition to Disease, Genome, Human, Genome-Wide Association Study, Humans, Mutation, Neoplasm Proteins, Neoplasms, Polymorphism, Single Nucleotide, Signal Transduction
Abstract

Systematic efforts to sequence the cancer genome have identified large numbers of mutations and copy number alterations in human cancers. However, elucidating the functional consequences of these variants, and their interactions to drive or maintain oncogenic states, remains a challenge in cancer research. We developed REVEALER, a computational method that identifies combinations of mutually exclusive genomic alterations correlated with functional phenotypes, such as the activation or gene dependency of oncogenic pathways or sensitivity to a drug treatment. We used REVEALER to uncover complementary genomic alterations associated with the transcriptional activation of β-catenin and NRF2, MEK-inhibitor sensitivity, and KRAS dependency. REVEALER successfully identified both known and new associations, demonstrating the power of combining functional profiles with extensive characterization of genomic alterations in cancer genomes.

Published
2016

10. Quantitative Proteomics of the Cancer Cell Line Encyclopedia

Author

Nusinow, David P., Szpyt, John, Ghandi, Mahmoud, Rose, Christopher M., McDonald, E. Robert, III, Kalocsay, Marian, Jané-Valbuena, Judit, Gelfand, Ellen, Schweppe, Devin K., Jedrychowski, Mark, Golji, Javad, Porter, Dale A., Rejtar, Tomas, Wang, Y. Karen, Kryukov, Gregory V., Stegmeier, Frank, Erickson, Brian K., Garraway, Levi A., Sellers, William R., and Gygi, Steven P.

Published
2020
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11. The Molecular Signatures Database (MSigDB) hallmark gene set collection.

Author

Liberzon, Arthur, Birger, Chet, Thorvaldsdóttir, Helga, Ghandi, Mahmoud, Mesirov, Jill P, and Tamayo, Pablo

Subjects
gene expression, gene set enrichment analysis, gene sets, Biotechnology, Genetics, Biochemistry and Cell Biology
Abstract

The Molecular Signatures Database (MSigDB) is one of the most widely used and comprehensive databases of gene sets for performing gene set enrichment analysis. Since its creation, MSigDB has grown beyond its roots in metabolic disease and cancer to include >10,000 gene sets. These better represent a wider range of biological processes and diseases, but the utility of the database is reduced by increased redundancy across, and heterogeneity within, gene sets. To address this challenge, here we use a combination of automated approaches and expert curation to develop a collection of "hallmark" gene sets as part of MSigDB. Each hallmark in this collection consists of a "refined" gene set, derived from multiple "founder" sets, that conveys a specific biological state or process and displays coherent expression. The hallmarks effectively summarize most of the relevant information of the original founder sets and, by reducing both variation and redundancy, provide more refined and concise inputs for gene set enrichment analysis.

Published
2015

12. Small-Molecule and CRISPR Screening Converge to Reveal Receptor Tyrosine Kinase Dependencies in Pediatric Rhabdoid Tumors

Author

Oberlick, Elaine M., Rees, Matthew G., Seashore-Ludlow, Brinton, Vazquez, Francisca, Nelson, Geoffrey M., Dharia, Neekesh V., Weir, Barbara A., Tsherniak, Aviad, Ghandi, Mahmoud, Krill-Burger, John M., Meyers, Robin M., Wang, Xiaofeng, Montgomery, Phil, Root, David E., Bieber, Jake M., Radko, Sandi, Cheah, Jaime H., Hon, C. Suk-Yee, Shamji, Alykhan F., Clemons, Paul A., Park, Peter J., Dyer, Michael A., Golub, Todd R., Stegmaier, Kimberly, Hahn, William C., Stewart, Elizabeth A., Schreiber, Stuart L., and Roberts, Charles W.M.

Published
2019
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13. RPL22 is a tumor suppressor in MSI-high cancers and a key splicing regulator of MDM4

Author

Weinstein, Hannah N.W., primary, Hu, Kevin, additional, Fish, Lisa, additional, Chen, Yih-An, additional, Allegakoen, Paul, additional, Hui, Keliana S. F., additional, Pham, Julia H., additional, Baco, Maria B., additional, Song, Hanbing, additional, Giacomelli, Andrew O., additional, Vazquez, Francisca, additional, Ghandi, Mahmoud, additional, Goodarzi, Hani, additional, and Huang, Franklin W., additional

Published
2023
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15. DNA methyltransferase inhibition overcomes diphthamide pathway deficiencies underlying CD123-targeted treatment resistance

Author

Togami, Katsuhiro, Pastika, Timothy, Stephansky, Jason, Ghandi, Mahmoud, Christie, Amanda L., Jones, Kristen L., Johnson, Carl A., Lindsay, Ross W., Brooks, Christopher L., Letai, Anthony, Craig, Jeffrey W., Pozdnyakova, Olga, Weinstock, David M., Montero, Joan, Aster, Jon C., Johannessen, Cory M., and Lane, Andrew A.

Subjects
Thermo Fisher Scientific Inc., Interleukins, Blinatumomab, Methylation, Transferases, DNA, Dendritic cells, Inotuzumab ozogamicin, Scientific equipment industry, Tagraxofusp, Acute myelocytic leukemia, Cancer, Myeloid leukemia, Tumors, Genomes, Enzymes, Diphtheria, Health care industry
Abstract

The interleukin-3 receptor [alpha] subunit, CD123, is expressed in many hematologic malignancies including acute myeloid leukemia (AML) and blastic plasmacytoid dendritic cell neoplasm (BPDCN). Tagraxofusp (SL-401) is a CD123-targeted therapy consisting of interleukin-3 fused to a truncated diphtheria toxin payload. Factors influencing response to tagraxofusp other than CD123 expression are largely unknown. We interrogated tagraxofusp resistance in patients and experimental models and found that it was not associated with CD123 loss. Rather, resistant AML and BPDCN cells frequently acquired deficiencies in the diphthamide synthesis pathway, impairing tagraxofusp's ability to ADP- ribosylate cellular targets. Expression of DPH1, encoding a diphthamide pathway enzyme, was reduced by DNA CpG methylation in resistant cells. Treatment with the DNA methyltransferase inhibitor azacitidine restored DPH1 expression and tagraxofusp sensitivity. We also developed a drug-dependent ADP-ribosylation assay in primary cells that correlated with tagraxofusp activity and may represent an additional novel biomarker. As predicted by these results and our observation that resistance also increased mitochondrial apoptotic priming, we found that the combination of tagraxofusp and azacitidine was effective in patient-derived xenografts treated in vivo. These data have important implications for clinical use of tagraxofusp and led to a phase 1 study combining tagraxofusp and azacitidine in myeloid malignancies., Introduction CD123, or the interleukin-3 (IL-3) receptor (IL-3R) [alpha] chain, is a cell-surface marker associated with a variety of hematologic malignancies and is often enriched on tumor cells compared with [...]

Published
2019
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16. WRN helicase is a synthetic lethal target in microsatellite unstable cancers

Author

Chan, Edmond M., Shibue, Tsukasa, McFarland, James M., Gaeta, Benjamin, Ghandi, Mahmoud, Dumont, Nancy, and Gonzalez, Alfredo

Subjects
Helicases -- Analysis, CRISPR-Cas technology -- Usage, Synthetic biology -- Usage, Werner syndrome -- Research, Genetic research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Synthetic lethality--an interaction between two genetic events through which the co-occurrence of these two genetic events leads to cell death, but each event alone does not--can be exploited for cancer therapeutics.sup.1. DNA repair processes represent attractive synthetic lethal targets, because many cancers exhibit an impairment of a DNA repair pathway, which can lead to dependence on specific repair proteins.sup.2. The success of poly(ADP-ribose) polymerase 1 (PARP-1) inhibitors in cancers with deficiencies in homologous recombination highlights the potential of this approach.sup.3. Hypothesizing that other DNA repair defects would give rise to synthetic lethal relationships, we queried dependencies in cancers with microsatellite instability (MSI), which results from deficient DNA mismatch repair. Here we analysed data from large-scale silencing screens using CRISPR-Cas9-mediated knockout and RNA interference, and found that the RecQ DNA helicase WRN was selectively essential in MSI models in vitro and in vivo, yet dispensable in models of cancers that are microsatellite stable. Depletion of WRN induced double-stranded DNA breaks and promoted apoptosis and cell cycle arrest selectively in MSI models. MSI cancer models required the helicase activity of WRN, but not its exonuclease activity. These findings show that WRN is a synthetic lethal vulnerability and promising drug target for MSI cancers. Depletion of the DNA helicase WRN induced double-stranded DNA breaks, and promoted apoptosis and cell cycle arrest selectively in cancers with microsatellite instability, indicating that WRN is a promising drug target for the treatment of these cancers., Author(s): Edmond M. Chan [sup.1] [sup.2] , Tsukasa Shibue [sup.1] , James M. McFarland [sup.1] , Benjamin Gaeta [sup.1] , Mahmoud Ghandi [sup.1] , Nancy Dumont [sup.1] , Alfredo Gonzalez [...]

Published
2019
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17. The landscape of cancer cell line metabolism

Author

Li, Haoxin, Ning, Shaoyang, Ghandi, Mahmoud, Kryukov, Gregory V., Gopal, Shuba, Deik, Amy, Souza, Amanda, Pierce, Kerry, Keskula, Paula, Hernandez, Desiree, Ann, Julie, Shkoza, Dojna, Apfel, Verena, Zou, Yilong, Vazquez, Francisca, Barretina, Jordi, Pagliarini, Raymond A., Galli, Giorgio G., Root, David E., Hahn, William C., Tsherniak, Aviad, Giannakis, Marios, Schreiber, Stuart L., Clish, Clary B., Garraway, Levi A., and Sellers, William R.

Published
2019
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18. Defining a Cancer Dependency Map

Author

Tsherniak, Aviad, Vazquez, Francisca, Montgomery, Phil G., Weir, Barbara A., Kryukov, Gregory, Cowley, Glenn S., Gill, Stanley, Harrington, William F., Pantel, Sasha, Krill-Burger, John M., Meyers, Robin M., Ali, Levi, Goodale, Amy, Lee, Yenarae, Jiang, Guozhi, Hsiao, Jessica, Gerath, William F.J., Howell, Sara, Merkel, Erin, Ghandi, Mahmoud, Garraway, Levi A., Root, David E., Golub, Todd R., Boehm, Jesse S., and Hahn, William C.

Published
2017
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19. Multiplexed single-cell transcriptional response profiling to define cancer vulnerabilities and therapeutic mechanism of action

Author

McFarland, James M., Paolella, Brenton R., Warren, Allison, Geiger-Schuller, Kathryn, Shibue, Tsukasa, Rothberg, Michael, Kuksenko, Olena, Colgan, William N., Jones, Andrew, Chambers, Emily, Dionne, Danielle, Bender, Samantha, Wolpin, Brian M., Ghandi, Mahmoud, Tirosh, Itay, Rozenblatt-Rosen, Orit, Roth, Jennifer A., Golub, Todd R., Regev, Aviv, Aguirre, Andrew J., Vazquez, Francisca, and Tsherniak, Aviad

Published
2020
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20. Genetic and transcriptional evolution alters cancer cell line drug response

Author

Ben-David, Uri, Siranosian, Benjamin, Ha, Gavin, Tang, Helen, Oren, Yaara, Hinohara, Kunihiko, Strathdee, Craig A., Dempster, Joshua, Lyons, Nicholas J., Burns, Robert, Nag, Anwesha, Kugener, Guillaume, Cimini, Beth, Tsvetkov, Peter, Maruvka, Yosef E., O’Rourke, Ryan, Garrity, Anthony, Tubelli, Andrew A., Bandopadhayay, Pratiti, Tsherniak, Aviad, Vazquez, Francisca, Wong, Bang, Birger, Chet, Ghandi, Mahmoud, Thorner, Aaron R., Bittker, Joshua A., Meyerson, Matthew, Getz, Gad, Beroukhim, Rameen, and Golub, Todd R.

Published
2018
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21. Pediatric-type nodal follicular lymphoma: a biologically distinct lymphoma with frequent MAPK pathway mutations

Author

Louissaint, Abner, Jr, Schafernak, Kristian T., Geyer, Julia T., Kovach, Alexandra E., Ghandi, Mahmoud, Gratzinger, Dita, Roth, Christine G., Paxton, Christian N., Kim, Sunhee, Namgyal, Chungdak, Morin, Ryan, Morgan, Elizabeth A., Neuberg, Donna S., South, Sarah T., Harris, Marian H., Hasserjian, Robert P., Hochberg, Ephraim P., Garraway, Levi A., Harris, Nancy Lee, and Weinstock, David M.

Published
2016
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23. Supplementary Tables from Sex-Biased ZRSR2 Mutations in Myeloid Malignancies Impair Plasmacytoid Dendritic Cell Activation and Apoptosis

Author

Togami, Katsuhiro, primary, Chung, Sun Sook, primary, Madan, Vikas, primary, Booth, Christopher A.G., primary, Kenyon, Christopher M., primary, Cabal-Hierro, Lucia, primary, Taylor, Justin, primary, Kim, Sunhee S., primary, Griffin, Gabriel K., primary, Ghandi, Mahmoud, primary, Li, Jia, primary, Li, Yvonne Y., primary, Angelot-Delettre, Fanny, primary, Biichle, Sabeha, primary, Seiler, Michael, primary, Buonamici, Silvia, primary, Lovitch, Scott B., primary, Louissaint, Abner, primary, Morgan, Elizabeth A., primary, Jardin, Fabrice, primary, Piccaluga, Pier Paolo, primary, Weinstock, David M., primary, Hammerman, Peter S., primary, Yang, Henry, primary, Konopleva, Marina, primary, Pemmaraju, Naveen, primary, Garnache-Ottou, Francine, primary, Abdel-Wahab, Omar, primary, Koeffler, H. Phillip, primary, and Lane, Andrew A., primary

Published
2023
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24. Supplementary Figures S1-S8 from Sex-Biased ZRSR2 Mutations in Myeloid Malignancies Impair Plasmacytoid Dendritic Cell Activation and Apoptosis

Author

Togami, Katsuhiro, primary, Chung, Sun Sook, primary, Madan, Vikas, primary, Booth, Christopher A.G., primary, Kenyon, Christopher M., primary, Cabal-Hierro, Lucia, primary, Taylor, Justin, primary, Kim, Sunhee S., primary, Griffin, Gabriel K., primary, Ghandi, Mahmoud, primary, Li, Jia, primary, Li, Yvonne Y., primary, Angelot-Delettre, Fanny, primary, Biichle, Sabeha, primary, Seiler, Michael, primary, Buonamici, Silvia, primary, Lovitch, Scott B., primary, Louissaint, Abner, primary, Morgan, Elizabeth A., primary, Jardin, Fabrice, primary, Piccaluga, Pier Paolo, primary, Weinstock, David M., primary, Hammerman, Peter S., primary, Yang, Henry, primary, Konopleva, Marina, primary, Pemmaraju, Naveen, primary, Garnache-Ottou, Francine, primary, Abdel-Wahab, Omar, primary, Koeffler, H. Phillip, primary, and Lane, Andrew A., primary

Published
2023
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25. Data from Sex-Biased ZRSR2 Mutations in Myeloid Malignancies Impair Plasmacytoid Dendritic Cell Activation and Apoptosis

Author

Togami, Katsuhiro, primary, Chung, Sun Sook, primary, Madan, Vikas, primary, Booth, Christopher A.G., primary, Kenyon, Christopher M., primary, Cabal-Hierro, Lucia, primary, Taylor, Justin, primary, Kim, Sunhee S., primary, Griffin, Gabriel K., primary, Ghandi, Mahmoud, primary, Li, Jia, primary, Li, Yvonne Y., primary, Angelot-Delettre, Fanny, primary, Biichle, Sabeha, primary, Seiler, Michael, primary, Buonamici, Silvia, primary, Lovitch, Scott B., primary, Louissaint, Abner, primary, Morgan, Elizabeth A., primary, Jardin, Fabrice, primary, Piccaluga, Pier Paolo, primary, Weinstock, David M., primary, Hammerman, Peter S., primary, Yang, Henry, primary, Konopleva, Marina, primary, Pemmaraju, Naveen, primary, Garnache-Ottou, Francine, primary, Abdel-Wahab, Omar, primary, Koeffler, H. Phillip, primary, and Lane, Andrew A., primary

Published
2023
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26. Supplementary Methods from Sex-Biased ZRSR2 Mutations in Myeloid Malignancies Impair Plasmacytoid Dendritic Cell Activation and Apoptosis

Author

Togami, Katsuhiro, primary, Chung, Sun Sook, primary, Madan, Vikas, primary, Booth, Christopher A.G., primary, Kenyon, Christopher M., primary, Cabal-Hierro, Lucia, primary, Taylor, Justin, primary, Kim, Sunhee S., primary, Griffin, Gabriel K., primary, Ghandi, Mahmoud, primary, Li, Jia, primary, Li, Yvonne Y., primary, Angelot-Delettre, Fanny, primary, Biichle, Sabeha, primary, Seiler, Michael, primary, Buonamici, Silvia, primary, Lovitch, Scott B., primary, Louissaint, Abner, primary, Morgan, Elizabeth A., primary, Jardin, Fabrice, primary, Piccaluga, Pier Paolo, primary, Weinstock, David M., primary, Hammerman, Peter S., primary, Yang, Henry, primary, Konopleva, Marina, primary, Pemmaraju, Naveen, primary, Garnache-Ottou, Francine, primary, Abdel-Wahab, Omar, primary, Koeffler, H. Phillip, primary, and Lane, Andrew A., primary

Published
2023
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27. Abstract 3449: Development of MRT-2359, an orally bioavailable GSPT1 molecular glue degrader, for the treatment of lung cancers with MYC-induced translational addiction

Author

Gavory, Gerald, primary, Ghandi, Mahmoud, additional, d’Alessandro, Anne-Cecile, additional, Bonenfant, Debora, additional, Cabanski, Maciej, additional, Cantagallo, Lisa, additional, Chicas, Agustin, additional, Chen, Qian, additional, Diesslin, Anna, additional, King, Christopher, additional, Massafra, Vittoria, additional, Narayan, Rajiv, additional, Osmont, Arnaud, additional, Peck, Dave, additional, Ortiz, Carolina Perdomo, additional, Schillo, Martin, additional, Singh, Ambika, additional, Tiedt, Ralph, additional, Tortoioli, Simone, additional, Buonamici, Silvia, additional, Janku, Filip, additional, Wallace, Owen, additional, and Fasching, Bernhard, additional

Published
2023
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34. RPL22 Is a Tumor Suppressor in MSI-High Cancers and a Key Splicing Regulator of MDM4

Author

Weinstein, Hannah Nicole Weber, primary, Hu, Kevin, additional, Fish, Lisa, additional, Chen, Yih-An, additional, Allegakoen, Paul, additional, Hui, Keliana S. F., additional, Pham, Julia H., additional, Baco, Maria B., additional, Song, Hanbing, additional, Giacomelli, Andrew O., additional, Vazquez, Francisca, additional, Ghandi, Mahmoud, additional, Goodarzi, Hani, additional, and Huang, Franklin W., additional

Published
2023
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35. Locally Disordered Methylation Forms the Basis of Intratumor Methylome Variation in Chronic Lymphocytic Leukemia

Author

Landau, Dan A., Clement, Kendell, Ziller, Michael J., Boyle, Patrick, Fan, Jean, Gu, Hongcang, Stevenson, Kristen, Sougnez, Carrie, Wang, Lili, Li, Shuqiang, Kotliar, Dylan, Zhang, Wandi, Ghandi, Mahmoud, Garraway, Levi, Fernandes, Stacey M., Livak, Kenneth J., Gabriel, Stacey, Gnirke, Andreas, Lander, Eric S., Brown, Jennifer R., Neuberg, Donna, Kharchenko, Peter V., Hacohen, Nir, Getz, Gad, Meissner, Alexander, and Wu, Catherine J.

Published
2014
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36. Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models

Author

Ng, Samuel Y., Yoshida, Noriaki, Christie, Amanda L., Ghandi, Mahmoud, Dharia, Neekesh V., Dempster, Joshua, Murakami, Mark, Shigemori, Kay, Morrow, Sara N., Van Scoyk, Alexandria, Cordero, Nicolas A., Stevenson, Kristen E., Puligandla, Maneka, Haas, Brian, Lo, Christopher, Meyers, Robin, Gao, Galen, Cherniack, Andrew, Louissaint, Jr, Abner, Nardi, Valentina, Thorner, Aaron R., Long, Henry, Qiu, Xintao, Morgan, Elizabeth A., Dorfman, David M., Fiore, Danilo, Jang, Julie, Epstein, Alan L., Dogan, Ahmet, Zhang, Yanming, Horwitz, Steven M., Jacobsen, Eric D., Santiago, Solimar, Ren, Jian-Guo, Guerlavais, Vincent, Annis, D. Allen, Aivado, Manuel, Saleh, Mansoor N., Mehta, Amitkumar, Tsherniak, Aviad, Root, David, Vazquez, Francisca, Hahn, William C., Inghirami, Giorgio, Aster, Jon C., Weinstock, David M., and Koch, Raphael

Published
2018
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37. Punctuated Evolution of Prostate Cancer Genomes

Author

Baca, Sylvan C., Prandi, Davide, Lawrence, Michael S., Mosquera, Juan Miguel, Romanel, Alessandro, Drier, Yotam, Park, Kyung, Kitabayashi, Naoki, MacDonald, Theresa Y., Ghandi, Mahmoud, Van Allen, Eliezer, Kryukov, Gregory V., Sboner, Andrea, Theurillat, Jean-Philippe, Soong, T. David, Nickerson, Elizabeth, Auclair, Daniel, Tewari, Ashutosh, Beltran, Himisha, Onofrio, Robert C., Boysen, Gunther, Guiducci, Candace, Barbieri, Christopher E., Cibulskis, Kristian, Sivachenko, Andrey, Carter, Scott L., Saksena, Gordon, Voet, Douglas, Ramos, Alex H., Winckler, Wendy, Cipicchio, Michelle, Ardlie, Kristin, Kantoff, Philip W., Berger, Michael F., Gabriel, Stacey B., Golub, Todd R., Meyerson, Matthew, Lander, Eric S., Elemento, Olivier, Getz, Gad, Demichelis, Francesca, Rubin, Mark A., and Garraway, Levi A.

Published
2013
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38. Abstract 3929: Identification of MRT-2359 a potent, selective and orally bioavailable GSPT1-directed molecular glue degrader (MGD) for the treatment of cancers with Myc-induced translational addiction

Author

Gavory, Gerald, primary, Ghandi, Mahmoud, additional, d’Alessandro, Anne-Cecile, additional, Bonenfant, Debora, additional, Chicas, Agustin, additional, Delobel, Frederic, additional, Demarco, Brad, additional, Flohr, Alexander, additional, King, Christopher, additional, Laine, Anne-Laure, additional, Massafra, Vittoria, additional, Narayan, Rajiv, additional, Osmont, Arnaud, additional, Ottaviani, Giorgio, additional, Peck, Dave, additional, Pessa, Sarah, additional, Rubin, Nooreen, additional, Ryckmans, Thomas, additional, Schillo, Martin, additional, Singh, Ambika, additional, Tortoioli, Simone, additional, Vigil, Dominico, additional, Zarayskiy, Vladislav, additional, Castle, John, additional, Janku, Filip, additional, Wallace, Owen, additional, Buonamici, Silvia, additional, and Fasching, Bernhard, additional

Published
2022
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39. Multiplexed single-cell transcriptional response profiling to define cancer vulnerabilities and therapeutic mechanism of action

Author

McFarland, James M., Paolella, Brenton R., Warren, Allison, Geiger-Schuller, Kathryn, Shibue, Tsukasa, Rothberg, Michael, Kuksenko, Olena, Colgan, William N., Jones, Andrew, Chambers, Emily, Dionne, Danielle, Bender, Samantha, Wolpin, Brian M., Ghandi, Mahmoud, Tirosh, Itay, Rozenblatt-Rosen, Orit, Roth, Jennifer A., Golub, Todd R., Regev, Aviv, Aguirre, Andrew J., Vazquez, Francisca, Tsherniak, Aviad, McFarland, James M., Paolella, Brenton R., Warren, Allison, Geiger-Schuller, Kathryn, Shibue, Tsukasa, Rothberg, Michael, Kuksenko, Olena, Colgan, William N., Jones, Andrew, Chambers, Emily, Dionne, Danielle, Bender, Samantha, Wolpin, Brian M., Ghandi, Mahmoud, Tirosh, Itay, Rozenblatt-Rosen, Orit, Roth, Jennifer A., Golub, Todd R., Regev, Aviv, Aguirre, Andrew J., Vazquez, Francisca, and Tsherniak, Aviad

Abstract

© 2020, The Author(s). Assays to study cancer cell responses to pharmacologic or genetic perturbations are typically restricted to using simple phenotypic readouts such as proliferation rate. Information-rich assays, such as gene-expression profiling, have generally not permitted efficient profiling of a given perturbation across multiple cellular contexts. Here, we develop MIX-Seq, a method for multiplexed transcriptional profiling of post-perturbation responses across a mixture of samples with single-cell resolution, using SNP-based computational demultiplexing of single-cell RNA-sequencing data. We show that MIX-Seq can be used to profile responses to chemical or genetic perturbations across pools of 100 or more cancer cell lines. We combine it with Cell Hashing to further multiplex additional experimental conditions, such as post-treatment time points or drug doses. Analyzing the high-content readout of scRNA-seq reveals both shared and context-specific transcriptional response components that can identify drug mechanism of action and enable prediction of long-term cell viability from short-term transcriptional responses to treatment.

Published
2022

41. ARID1B is a specific vulnerability in ARID1A-mutant cancers

Author

Helming, Katherine C., Wang, Xiaofeng, Wilson, Boris G., Vazquez, Francisca, Haswell, Jeffrey R., Manchester, Haley E., Kim, Youngha, Kryukov, Gregory V., Ghandi, Mahmoud, Aguirre, Andrew J., Jagani, Zainab, Wang, Zhong, Garraway, Levi A., Hahn, William C., and Roberts, Charles W. M.

Subjects
Gene mutations -- Physiological aspects -- Research, Antineoplastic agents -- Dosage and administration -- Complications and side effects, Cancer -- Genetic aspects -- Drug therapy -- Research, Antimitotic agents -- Dosage and administration -- Complications and side effects, Biological sciences, Health
Abstract

Recent studies have revealed that ARID1A, encoding AT-rich interactive domain 1A (SWI-like), is frequently mutated across a variety of human cancers and also has bona fide tumor suppressor properties. Consequently, identification of vulnerabilities conferred by ARID1A mutation would have major relevance for human cancer. Here, using a broad screening approach, we identify ARID1B, an ARID1A homolog whose gene product is mutually exclusive with ARID1A in SWI/SNF complexes, as the number 1 gene preferentially required for the survival of ARID1A-mutant cancer cell lines. We show that loss of ARID1B in ARID1A-deficient backgrounds destabilizes SWI/SNF and impairs proliferation in both cancer cells and primary cells. We also find that ARID1A and ARID1B are frequently co-mutated in cancer but that ARID1A-deficient cancers retain at least one functional ARID1B allele. These results suggest that loss of ARID1A and ARID1B alleles cooperatively promotes cancer formation but also results in a unique functional dependence. The results further identify ARID1B as a potential therapeutic target for ARID1A-mutant cancers., To search for specific vulnerabilities created by ARID1A mutation, we used data from Project Achilles, a large-scale project focused on identifying essential genes in a wide panel of cancer cell [...]

Published
2014
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43. Abstract LBA004: Identification of GSPT1-directed molecular glue degrader (MGD) for the treatment of Myc-driven breast cancer

Author

Gavory, Gerald, primary, Fasching, Bernhard, additional, Bonenfant, Debora, additional, Sadok, Amine, additional, Singh, Ambika, additional, Schillo, Martin, additional, Massafra, Vittoria, additional, d’Alessandro, Anne-Cecile, additional, Castle, John, additional, Ghandi, Mahmoud, additional, Chicas, Agustin, additional, Delobel, Frederic, additional, Flohr, Alexander, additional, Ottaviani, Giorgio, additional, Ryckmans, Thomas, additional, Laine, Anne-Laure, additional, Eidam, Oliv, additional, Wang, Hannah, additional, Bernett, Ilona, additional, Chan, Laura, additional, Gorrini, Chiara, additional, Roumiliotis, Theo, additional, Choudhary, Jyoti, additional, LeBihan, Yann-Vai, additional, Cabry, Marc, additional, Stubbs, Mark, additional, Burke, Rosemary, additional, Van Montfort, Rob, additional, Caldwell, John, additional, Chopra, Rajesh, additional, Collins, Ian, additional, and Buonamici, Silvia, additional

Published
2021
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44. Pharmacogenomic agreement between two cancer cell line data sets

Author

Stransky, Nicolas, Ghandi, Mahmoud, Kryukov, Gregory V., Garraway, Levi A., Lehár, Joseph, Liu, Manway, Sonkin, Dmitriy, Kauffmann, Audrey, Venkatesan, Kavitha, Edelman, Elena J., Riester, Markus, Barretina, Jordi, Caponigro, Giordano, Schlegel, Robert, Sellers, William R., Stegmeier, Frank, Morrissey, Michael, Amzallag, Arnaud, Pruteanu-Malinici, Iulian, Haber, Daniel A., Ramaswamy, Sridhar, Benes, Cyril H., Menden, Michael P., Iorio, Francesco, Stratton, Michael R., McDermott, Ultan, Garnett, Mathew J., and Saez-Rodriguez, Julio

Published
2015
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45. Sex-Biased ZRSR2 Mutations in Myeloid Malignancies Impair Plasmacytoid Dendritic Cell Activation and Apoptosis

Author

Togami, Katsuhiro, primary, Chung, Sun Sook, additional, Madan, Vikas, additional, Booth, Christopher A.G., additional, Kenyon, Christopher M., additional, Cabal-Hierro, Lucia, additional, Taylor, Justin, additional, Kim, Sunhee S., additional, Griffin, Gabriel K., additional, Ghandi, Mahmoud, additional, Li, Jia, additional, Li, Yvonne Y., additional, Angelot-Delettre, Fanny, additional, Biichle, Sabeha, additional, Seiler, Michael, additional, Buonamici, Silvia, additional, Lovitch, Scott B., additional, Louissaint, Abner, additional, Morgan, Elizabeth A., additional, Jardin, Fabrice, additional, Piccaluga, Pier Paolo, additional, Weinstock, David M., additional, Hammerman, Peter S., additional, Yang, Henry, additional, Konopleva, Marina, additional, Pemmaraju, Naveen, additional, Garnache-Ottou, Francine, additional, Abdel-Wahab, Omar, additional, Koeffler, H. Phillip, additional, and Lane, Andrew A., additional

Published
2021
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