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361 results on '"Buonamici, Silvia"'

1. 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

2. Splicing modulation sensitizes chronic lymphocytic leukemia cells to venetoclax by remodeling mitochondrial apoptotic dependencies

Author

Hacken, Elisa ten, Valentin, Rebecca, Regis, Fara Faye D, Sun, Jing, Yin, Shanye, Werner, Lillian, Deng, Jing, Gruber, Michaela, Wong, Jessica, Zheng, Mei, Gill, Amy L, Seiler, Michael, Smith, Peter, Thomas, Michael, Buonamici, Silvia, Ghia, Emanuela M, Kim, Ekaterina, Rassenti, Laura Z, Burger, Jan A, Kipps, Thomas J, Meyerson, Matthew L, Bachireddy, Pavan, Wang, Lili, Reed, Robin, Neuberg, Donna, Carrasco, Ruben D, Brooks, Angela N, Letai, Anthony, Davids, Matthew S, and Wu, Catherine J

Subjects
Hematology, Genetics, Cancer, Rare Diseases, Orphan Drug, Clinical Research, Lymphoma, Adult, Aged, Aged, 80 and over, Alternative Splicing, Animals, Antineoplastic Combined Chemotherapy Protocols, Apoptosis, Bridged Bicyclo Compounds, Heterocyclic, Disease Models, Animal, Drug Resistance, Neoplasm, Drug Screening Assays, Antitumor, Epoxy Compounds, Female, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Macrolides, Male, Mice, Mice, Transgenic, Middle Aged, Mitochondria, Mutation, Myeloid Cell Leukemia Sequence 1 Protein, Phosphoproteins, Primary Cell Culture, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Pyrimidines, RNA Splicing Factors, Spliceosomes, Sulfonamides, Thiophenes, Apoptosis inhibitors, Therapeutics, Transcription
Abstract

The identification of targetable vulnerabilities in the context of therapeutic resistance is a key challenge in cancer treatment. We detected pervasive aberrant splicing as a characteristic feature of chronic lymphocytic leukemia (CLL), irrespective of splicing factor mutation status, which was associated with sensitivity to the spliceosome modulator, E7107. Splicing modulation affected CLL survival pathways, including members of the B cell lymphoma-2 (BCL2) family of proteins, remodeling antiapoptotic dependencies of human and murine CLL cells. E7107 treatment decreased myeloid cell leukemia-1 (MCL1) dependence and increased BCL2 dependence, sensitizing primary human CLL cells and venetoclax-resistant CLL-like cells from an Eμ-TCL1-based adoptive transfer murine model to treatment with the BCL2 inhibitor venetoclax. Our data provide preclinical rationale to support the combination of venetoclax with splicing modulators to reprogram apoptotic dependencies in CLL for treating venetoclax-resistant CLL cases.

Published
2018

3. Splicing modulators impair DNA damage response and induce killing of cohesin-mutant MDS and AML

Author

Wheeler, Emily C., primary, Martin, Benjamin J. E., additional, Doyle, William C., additional, Neaher, Sofia, additional, Conway, Caroline A., additional, Pitton, Caroline N., additional, Gorelov, Rebecca A., additional, Donahue, Melanie, additional, Jann, Johann C., additional, Abdel-Wahab, Omar, additional, Taylor, Justin, additional, Seiler, Michael, additional, Buonamici, Silvia, additional, Pikman, Yana, additional, Garcia, Jacqueline S., additional, Belizaire, Roger, additional, Adelman, Karen, additional, and Tothova, Zuzana, additional

Published
2024
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4. Transcriptomic Characterization of SF3B1 Mutation Reveals Its Pleiotropic Effects in Chronic Lymphocytic Leukemia

Author

Wang, Lili, Brooks, Angela N, Fan, Jean, Wan, Youzhong, Gambe, Rutendo, Li, Shuqiang, Hergert, Sarah, Yin, Shanye, Freeman, Samuel S, Levin, Joshua Z, Fan, Lin, Seiler, Michael, Buonamici, Silvia, Smith, Peter G, Chau, Kevin F, Cibulskis, Carrie L, Zhang, Wandi, Rassenti, Laura Z, Ghia, Emanuela M, Kipps, Thomas J, Fernandes, Stacey, Bloch, Donald B, Kotliar, Dylan, Landau, Dan A, Shukla, Sachet A, Aster, Jon C, Reed, Robin, DeLuca, David S, Brown, Jennifer R, Neuberg, Donna, Getz, Gad, Livak, Kenneth J, Meyerson, Matthew M, Kharchenko, Peter V, and Wu, Catherine J

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Lymphoma, Genetics, Clinical Research, Cancer, Rare Diseases, Hematology, 2.1 Biological and endogenous factors, Aetiology, Alternative Splicing, Cell Line, Tumor, Dishevelled Proteins, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Mutation, Phosphoproteins, RNA Splicing Factors, Receptors, Notch, Signal Transduction, CLL, Notch signaling, RNA sequencing, SF3B1, alternative splicing, Neurosciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Mutations in SF3B1, which encodes a spliceosome component, are associated with poor outcome in chronic lymphocytic leukemia (CLL), but how these contribute to CLL progression remains poorly understood. We undertook a transcriptomic characterization of primary human CLL cells to identify transcripts and pathways affected by SF3B1 mutation. Splicing alterations, identified in the analysis of bulk cells, were confirmed in single SF3B1-mutated CLL cells and also found in cell lines ectopically expressing mutant SF3B1. SF3B1 mutation was found to dysregulate multiple cellular functions including DNA damage response, telomere maintenance, and Notch signaling (mediated through KLF8 upregulation, increased TERC and TERT expression, or altered splicing of DVL2 transcript, respectively). SF3B1 mutation leads to diverse changes in CLL-related pathways.

Published
2016

5. Somatic Mutational Landscape of Splicing Factor Genes and Their Functional Consequences across 33 Cancer Types

Author

Caesar-Johnson, Samantha J., Demchok, John A., Felau, Ina, Kasapi, Melpomeni, Ferguson, Martin L., Hutter, Carolyn M., Sofia, Heidi J., Tarnuzzer, Roy, Wang, Zhining, Yang, Liming, Zenklusen, Jean C., Zhang, Jiashan (Julia), Chudamani, Sudha, Liu, Jia, Lolla, Laxmi, Naresh, Rashi, Pihl, Todd, Sun, Qiang, Wan, Yunhu, Wu, Ye, Cho, Juok, DeFreitas, Timothy, Frazer, Scott, Gehlenborg, Nils, Getz, Gad, Heiman, David I., Kim, Jaegil, Lawrence, Michael S., Lin, Pei, Meier, Sam, Noble, Michael S., Saksena, Gordon, Voet, Doug, Zhang, Hailei, Bernard, Brady, Chambwe, Nyasha, Dhankani, Varsha, Knijnenburg, Theo, Kramer, Roger, Leinonen, Kalle, Liu, Yuexin, Miller, Michael, Reynolds, Sheila, Shmulevich, Ilya, Thorsson, Vesteinn, Zhang, Wei, Akbani, Rehan, Broom, Bradley M., Hegde, Apurva M., Ju, Zhenlin, Kanchi, Rupa S., Korkut, Anil, Li, Jun, Liang, Han, Ling, Shiyun, Liu, Wenbin, Lu, Yiling, Mills, Gordon B., Ng, Kwok-Shing, Rao, Arvind, Ryan, Michael, Wang, Jing, Weinstein, John N., Zhang, Jiexin, Abeshouse, Adam, Armenia, Joshua, Chakravarty, Debyani, Chatila, Walid K., de Bruijn, Ino, Gao, Jianjiong, Gross, Benjamin E., Heins, Zachary J., Kundra, Ritika, La, Konnor, Ladanyi, Marc, Luna, Augustin, Nissan, Moriah G., Ochoa, Angelica, Phillips, Sarah M., Reznik, Ed, Sanchez-Vega, Francisco, Sander, Chris, Schultz, Nikolaus, Sheridan, Robert, Sumer, S. Onur, Sun, Yichao, Taylor, Barry S., Wang, Jioajiao, Zhang, Hongxin, Anur, Pavana, Peto, Myron, Spellman, Paul, Benz, Christopher, Stuart, Joshua M., Wong, Christopher K., Yau, Christina, Hayes, D. Neil, Parker, Joel S., Wilkerson, Matthew D., Ally, Adrian, Balasundaram, Miruna, Bowlby, Reanne, Brooks, Denise, Carlsen, Rebecca, Chuah, Eric, Dhalla, Noreen, Holt, Robert, Jones, Steven J.M., Kasaian, Katayoon, Lee, Darlene, Ma, Yussanne, Marra, Marco A., Mayo, Michael, Moore, Richard A., Mungall, Andrew J., Mungall, Karen, Robertson, A. Gordon, Sadeghi, Sara, Schein, Jacqueline E., Sipahimalani, Payal, Tam, Angela, Thiessen, Nina, Tse, Kane, Wong, Tina, Berger, Ashton C., Beroukhim, Rameen, Cherniack, Andrew D., Cibulskis, Carrie, Gabriel, Stacey B., Gao, Galen F., Ha, Gavin, Meyerson, Matthew, Schumacher, Steven E., Shih, Juliann, Kucherlapati, Melanie H., Kucherlapati, Raju S., Baylin, Stephen, Cope, Leslie, Danilova, Ludmila, Bootwalla, Moiz S., Lai, Phillip H., Maglinte, Dennis T., Van Den Berg, David J., Weisenberger, Daniel J., Auman, J. Todd, Balu, Saianand, Bodenheimer, Tom, Fan, Cheng, Hoadley, Katherine A., Hoyle, Alan P., Jefferys, Stuart R., Jones, Corbin D., Meng, Shaowu, Mieczkowski, Piotr A., Mose, Lisle E., Perou, Amy H., Perou, Charles M., Roach, Jeffrey, Shi, Yan, Simons, Janae V., Skelly, Tara, Soloway, Matthew G., Tan, Donghui, Veluvolu, Umadevi, Fan, Huihui, Hinoue, Toshinori, Laird, Peter W., Shen, Hui, Zhou, Wanding, Bellair, Michelle, Chang, Kyle, Covington, Kyle, Creighton, Chad J., Dinh, Huyen, Doddapaneni, HarshaVardhan, Donehower, Lawrence A., Drummond, Jennifer, Gibbs, Richard A., Glenn, Robert, Hale, Walker, Han, Yi, Hu, Jianhong, Korchina, Viktoriya, Lee, Sandra, Lewis, Lora, Li, Wei, Liu, Xiuping, Morgan, Margaret, Morton, Donna, Muzny, Donna, Santibanez, Jireh, Sheth, Margi, Shinbrot, Eve, Wang, Linghua, Wang, Min, Wheeler, David A., Xi, Liu, Zhao, Fengmei, Hess, Julian, Appelbaum, Elizabeth L., Bailey, Matthew, Cordes, Matthew G., Ding, Li, Fronick, Catrina C., Fulton, Lucinda A., Fulton, Robert S., Kandoth, Cyriac, Mardis, Elaine R., McLellan, Michael D., Miller, Christopher A., Schmidt, Heather K., Wilson, Richard K., Crain, Daniel, Curley, Erin, Gardner, Johanna, Lau, Kevin, Mallery, David, Morris, Scott, Paulauskis, Joseph, Penny, Robert, Shelton, Candace, Shelton, Troy, Sherman, Mark, Thompson, Eric, Yena, Peggy, Bowen, Jay, Gastier-Foster, Julie M., Gerken, Mark, Leraas, Kristen M., Lichtenberg, Tara M., Ramirez, Nilsa C., Wise, Lisa, Zmuda, Erik, Corcoran, Niall, Costello, Tony, Hovens, Christopher, Carvalho, Andre L., de Carvalho, Ana C., Fregnani, José H., Longatto-Filho, Adhemar, Reis, Rui M., Scapulatempo-Neto, Cristovam, Silveira, Henrique C.S., Vidal, Daniel O., Burnette, Andrew, Eschbacher, Jennifer, Hermes, Beth, Noss, Ardene, Singh, Rosy, Anderson, Matthew L., Castro, Patricia D., Ittmann, Michael, Huntsman, David, Kohl, Bernard, Le, Xuan, Thorp, Richard, Andry, Chris, Duffy, Elizabeth R., Lyadov, Vladimir, Paklina, Oxana, Setdikova, Galiya, Shabunin, Alexey, Tavobilov, Mikhail, McPherson, Christopher, Warnick, Ronald, Berkowitz, Ross, Cramer, Daniel, Feltmate, Colleen, Horowitz, Neil, Kibel, Adam, Muto, Michael, Raut, Chandrajit P., Malykh, Andrei, Barnholtz-Sloan, Jill S., Barrett, Wendi, Devine, Karen, Fulop, Jordonna, Ostrom, Quinn T., Shimmel, Kristen, Wolinsky, Yingli, Sloan, Andrew E., De Rose, Agostino, Giuliante, Felice, Goodman, Marc, Karlan, Beth Y., Hagedorn, Curt H., Eckman, John, Harr, Jodi, Myers, Jerome, Tucker, Kelinda, Zach, Leigh Anne, Deyarmin, Brenda, Hu, Hai, Kvecher, Leonid, Larson, Caroline, Mural, Richard J., Somiari, Stella, Vicha, Ales, Zelinka, Tomas, Bennett, Joseph, Iacocca, Mary, Rabeno, Brenda, Swanson, Patricia, Latour, Mathieu, Lacombe, Louis, Têtu, Bernard, Bergeron, Alain, McGraw, Mary, Staugaitis, Susan M., Chabot, John, Hibshoosh, Hanina, Sepulveda, Antonia, Su, Tao, Wang, Timothy, Potapova, Olga, Voronina, Olga, Desjardins, Laurence, Mariani, Odette, Roman-Roman, Sergio, Sastre, Xavier, Stern, Marc-Henri, Cheng, Feixiong, Signoretti, Sabina, Berchuck, Andrew, Bigner, Darell, Lipp, Eric, Marks, Jeffrey, McCall, Shannon, McLendon, Roger, Secord, Angeles, Sharp, Alexis, Behera, Madhusmita, Brat, Daniel J., Chen, Amy, Delman, Keith, Force, Seth, Khuri, Fadlo, Magliocca, Kelly, Maithel, Shishir, Olson, Jeffrey J., Owonikoko, Taofeek, Pickens, Alan, Ramalingam, Suresh, Shin, Dong M., Sica, Gabriel, Van Meir, Erwin G., Zhang, Hongzheng, Eijckenboom, Wil, Gillis, Ad, Korpershoek, Esther, Looijenga, Leendert, Oosterhuis, Wolter, Stoop, Hans, van Kessel, Kim E., Zwarthoff, Ellen C., Calatozzolo, Chiara, Cuppini, Lucia, Cuzzubbo, Stefania, DiMeco, Francesco, Finocchiaro, Gaetano, Mattei, Luca, Perin, Alessandro, Pollo, Bianca, Chen, Chu, Houck, John, Lohavanichbutr, Pawadee, Hartmann, Arndt, Stoehr, Christine, Stoehr, Robert, Taubert, Helge, Wach, Sven, Wullich, Bernd, Kycler, Witold, Murawa, Dawid, Wiznerowicz, Maciej, Chung, Ki, Edenfield, W. Jeffrey, Martin, Julie, Baudin, Eric, Bubley, Glenn, Bueno, Raphael, De Rienzo, Assunta, Richards, William G., Kalkanis, Steven, Mikkelsen, Tom, Noushmehr, Houtan, Scarpace, Lisa, Girard, Nicolas, Aymerich, Marta, Campo, Elias, Giné, Eva, Guillermo, Armando López, Van Bang, Nguyen, Hanh, Phan Thi, Phu, Bui Duc, Tang, Yufang, Colman, Howard, Evason, Kimberley, Dottino, Peter R., Martignetti, John A., Gabra, Hani, Juhl, Hartmut, Akeredolu, Teniola, Stepa, Serghei, Hoon, Dave, Ahn, Keunsoo, Kang, Koo Jeong, Beuschlein, Felix, Breggia, Anne, Birrer, Michael, Bell, Debra, Borad, Mitesh, Bryce, Alan H., Castle, Erik, Chandan, Vishal, Cheville, John, Copland, John A., Farnell, Michael, Flotte, Thomas, Giama, Nasra, Ho, Thai, Kendrick, Michael, Kocher, Jean-Pierre, Kopp, Karla, Moser, Catherine, Nagorney, David, O’Brien, Daniel, O’Neill, Brian Patrick, Patel, Tushar, Petersen, Gloria, Que, Florencia, Rivera, Michael, Roberts, Lewis, Smallridge, Robert, Smyrk, Thomas, Stanton, Melissa, Thompson, R. Houston, Torbenson, Michael, Yang, Ju Dong, Zhang, Lizhi, Brimo, Fadi, Ajani, Jaffer A., Angulo Gonzalez, Ana Maria, Behrens, Carmen, Bondaruk, Jolanta, Broaddus, Russell, Czerniak, Bogdan, Esmaeli, Bita, Fujimoto, Junya, Gershenwald, Jeffrey, Guo, Charles, Lazar, Alexander J., Logothetis, Christopher, Meric-Bernstam, Funda, Moran, Cesar, Ramondetta, Lois, Rice, David, Sood, Anil, Tamboli, Pheroze, Thompson, Timothy, Troncoso, Patricia, Tsao, Anne, Wistuba, Ignacio, Carter, Candace, Haydu, Lauren, Hersey, Peter, Jakrot, Valerie, Kakavand, Hojabr, Kefford, Richard, Lee, Kenneth, Long, Georgina, Mann, Graham, Quinn, Michael, Saw, Robyn, Scolyer, Richard, Shannon, Kerwin, Spillane, Andrew, Stretch, Jonathan, Synott, Maria, Thompson, John, Wilmott, James, Al-Ahmadie, Hikmat, Chan, Timothy A., Ghossein, Ronald, Gopalan, Anuradha, Levine, Douglas A., Reuter, Victor, Singer, Samuel, Singh, Bhuvanesh, Tien, Nguyen Viet, Broudy, Thomas, Mirsaidi, Cyrus, Nair, Praveen, Drwiega, Paul, Miller, Judy, Smith, Jennifer, Zaren, Howard, Park, Joong-Won, Hung, Nguyen Phi, Kebebew, Electron, Linehan, W. Marston, Metwalli, Adam R., Pacak, Karel, Pinto, Peter A., Schiffman, Mark, Schmidt, Laura S., Vocke, Cathy D., Wentzensen, Nicolas, Worrell, Robert, Yang, Hannah, Moncrieff, Marc, Goparaju, Chandra, Melamed, Jonathan, Pass, Harvey, Botnariuc, Natalia, Caraman, Irina, Cernat, Mircea, Chemencedji, Inga, Clipca, Adrian, Doruc, Serghei, Gorincioi, Ghenadie, Mura, Sergiu, Pirtac, Maria, Stancul, Irina, Tcaciuc, Diana, Albert, Monique, Alexopoulou, Iakovina, Arnaout, Angel, Bartlett, John, Engel, Jay, Gilbert, Sebastien, Parfitt, Jeremy, Sekhon, Harman, Thomas, George, Rassl, Doris M., Rintoul, Robert C., Bifulco, Carlo, Tamakawa, Raina, Urba, Walter, Hayward, Nicholas, Timmers, Henri, Antenucci, Anna, Facciolo, Francesco, Grazi, Gianluca, Marino, Mirella, Merola, Roberta, de Krijger, Ronald, Gimenez-Roqueplo, Anne-Paule, Piché, Alain, Chevalier, Simone, McKercher, Ginette, Birsoy, Kivanc, Barnett, Gene, Brewer, Cathy, Farver, Carol, Naska, Theresa, Pennell, Nathan A., Raymond, Daniel, Schilero, Cathy, Smolenski, Kathy, Williams, Felicia, Morrison, Carl, Borgia, Jeffrey A., Liptay, Michael J., Pool, Mark, Seder, Christopher W., Junker, Kerstin, Omberg, Larsson, Dinkin, Mikhail, Manikhas, George, Alvaro, Domenico, Bragazzi, Maria Consiglia, Cardinale, Vincenzo, Carpino, Guido, Gaudio, Eugenio, Chesla, David, Cottingham, Sandra, Dubina, Michael, Moiseenko, Fedor, Dhanasekaran, Renumathy, Becker, Karl-Friedrich, Janssen, Klaus-Peter, Slotta-Huspenina, Julia, Abdel-Rahman, Mohamed H., Aziz, Dina, Bell, Sue, Cebulla, Colleen M., Davis, Amy, Duell, Rebecca, Elder, J. Bradley, Hilty, Joe, Kumar, Bahavna, Lang, James, Lehman, Norman L., Mandt, Randy, Nguyen, Phuong, Pilarski, Robert, Rai, Karan, Schoenfield, Lynn, Senecal, Kelly, Wakely, Paul, Hansen, Paul, Lechan, Ronald, Powers, James, Tischler, Arthur, Grizzle, William E., Sexton, Katherine C., Kastl, Alison, Henderson, Joel, Porten, Sima, Waldmann, Jens, Fassnacht, Martin, Asa, Sylvia L., Schadendorf, Dirk, Couce, Marta, Graefen, Markus, Huland, Hartwig, Sauter, Guido, Schlomm, Thorsten, Simon, Ronald, Tennstedt, Pierre, Olabode, Oluwole, Nelson, Mark, Bathe, Oliver, Carroll, Peter R., Chan, June M., Disaia, Philip, Glenn, Pat, Kelley, Robin K., Landen, Charles N., Phillips, Joanna, Prados, Michael, Simko, Jeffry, Smith-McCune, Karen, VandenBerg, Scott, Roggin, Kevin, Fehrenbach, Ashley, Kendler, Ady, Sifri, Suzanne, Steele, Ruth, Jimeno, Antonio, Carey, Francis, Forgie, Ian, Mannelli, Massimo, Carney, Michael, Hernandez, Brenda, Campos, Benito, Herold-Mende, Christel, Jungk, Christin, Unterberg, Andreas, von Deimling, Andreas, Bossler, Aaron, Galbraith, Joseph, Jacobus, Laura, Knudson, Michael, Knutson, Tina, Ma, Deqin, Milhem, Mohammed, Sigmund, Rita, Godwin, Andrew K., Madan, Rashna, Rosenthal, Howard G., Adebamowo, Clement, Adebamowo, Sally N., Boussioutas, Alex, Beer, David, Giordano, Thomas, Mes-Masson, Anne-Marie, Saad, Fred, Bocklage, Therese, Landrum, Lisa, Mannel, Robert, Moore, Kathleen, Moxley, Katherine, Postier, Russel, Walker, Joan, Zuna, Rosemary, Feldman, Michael, Valdivieso, Federico, Dhir, Rajiv, Luketich, James, Mora Pinero, Edna M., Quintero-Aguilo, Mario, Carlotti, Carlos Gilberto, Jr., Dos Santos, Jose Sebastião, Kemp, Rafael, Sankarankuty, Ajith, Tirapelli, Daniela, Catto, James, Agnew, Kathy, Swisher, Elizabeth, Creaney, Jenette, Robinson, Bruce, Shelley, Carl Simon, Godwin, Eryn M., Kendall, Sara, Shipman, Cassaundra, Bradford, Carol, Carey, Thomas, Haddad, Andrea, Moyer, Jeffey, Peterson, Lisa, Prince, Mark, Rozek, Laura, Wolf, Gregory, Bowman, Rayleen, Fong, Kwun M., Yang, Ian, Korst, Robert, Rathmell, W. Kimryn, Fantacone-Campbell, J. Leigh, Hooke, Jeffrey A., Kovatich, Albert J., Shriver, Craig D., DiPersio, John, Drake, Bettina, Govindan, Ramaswamy, Heath, Sharon, Ley, Timothy, Van Tine, Brian, Westervelt, Peter, Rubin, Mark A., Lee, Jung Il, Aredes, Natália D., Mariamidze, Armaz, Seiler, Michael, Peng, Shouyong, Agrawal, Anant A., Palacino, James, Teng, Teng, Zhu, Ping, Smith, Peter G., Buonamici, Silvia, and Yu, Lihua

Published
2018
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7. H3B-8800, an orally available small-molecule splicing modulator, induces lethality in spliceosome-mutant cancers

Author

Seiler, Michael, Yoshimi, Akihide, Darman, Rachel, Chan, Betty, Keaney, Gregg, Thomas, Michael, Agrawal, Anant A, Caleb, Benjamin, Csibi, Alfredo, Sean, Eckley, Fekkes, Peter, Karr, Craig, Klimek, Virginia, Lai, George, Lee, Linda, Kumar, Pavan, Lee, Stanley Chun-Wei, Liu, Xiang, Mackenzie, Crystal, Meeske, Carol, Mizui, Yoshiharu, Padron, Eric, Park, Eunice, Pazolli, Ermira, Peng, Shouyong, Prajapati, Sudeep, Taylor, Justin, Teng, Teng, Wang, John, Warmuth, Markus, Yao, Huilan, Yu, Lihua, Zhu, Ping, Abdel-Wahab, Omar, Smith, Peter G, and Buonamici, Silvia

Subjects
RNA splicing -- Health aspects, Gene mutation -- Health aspects, Carcinogenesis -- Genetic aspects, Biological sciences, Health
Abstract

Author(s): Michael Seiler [1]; Akihide Yoshimi [2]; Rachel Darman [1]; Betty Chan [1]; Gregg Keaney [1]; Michael Thomas [1]; Anant A Agrawal [1]; Benjamin Caleb [1]; Alfredo Csibi [1]; Eckley [...]

Published
2018
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8. 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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9. 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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10. 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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11. 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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12. 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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13. Figures S1-S6 from Discovery of Selective Estrogen Receptor Covalent Antagonists for the Treatment of ERαWT and ERαMUT Breast Cancer

Author

Puyang, Xiaoling, primary, Furman, Craig, primary, Zheng, Guo Zhu, primary, Wu, Zhenhua J., primary, Banka, Deepti, primary, Aithal, Kiran, primary, Agoulnik, Sergei, primary, Bolduc, David M., primary, Buonamici, Silvia, primary, Caleb, Benjamin, primary, Das, Subhasree, primary, Eckley, Sean, primary, Fekkes, Peter, primary, Hao, Ming-Hong, primary, Hart, Andrew, primary, Houtman, René, primary, Irwin, Sean, primary, Joshi, Jaya J., primary, Karr, Craig, primary, Kim, Amy, primary, Kumar, Namita, primary, Kumar, Pavan, primary, Kuznetsov, Galina, primary, Lai, Weidong G., primary, Larsen, Nicholas, primary, Mackenzie, Crystal, primary, Martin, Lesley-Ann, primary, Melchers, Diana, primary, Moriarty, Alyssa, primary, Nguyen, Tuong-Vi, primary, Norris, John, primary, O'Shea, Morgan, primary, Pancholi, Sunil, primary, Prajapati, Sudeep, primary, Rajagopalan, Sujatha, primary, Reynolds, Dominic J., primary, Rimkunas, Victoria, primary, Rioux, Nathalie, primary, Ribas, Ricardo, primary, Siu, Amy, primary, Sivakumar, Sasirekha, primary, Subramanian, Vanitha, primary, Thomas, Michael, primary, Vaillancourt, Frédéric H., primary, Wang, John, primary, Wardell, Suzanne, primary, Wick, Michael J., primary, Yao, Shihua, primary, Yu, Lihua, primary, Warmuth, Markus, primary, Smith, Peter G., primary, Zhu, Ping, primary, and Korpal, Manav, primary

Published
2023
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17. Data from Discovery of Selective Estrogen Receptor Covalent Antagonists for the Treatment of ERαWT and ERαMUT Breast Cancer

Author

Puyang, Xiaoling, primary, Furman, Craig, primary, Zheng, Guo Zhu, primary, Wu, Zhenhua J., primary, Banka, Deepti, primary, Aithal, Kiran, primary, Agoulnik, Sergei, primary, Bolduc, David M., primary, Buonamici, Silvia, primary, Caleb, Benjamin, primary, Das, Subhasree, primary, Eckley, Sean, primary, Fekkes, Peter, primary, Hao, Ming-Hong, primary, Hart, Andrew, primary, Houtman, René, primary, Irwin, Sean, primary, Joshi, Jaya J., primary, Karr, Craig, primary, Kim, Amy, primary, Kumar, Namita, primary, Kumar, Pavan, primary, Kuznetsov, Galina, primary, Lai, Weidong G., primary, Larsen, Nicholas, primary, Mackenzie, Crystal, primary, Martin, Lesley-Ann, primary, Melchers, Diana, primary, Moriarty, Alyssa, primary, Nguyen, Tuong-Vi, primary, Norris, John, primary, O'Shea, Morgan, primary, Pancholi, Sunil, primary, Prajapati, Sudeep, primary, Rajagopalan, Sujatha, primary, Reynolds, Dominic J., primary, Rimkunas, Victoria, primary, Rioux, Nathalie, primary, Ribas, Ricardo, primary, Siu, Amy, primary, Sivakumar, Sasirekha, primary, Subramanian, Vanitha, primary, Thomas, Michael, primary, Vaillancourt, Frédéric H., primary, Wang, John, primary, Wardell, Suzanne, primary, Wick, Michael J., primary, Yao, Shihua, primary, Yu, Lihua, primary, Warmuth, Markus, primary, Smith, Peter G., primary, Zhu, Ping, primary, and Korpal, Manav, primary

Published
2023
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18. Tables S3-S4 from Discovery of Selective Estrogen Receptor Covalent Antagonists for the Treatment of ERαWT and ERαMUT Breast Cancer

Author

Puyang, Xiaoling, primary, Furman, Craig, primary, Zheng, Guo Zhu, primary, Wu, Zhenhua J., primary, Banka, Deepti, primary, Aithal, Kiran, primary, Agoulnik, Sergei, primary, Bolduc, David M., primary, Buonamici, Silvia, primary, Caleb, Benjamin, primary, Das, Subhasree, primary, Eckley, Sean, primary, Fekkes, Peter, primary, Hao, Ming-Hong, primary, Hart, Andrew, primary, Houtman, René, primary, Irwin, Sean, primary, Joshi, Jaya J., primary, Karr, Craig, primary, Kim, Amy, primary, Kumar, Namita, primary, Kumar, Pavan, primary, Kuznetsov, Galina, primary, Lai, Weidong G., primary, Larsen, Nicholas, primary, Mackenzie, Crystal, primary, Martin, Lesley-Ann, primary, Melchers, Diana, primary, Moriarty, Alyssa, primary, Nguyen, Tuong-Vi, primary, Norris, John, primary, O'Shea, Morgan, primary, Pancholi, Sunil, primary, Prajapati, Sudeep, primary, Rajagopalan, Sujatha, primary, Reynolds, Dominic J., primary, Rimkunas, Victoria, primary, Rioux, Nathalie, primary, Ribas, Ricardo, primary, Siu, Amy, primary, Sivakumar, Sasirekha, primary, Subramanian, Vanitha, primary, Thomas, Michael, primary, Vaillancourt, Frédéric H., primary, Wang, John, primary, Wardell, Suzanne, primary, Wick, Michael J., primary, Yao, Shihua, primary, Yu, Lihua, primary, Warmuth, Markus, primary, Smith, Peter G., primary, Zhu, Ping, primary, and Korpal, Manav, primary

Published
2023
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20. Supplementary Methods from Discovery of Selective Estrogen Receptor Covalent Antagonists for the Treatment of ERαWT and ERαMUT Breast Cancer

Author

Puyang, Xiaoling, primary, Furman, Craig, primary, Zheng, Guo Zhu, primary, Wu, Zhenhua J., primary, Banka, Deepti, primary, Aithal, Kiran, primary, Agoulnik, Sergei, primary, Bolduc, David M., primary, Buonamici, Silvia, primary, Caleb, Benjamin, primary, Das, Subhasree, primary, Eckley, Sean, primary, Fekkes, Peter, primary, Hao, Ming-Hong, primary, Hart, Andrew, primary, Houtman, René, primary, Irwin, Sean, primary, Joshi, Jaya J., primary, Karr, Craig, primary, Kim, Amy, primary, Kumar, Namita, primary, Kumar, Pavan, primary, Kuznetsov, Galina, primary, Lai, Weidong G., primary, Larsen, Nicholas, primary, Mackenzie, Crystal, primary, Martin, Lesley-Ann, primary, Melchers, Diana, primary, Moriarty, Alyssa, primary, Nguyen, Tuong-Vi, primary, Norris, John, primary, O'Shea, Morgan, primary, Pancholi, Sunil, primary, Prajapati, Sudeep, primary, Rajagopalan, Sujatha, primary, Reynolds, Dominic J., primary, Rimkunas, Victoria, primary, Rioux, Nathalie, primary, Ribas, Ricardo, primary, Siu, Amy, primary, Sivakumar, Sasirekha, primary, Subramanian, Vanitha, primary, Thomas, Michael, primary, Vaillancourt, Frédéric H., primary, Wang, John, primary, Wardell, Suzanne, primary, Wick, Michael J., primary, Yao, Shihua, primary, Yu, Lihua, primary, Warmuth, Markus, primary, Smith, Peter G., primary, Zhu, Ping, primary, and Korpal, Manav, primary

Published
2023
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23. Sensitivity to splicing modulation of BCL2 family genes defines cancer therapeutic strategies for splicing modulators

Author

Aird, Daniel, Teng, Teng, Huang, Chia-Ling, Pazolli, Ermira, Banka, Deepti, Cheung-Ong, Kahlin, Eifert, Cheryl, Furman, Craig, Wu, Zhenhua Jeremy, Seiler, Michael, Buonamici, Silvia, Fekkes, Peter, Karr, Craig, Palacino, James, Park, Eunice, Smith, Peter G., Yu, Lihua, Mizui, Yoshiharu, Warmuth, Markus, Chicas, Agustin, Corson, Laura, and Zhu, Ping

Published
2019
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24. Supplementary Figure S7 from H3B-6527 Is a Potent and Selective Inhibitor of FGFR4 in FGF19-Driven Hepatocellular Carcinoma

Author

Joshi, Jaya Julie, primary, Coffey, Heather, primary, Corcoran, Erik, primary, Tsai, Jennifer, primary, Huang, Chia-Ling, primary, Ichikawa, Kana, primary, Prajapati, Sudeep, primary, Hao, Ming-Hong, primary, Bailey, Suzanna, primary, Wu, Jeremy, primary, Rimkunas, Victoria, primary, Karr, Craig, primary, Subramanian, Vanitha, primary, Kumar, Pavan, primary, MacKenzie, Crystal, primary, Hurley, Raelene, primary, Satoh, Takashi, primary, Yu, Kun, primary, Park, Eunice, primary, Rioux, Nathalie, primary, Kim, Amy, primary, Lai, Weidong G., primary, Yu, Lihua, primary, Zhu, Ping, primary, Buonamici, Silvia, primary, Larsen, Nicholas, primary, Fekkes, Peter, primary, Wang, John, primary, Warmuth, Markus, primary, Reynolds, Dominic J., primary, Smith, Peter G., primary, and Selvaraj, Anand, primary

Published
2023
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25. Supplementary Table S2andS3 from H3B-6527 Is a Potent and Selective Inhibitor of FGFR4 in FGF19-Driven Hepatocellular Carcinoma

Author

Joshi, Jaya Julie, primary, Coffey, Heather, primary, Corcoran, Erik, primary, Tsai, Jennifer, primary, Huang, Chia-Ling, primary, Ichikawa, Kana, primary, Prajapati, Sudeep, primary, Hao, Ming-Hong, primary, Bailey, Suzanna, primary, Wu, Jeremy, primary, Rimkunas, Victoria, primary, Karr, Craig, primary, Subramanian, Vanitha, primary, Kumar, Pavan, primary, MacKenzie, Crystal, primary, Hurley, Raelene, primary, Satoh, Takashi, primary, Yu, Kun, primary, Park, Eunice, primary, Rioux, Nathalie, primary, Kim, Amy, primary, Lai, Weidong G., primary, Yu, Lihua, primary, Zhu, Ping, primary, Buonamici, Silvia, primary, Larsen, Nicholas, primary, Fekkes, Peter, primary, Wang, John, primary, Warmuth, Markus, primary, Reynolds, Dominic J., primary, Smith, Peter G., primary, and Selvaraj, Anand, primary

Published
2023
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26. Data from H3B-6527 Is a Potent and Selective Inhibitor of FGFR4 in FGF19-Driven Hepatocellular Carcinoma

Author

Joshi, Jaya Julie, primary, Coffey, Heather, primary, Corcoran, Erik, primary, Tsai, Jennifer, primary, Huang, Chia-Ling, primary, Ichikawa, Kana, primary, Prajapati, Sudeep, primary, Hao, Ming-Hong, primary, Bailey, Suzanna, primary, Wu, Jeremy, primary, Rimkunas, Victoria, primary, Karr, Craig, primary, Subramanian, Vanitha, primary, Kumar, Pavan, primary, MacKenzie, Crystal, primary, Hurley, Raelene, primary, Satoh, Takashi, primary, Yu, Kun, primary, Park, Eunice, primary, Rioux, Nathalie, primary, Kim, Amy, primary, Lai, Weidong G., primary, Yu, Lihua, primary, Zhu, Ping, primary, Buonamici, Silvia, primary, Larsen, Nicholas, primary, Fekkes, Peter, primary, Wang, John, primary, Warmuth, Markus, primary, Reynolds, Dominic J., primary, Smith, Peter G., primary, and Selvaraj, Anand, primary

Published
2023
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27. Supplementary Legends from H3B-6527 Is a Potent and Selective Inhibitor of FGFR4 in FGF19-Driven Hepatocellular Carcinoma

Author

Joshi, Jaya Julie, primary, Coffey, Heather, primary, Corcoran, Erik, primary, Tsai, Jennifer, primary, Huang, Chia-Ling, primary, Ichikawa, Kana, primary, Prajapati, Sudeep, primary, Hao, Ming-Hong, primary, Bailey, Suzanna, primary, Wu, Jeremy, primary, Rimkunas, Victoria, primary, Karr, Craig, primary, Subramanian, Vanitha, primary, Kumar, Pavan, primary, MacKenzie, Crystal, primary, Hurley, Raelene, primary, Satoh, Takashi, primary, Yu, Kun, primary, Park, Eunice, primary, Rioux, Nathalie, primary, Kim, Amy, primary, Lai, Weidong G., primary, Yu, Lihua, primary, Zhu, Ping, primary, Buonamici, Silvia, primary, Larsen, Nicholas, primary, Fekkes, Peter, primary, Wang, John, primary, Warmuth, Markus, primary, Reynolds, Dominic J., primary, Smith, Peter G., primary, and Selvaraj, Anand, primary

Published
2023
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28. Splicing Modulators Impair DNA Damage Response and Induce Killing of Cohesin-Mutant MDS/AML

Author

Wheeler, Emily C, primary, Martin, Benjamin, additional, Doyle, William, additional, Gorelov, Rebecca, additional, Donahue, Melanie, additional, Jann, Johann-Christoph, additional, Abdel-Wahab, Omar, additional, Taylor, Justin, additional, Seiler, Michael, additional, Buonamici, Silvia, additional, Belizaire, Roger, additional, Adelman, Karen, additional, and Tothova, Zuzana, additional

Published
2022
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29. SRPK1 maintains acute myeloid leukemia through effects on isoform usage of epigenetic regulators including BRD4

Author

Tzelepis, Konstantinos, De Braekeleer, Etienne, Aspris, Demetrios, Barbieri, Isaia, Vijayabaskar, M. S., Liu, Wen-Hsin, Gozdecka, Malgorzata, Metzakopian, Emmanouil, Toop, Hamish D., Dudek, Monika, Robson, Samuel C., Hermida-Prado, Francisco, Yang, Yu Hsuen, Babaei-Jadidi, Roya, Garyfallos, Dimitrios A., Ponstingl, Hannes, Dias, Joao M. L., Gallipoli, Paolo, Seiler, Michael, Buonamici, Silvia, Vick, Binje, Bannister, Andrew J., Rad, Roland, Prinjha, Rab K., Marioni, John C., Huntly, Brian, Batson, Jennifer, Morris, Jonathan C., Pina, Cristina, Bradley, Allan, Jeremias, Irmela, Bates, David O., Yusa, Kosuke, Kouzarides, Tony, and Vassiliou, George S.

Published
2018
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30. Modulation of splicing catalysis for therapeutic targeting of leukemia with mutations in genes encoding spliceosomal proteins

Author

Lee, Stanley Chun-Wei, Dvinge, Heidi, Kim, Eunhee, Cho, Hana, Micol, Jean-Baptiste, Chung, Young Rock, Durham, Benjamin H, Yoshimi, Akihide, Kim, Young Joon, Thomas, Michael, Lobry, Camille, Chen, Chun-Wei, Pastore, Alessandro, Taylor, Justin, Wang, Xujun, Krivtsov, Andrei, Armstrong, Scott A, Palacino, James, Buonamici, Silvia, Smith, Peter G, Bradley, Robert K, and Abdel-Wahab, Omar

Subjects
Catalysis -- Health aspects -- Research, Gene mutation -- Research, Leukemia -- Genetic aspects -- Risk factors -- Care and treatment, Biological sciences, Health
Abstract

Author(s): Stanley Chun-Wei Lee [1]; Heidi Dvinge [2, 3]; Eunhee Kim [1]; Hana Cho [1]; Jean-Baptiste Micol [1]; Young Rock Chung [1]; Benjamin H Durham [1]; Akihide Yoshimi [1]; Young [...]

Published
2016
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31. The allosteric inhibitor ABL001 enables dual targeting of BCR-ABL1

Author

Wylie, Andrew A., Schoepfer, Joseph, Jahnke, Wolfgang, Cowan-Jacob, Sandra W., Loo, Alice, Furet, Pascal, Marzinzik, Andreas L., Pelle, Xavier, Donovan, Jerry, Zhu, Wenjing, Buonamici, Silvia, Hassan, Quamrul A., Lombardo, Franco, Iyer, Varsha, Palmer, Michael, Berellini, Giuliano, Dodd, Stephanie, Thohan, Sanjeev, Bitter, Hans, Branford, Susan, Ross, David M., Hughes, Timothy P., Petruzzelli, Lilli, Vanasse, Gary K., Warmuth, Markus, Hofmann, Francesco, Keen, Nicholas J., and Sellers, William R.

Published
2017
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32. 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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33. 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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34. 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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35. Coordinate activation of Shh and PI3K signaling in PTEN-deficient glioblastoma: new therapeutic opportunities

Author

Filbin, Mariella Gruber, Dabral, Sukriti K., Pazyra-Murphy, Maria F., Ramkissoon, Shakti, Kung, Andrew L., Pak, Ekaterina, Chung, Jarom, Theisen, Matthew A., Sun, Yanping, Franchetti, Yoko, Sun, Yu, Shulman, David S., Redjal, Navid, Tabak, Barbara, Beroukhim, Rameen, Wang, Qi, Zhao, Jean, Dorsch, Marion, Buonamici, Silvia, Ligon, Keith L., Kelleher, Joseph F., and Segal, Rosalind A.

Subjects
Gene expression -- Research, Viral antibodies -- Properties, Glioblastoma multiforme -- Development and progression -- Care and treatment, Cellular signal transduction -- Genetic aspects, Cancer cells -- Genetic aspects, Antibodies -- Properties, Biological sciences, Health
Abstract

In glioblastoma, phosphatidylinositol 3-kinase (PI3K) signaling is frequently activated by loss of the tumor suppressor phosphatase and tensin homolog (PTEN) (1). However, it is not known whether inhibiting PI3K represents [...]

Published
2013
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36. Abstract 2197: Dysregulated alternative splicing landscape identifies intron retention as a hallmark and spliceosome as a therapeutic vulnerability in aggressive prostate cancer

Author

Zhang, Dingxiao, primary, Hu, qiang, additional, Liu, Xiaozhuo, additional, Ji, Yibing, additional, Chao, Hsueh-Ping, additional, Tracz, Amanda, additional, Kirk, Jason, additional, Buonamici, Silvia, additional, Zhu, Ping, additional, Wang, Jianmin, additional, liu, song, additional, and Tang, Dean, additional

Published
2021
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37. REM-422, a Potent, Selective, Oral Small Molecule mRNA Degrader of the MYB Oncogene, Demonstrates Anti-Tumor Activity in Mouse Xenograft Models of AML

Author

Prajapati, Sudeep, Cameron, Michael, Dunyak, Bryan M., Shan, Mengge, Siu, Y. Amy, Levin-Furtney, Samantha, Powe, Joshua, Burchfiel, Eileen T.M., Cabral, Sarah E., Harney, Alycen M., Keenan, Regina K., Larpenteur, Kevin M., Maag, Jesper L.V., Snyder, Andrew R., Nguyen, Dan T., Blaustein, Cecile, Buonamici, Silvia, Reynolds, Dominic, Schnaderbeck, Matthew J., Seiler, Michael, Vaillancourt, Frédéric H., Smith, Peter, Kaprielian, Zaven, and Kung, Charles

Published
2023
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38. A crucial requirement for Hedgehog signaling in small cell lung cancer

Author

Park, Kwon-Sik, Martelotto, Luciano G., Peifer, Martin, Sos, Martin L., Karnezis, Anthony N., Mahjoub, Moe R., Bernard, Katie, Conklin, Jamie F., Szczepny, Anette, Yuan, Jing, Guo, Ribo, Ospina, Beatrice, Falzon, Jeanette, Bennett, Samara, Brown, Tracey J., Markovic, Ana, Devereux, Wendy L., Ocasio, Cory A., Chen, James K., Stearns, Tim, Thomas, Roman K., Dorsch, Marion, Buonamici, Silvia, Watkins, D.Neil, Peacock, Craig D., and Sage, Julien

Subjects
Hedgehog proteins -- Physiological aspects -- Genetic aspects -- Research, Lung cancer, Non-small cell -- Development and progression -- Genetic aspects -- Care and treatment -- Research, Cellular signal transduction -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

Small-cell lung cancer (SCLC) is an aggressive neuroendocrine subtype of lung cancer for which there is no effective treatment (1,2). Using a mouse model in which deletion of Rbl and Trp53 in the lung epithelium of adult mice induces SCLC (3,4), we found that the Hedgehog signaling pathway is activated in SCLC cells independently of the lung microenvironment. Constitutive activation of the Hedgehog signaling molecule Smoothened (Smo) promoted the clonogenicity of human SCLC in vitro and the initiation and progression of mouse SCLC in vivo. Reciprocally, deletion of Smo in Rbl and Trp53-mutant lung epithelial cells strongly suppressed SCLC initiation and progression in mice. Furthermore, pharmacological blockade of Hedgehog signaling inhibited the growth of mouse and human SCLC, most notably following chemotherapy. These findings show a crucial cell-intrinsic role for Hedgehog signaling in the development and maintenance of SCLC and identify Hedgehog pathway inhibition as a therapeutic strategy to slow the progression of disease and delay cancer recurrence in individuals with SCLC., Activation of Hedgehog signaling has been reported in a subset of human SCLC cell lines and tumors (5-8) without changes in Hedgehog pathway gene copy numbers (9). Furthermore, we sequenced [...]

Published
2011
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39. A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia

Author

Klinakis, Apostolos, Lobry, Camille, Abdel-Wahab, Omar, Oh, Philmo, Haeno, Hiroshi, Buonamici, Silvia, van DeWalle, Inge, Cathelin, Severine, Trimarchi, Thomas, Araldi, Elisa, Liu, Cynthia, Ibrahim, Sherif, Beran, Miroslav, Zavadil, Jiri, Efstratiadis, Argiris, Taghon, Tom, Michor, Franziska, Levine, Ross L., and Aifantis, Iannis

Subjects
T cells -- Physiological aspects -- Research -- Genetic aspects, Hematopoietic stem cells -- Physiological aspects -- Research, Cellular signal transduction -- Research -- Genetic aspects -- Physiological aspects, Myelocytic leukemia -- Genetic aspects -- Research, Nonlymphoid leukemia -- Genetic aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Notch signalling is a central regulator of differentiation in a variety of organisms and tissue types1. Its activity is controlled by the multi-subunit γ-secretase (γSE) complex (2). Although Notch signalling can play both oncogenic and tumour-suppressor roles in solid tumours, in the haematopoietic system it is exclusively oncogenic, notably in T-cell acute lymphoblastic leukaemia, a disease characterized by Notch1-activating mutations (3). Here we identify novel somatic-inactivating Notch pathway mutations in a fraction of patients with chronic myelomonocytic leukaemia (CMML). Inactivation of Notch signalling in mouse haematopoietic stem cells (HSCs) results in an aberrant accumulation of granulocyte/monocyte progenitors (GMPs), extramedullary haematopoieisis and the induction of CMML-like disease. Transcriptome analysis revealed that Notch signalling regulates an extensive myelomonocytic-specific gene signature, through the direct suppression of gene transcription by the Notch target Hes1. Our studies identify a novel role for Notch signalling during early haematopoietic stem cell differentiation and suggest that the Notch pathway can play both tumour-promoting and -suppressive roles within the same tissue., Notch is essential for the emergence of definitive haematopoiesis (4), controls HSC differentiation to the T-cell lineage (5,6) and is a major oncogene, as most patients with T-cell acute lymphoblastic [...]

Published
2011
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40. Loss of the tumor suppressor Snf5 leads to aberrant activation of the Hedgehog-Gli pathway

Author

Jagani, Zainab, Mora-Blanco, E. Lorena, Sansam, Courtney G., McKenna, Elizabeth S., Wilson, Boris, Chen, Dongshu, Klekota, Justin, Tamayo, Pablo, Nguyen, Phuong T.L., Tolstorukov, Michael, Park, Peter J., Cho, Yoon-Jae, Hsiao, Kathy, Buonamici, Silvia, Pomeroy, Scott L., Mesirov, Jill P., Ruffner, Heinz, Bouwmeester, Tewis, Luchansky, Sarah J., Murtie, Joshua, Kelleher, Joseph F., Warmuth, Markus, Sellers, William R., Roberts, Charles W.M., and Dorsch, Marion

Subjects
Tumors -- Risk factors -- Genetic aspects -- Research, Gene expression -- Research, Tumor suppressor genes -- Health aspects -- Research, Hedgehog proteins -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

Aberrant activation of the Hedgehog (Hh) pathway can drive tumorigenesis (1). To investigate the mechanism by which glioma-associated oncogene family zinc finger-1 (GLI1), a crucial effector of Hh signaling (2), regulates Hh pathway activation, we searched for GLI1-interacting proteins. We report that the chromatin remodeling protein SNF5 (encoded by SMARCB1, hereafter called SNF5), which is inactivated in human malignant rhabdoid tumors (MRTs), interacts with GLI1. We show that Snf5 localizes to Gli1-regulated promoters and that loss of Snf5 leads to activation of the Hh-Gli pathway. Conversely, re-expression of SNF5 in MRT cells represses GLI1. Consistent with this, we show the presence of a Hh-Gli-activated gene expression profile in primary MRTs and show that GLI1 drives the growth of SNF5-deficient MRT cells in vitro and in vivo. Therefore, our studies reveal that SNF5 is a key mediator of Hh signaling and that aberrant activation of GLI1 is a previously undescribed targetable mechanism contributing to the growth of MRT cells., The Hh pathway has critical functions in tissue patterning and differentiation during development (1). Aberrant activation of the pathway resulting from mutations in the PTCH1 gene (encoding Patched-1 receptor) and [...]

Published
2010
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41. CCR7 signalling as an essential regulator of CNS infiltration in T-cell leukaemia

Author

Buonamici, Silvia, Trimarchi, Thomas, Ruocco, Maria Grazia, Reavie, Linsey, Cathelin, Severine, Mar, Brenton G., Klinakis, Apostolos, Lukyanov, Yevgeniy, Tseng, Jen-Chieh, Sen, Filiz, Gehrie, Eric, Li, Mengling, Newcomb, Elizabeth, Zavadil, Jiri, Meruelo, Daniel, Lipp, Martin, Ibrahim, Sherif, Efstratiadis, Argiris, Zagzag, David, Bromberg, Jonathan S., Dustin, Michael L., and Aifantis, Iannis

Published
2009
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42. Targeting the NF-[kappa]B signaling pathway in Notch1-induced T-cell leukemia

Author

Vilimas, Tomas, Mascarenhas, Joaquina, Palomero, Teresa, Mandal, Malay, Buonamici, Silvia, Meng, Fanyong, Thompson, Benjamin, Spaulding, Christina, Macaroun, Sami, Alegre, Maria-Luisa, Kee, Barbara L, Ferrando, Adolfo, Miele, Lucio, and Aifantis, Iannis

Abstract

T-cell acute lymphoblastic leukemia (T-ALL), unlike other ALL types, is only infrequently associated with chromosomal aberrations, but it was recently shown that most individuals with T-ALL carry activating mutations in the NOTCH1 gene. However, the signaling pathways and target genes responsible for Notch1-induced neoplastic transformation remain undefined. We report here that constitutively active Notch1 activates the NF-[kappa]B pathway transcriptionally and via the I[kappa]B kinase (IKK) complex, thereby causing increased expression of several well characterized target genes of NF-[kappa]B in bone marrow hematopoietic stem cells and progenitors. Our observations demonstrate that the NF-[kappa]B pathway is highly active in established human T-ALL and that inhibition of the pathway can efficiently restrict tumor growth both in vitro and in vivo. These findings identify NF-[kappa]B as one of the major mediators of Notch1-induced transformation and suggest that the NF-[kappa]B pathway is a potential target of future therapies of T-ALL., Author(s): Tomas Vilimas [1, 6, 7]; Joaquina Mascarenhas [2, 6]; Teresa Palomero [3]; Malay Mandal [1]; Silvia Buonamici [1, 4]; Fanyong Meng [1]; Benjamin Thompson [1, 4]; Christina Spaulding [5]; [...]

Published
2007
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43. Spliceosome-targeted therapies trigger an antiviral immune response in triple-negative breast cancer

Author

Bowling, Elizabeth A., primary, Wang, Jarey H., additional, Gong, Fade, additional, Wu, William, additional, Neill, Nicholas J., additional, Kim, Ik Sun, additional, Tyagi, Siddhartha, additional, Orellana, Mayra, additional, Kurley, Sarah J., additional, Dominguez-Vidaña, Rocio, additional, Chung, Hsiang-Ching, additional, Hsu, Tiffany Y.-T., additional, Dubrulle, Julien, additional, Saltzman, Alexander B., additional, Li, Heyuan, additional, Meena, Jitendra K., additional, Canlas, Gino M., additional, Chamakuri, Srinivas, additional, Singh, Swarnima, additional, Simon, Lukas M., additional, Olson, Calla M., additional, Dobrolecki, Lacey E., additional, Lewis, Michael T., additional, Zhang, Bing, additional, Golding, Ido, additional, Rosen, Jeffrey M., additional, Young, Damian W., additional, Malovannaya, Anna, additional, Stossi, Fabio, additional, Miles, George, additional, Ellis, Matthew J., additional, Yu, Lihua, additional, Buonamici, Silvia, additional, Lin, Charles Y., additional, Karlin, Kristen L., additional, Zhang, Xiang H.-F., additional, and Westbrook, Thomas F., additional

Published
2021
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44. Male-Biased Spliceosome Mutations in Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN) Impair pDC Activation and Apoptosis

Author

Togami, Katsuhiro, primary, Chung, Sun Sook, additional, Madan, Vikas, additional, Kenyon, Christopher M., additional, Cabal-Hierro, Lucia, additional, Taylor, Justin, additional, Kim, Sunhee, additional, Griffin, Gabriel K, additional, Ghandi, Mahmoud, additional, Li, Jia, additional, Li, Yvonne Y., additional, Angelot-Delletre, 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
2020
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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, 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
2020
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46. Erratum: Modulation of splicing catalysis for therapeutic targeting of leukemia with mutations in genes encoding spliceosomal proteins

Author

Lee, Stanley Chun-Wei, Dvinge, Heidi, Kim, Eunhee, Cho, Hana, Micol, Jean-Baptiste, Chung, Young Rock, Durham, Benjamin H, Yoshimi, Akihide, Kim, Young Joon, Thomas, Michael, Lobry, Camille, Chen, Chun-Wei, Pastore, Alessandro, Taylor, Justin, Wang, Xujun, Krivtsov, Andrei, Armstrong, Scott A, Palacino, James, Buonamici, Silvia, Smith, Peter G, Bradley, Robert K, and Abdel-Wahab, Omar

Published
2016
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47. Arsenic trioxide and thalidomide combination produces multi-lineage hematological responses in myelodysplastic syndromes patients, particularly in those with high pre-therapy EVI1 expression

Author

Raza, Azra, Buonamici, Silvia, Lisak, Laurie, Tahir, Sarah, Li, Donglan, Imran, Mehnaz, Chaudary, Nusrat Ijaz, Pervaiz, Hassan, Gallegos, J.Alejandro, Alvi, M.Imran, Mumtaz, Muhammad, Gezer, Sefer, Venugopal, Parameswaran, Reddy, Poluru, Galili, Naomi, Candoni, Anna, Singer, Jack, and Nucifora, Giuseppina

Published
2004
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50. Somatic Mutational Landscape of Splicing Factor Genes and Their Functional Consequences across 33 Cancer Types

Author

Seiler, Michael, Peng, Shouyong, Agrawal, Anant A, Palacino, James, Teng, Teng, Zhu, Ping, Smith, Peter G, Cancer Genome Atlas Research Network, Buonamici, Silvia, and Yu, Lihua

Subjects
RBM10, RNA Splicing, Medical Physiology, Cancer Genome Atlas Research Network, Cell Line, splicing, Rare Diseases, Mutation Rate, Loss of Function Mutation, Neoplasms, U2AF1, Genetics, Humans, cancer, 2.1 Biological and endogenous factors, Genetic Testing, Aetiology, Tumor, SF3B1, Human Genome, Oncogenes, Hematology, SRSF2, Genes, RNA Splicing Factors, Biochemistry and Cell Biology, FUBP1, mutation, Tumor Suppressor, Biotechnology
Abstract

Hotspot mutations in splicing factor genes have been recently reported at high frequency in hematological malignancies, suggesting the importance of RNA splicing in cancer. We analyzed whole-exome sequencing data across 33 tumor types in The Cancer Genome Atlas (TCGA), and we identified 119 splicing factor genes with significant non-silent mutation patterns, including mutation over-representation, recurrent loss of function (tumor suppressor-like), or hotspot mutation profile (oncogene-like). Furthermore, RNA sequencing analysis revealed altered splicing events associated with selected splicing factor mutations. In addition, we were able to identify common gene pathway profiles associated with the presence of these mutations. Our analysis suggests that somatic alteration of genes involved in the RNA-splicing process is common incancer and may represent an underappreciated hallmark of tumorigenesis.

Published
2018

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