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Your search keyword '"Jakubik, Charles T."' showing total 14 results
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14 results on '"Jakubik, Charles T."'

1. Exploitation of the Apoptosis-Primed State of MYCN-Amplified Neuroblastoma to Develop a Potent and Specific Targeted Therapy Combination

Author

Ham, Jungoh, Costa, Carlotta, Sano, Renata, Lochmann, Timothy L., Sennott, Erin M., Patel, Neha U., Dastur, Anahita, Gomez-Caraballo, Maria, Krytska, Kateryna, Hata, Aaron N., Floros, Konstantinos V., Hughes, Mark T., Jakubik, Charles T., Heisey, Daniel A.R., Ferrell, Justin T., Bristol, Molly L., March, Ryan J., Yates, Craig, Hicks, Mark A., Nakajima, Wataru, Gowda, Madhu, Windle, Brad E., Dozmorov, Mikhail G., Garnett, Mathew J., McDermott, Ultan, Harada, Hisashi, Taylor, Shirley M., Morgan, Iain M., Benes, Cyril H., Engelman, Jeffrey A., Mossé, Yael P., and Faber, Anthony C.

Published
2016
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2. Supplementary Data from PTEN Loss Mediates Clinical Cross-Resistance to CDK4/6 and PI3Kα Inhibitors in Breast Cancer

Author

Costa, Carlotta, primary, Wang, Ye, primary, Ly, Amy, primary, Hosono, Yasuyuki, primary, Murchie, Ellen, primary, Walmsley, Charlotte S., primary, Huynh, Tiffany, primary, Healy, Christopher, primary, Peterson, Rachel, primary, Yanase, Shogo, primary, Jakubik, Charles T., primary, Henderson, Laura E., primary, Damon, Leah J., primary, Timonina, Daria, primary, Sanidas, Ioannis, primary, Pinto, Christopher J., primary, Mino-Kenudson, Mari, primary, Stone, James R., primary, Dyson, Nicholas J., primary, Ellisen, Leif W., primary, Bardia, Aditya, primary, Ebi, Hiromichi, primary, Benes, Cyril H., primary, Engelman, Jeffrey A., primary, and Juric, Dejan, primary

Published
2023
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3. Data from PTEN Loss Mediates Clinical Cross-Resistance to CDK4/6 and PI3Kα Inhibitors in Breast Cancer

Author

Costa, Carlotta, primary, Wang, Ye, primary, Ly, Amy, primary, Hosono, Yasuyuki, primary, Murchie, Ellen, primary, Walmsley, Charlotte S., primary, Huynh, Tiffany, primary, Healy, Christopher, primary, Peterson, Rachel, primary, Yanase, Shogo, primary, Jakubik, Charles T., primary, Henderson, Laura E., primary, Damon, Leah J., primary, Timonina, Daria, primary, Sanidas, Ioannis, primary, Pinto, Christopher J., primary, Mino-Kenudson, Mari, primary, Stone, James R., primary, Dyson, Nicholas J., primary, Ellisen, Leif W., primary, Bardia, Aditya, primary, Ebi, Hiromichi, primary, Benes, Cyril H., primary, Engelman, Jeffrey A., primary, and Juric, Dejan, primary

Published
2023
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4. Assessment of ABT-263 activity across a cancer cell line collection leads to a potent combination therapy for small-cell lung cancer

Author

Faber, Anthony C., Farago, Anna F., Costa, Carlotta, Dastur, Anahita, Gomez-Caraballo, Maria, Robbins, Rebecca, Wagner, Bethany L., Rideout, William M., Jakubik, Charles T., Ham, Jungoh, Edelman, Elena J., Ebi, Hiromichi, Yeo, Alan T., Hata, Aaron N., Song, Youngchul, Patel, Neha U., March, Ryan J., Tam, Ah Ting, Milano, Randy J., Boisvert, Jessica L., Hicks, Mark A., Elmiligy, Sarah, Malstrom, Scott E., Rivera, Miguel N., Harada, Hisashi, Windle, Brad E., Ramaswamy, Sridhar, Benes, Cyril H., Jacks, Tyler, and Engelman, Jeffrey A.

Published
2015

6. Genomic screening reveals ubiquitin-like modifier activating enzyme 1 as a potent and druggable target in c-MYC-high triple negative breast cancer models

Author

Jacob, Sheeba, primary, Turner, Tia H, additional, Cai, Jinyang, additional, Floros, Konstantinos V, additional, Yu, Ann K, additional, Coon, Colin M, additional, Khatri, Rishabh, additional, Alzubi, Mohammad A, additional, Jakubik, Charles T, additional, Bouck, Ynes M, additional, Puchalapalli, Madhavi, additional, Shende, Mayuri, additional, Dozmorov, Mikhail G, additional, Boikos, Sosipatros A, additional, Hu, Bin, additional, Harrell, J Chuck, additional, Benes, Cyril H, additional, Koblinski, Jennifer E, additional, Costa, Carlotta, additional, and Faber, Anthony C, additional

Published
2022
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7. Genomic screening reveals UBA1 as a potent and druggable target in c-MYC-high TNBC models

Author

Jacob, Sheeba, primary, Turner, Tia H, additional, Cai, Jinyang, additional, Floros, Konstantinos V, additional, Yu, Ann K, additional, Coon, Colin M, additional, Khatri, Rishabh, additional, Alzubi, Mohammad A, additional, Jakubik, Charles T, additional, Bouck, Ynes M, additional, Puchalapalli, Madhavi, additional, Shende, Mayuri, additional, Dozmorov, Mikhail G, additional, Boikos, Sosipatros, additional, Hu, Bin, additional, Harrell, J Chuck, additional, Benes, Cyril H, additional, Koblinski, Jennifer, additional, Costa, Carlotta, additional, and Faber, Anthony C, additional

Published
2022
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9. Abstract 1903: PTEN loss mediates clinical cross-resistance to CDK4/6 and PI3Ká inhibitors in breast cancer

Author

Costa, Carlotta, primary, Wang, Ye, additional, Ly, Amy, additional, Hosono, Yasuyuki, additional, Murchie, Ellen, additional, Walmsley, Charlotte S., additional, Huynh, Tiffany, additional, Healy, Christopher, additional, Peterson, Rachel, additional, Yanase, Shogo, additional, Jakubik, Charles T., additional, Henderson, Laura E., additional, Damon, Leah J., additional, Timonina, Daria, additional, Sanidas, Ioannis, additional, Pinto, Christopher J., additional, Mino-Kenudson, Mari, additional, Stone, James, additional, Dyson, Nicholas J., additional, Ellisen, Leif W., additional, Bardia, Aditya, additional, Ebi, Hiromichi, additional, Benes, Cyril H., additional, Engelman, Jeffrey A., additional, and Juric, Dejan, additional

Published
2020
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10. Abstract P1-19-28: Genomic screening reveals UBA1 as a potent and druggable target in diverse models of triple negative breast cancer

Author

Jacob, Sheeba, primary, Turner, Tia H., additional, Yu, Ann K., additional, Coon, Colin M., additional, Alzubi, Mohammad A., additional, Jakubik, Charles T., additional, Bouck, Ynes, additional, Dozmorov, Mikhail G., additional, Boikos, Sosipatros A., additional, Koblinski, Jennifer, additional, Harrell, Joshua C., additional, Benes, Cyril H., additional, Costa, Carlotta, additional, and Faber, Anthony C., additional

Published
2020
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11. PIP3 abundance overcomes PI3K signaling selectivity in invadopodia.

Author

Jakubik, Charles T., Weckerly, Claire C., Hammond, Gerald R.V., Bresnick, Anne R., and Backer, Jonathan M.

Subjects
*PHOSPHATIDYLINOSITOL 3-kinases, *BREAST cancer, *CANCER cells
Abstract

PI3Kβ is required for invadopodia‐mediated matrix degradation by breast cancer cells. Invadopodia maturation requires GPCR activation of PI3Kβ and its coupling to SHIP2 to produce PI(3,4)P2. We now test whether selectivity for PI3Kβ is preserved under conditions of mutational increases in PI3K activity. In breast cancer cells where PI3Kβ is inhibited, short‐chain diC8‐PIP3 rescues gelatin degradation in a SHIP2‐dependent manner; rescue by diC8‐PI(3,4)P2 is SHIP2‐independent. Surprisingly, the expression of either activated PI3Kβ or PI3Kα mutants rescued the effects of PI3Kβ inhibition. In both cases, gelatin degradation was SHIP2‐dependent. These data confirm the requirement for PIP3 conversion to PI(3,4)P2 for invadopodia function and suggest that selectivity for distinct PI3K isotypes may be obviated by mutational activation of the PI3K pathway. [ABSTRACT FROM AUTHOR]

Published
2022
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12. PTEN Loss Mediates Clinical Cross-Resistance to CDK4/6 and PI3Kα Inhibitors in Breast Cancer

Author

Costa, Carlotta, primary, Wang, Ye, additional, Ly, Amy, additional, Hosono, Yasuyuki, additional, Murchie, Ellen, additional, Walmsley, Charlotte S., additional, Huynh, Tiffany, additional, Healy, Christopher, additional, Peterson, Rachel, additional, Yanase, Shogo, additional, Jakubik, Charles T., additional, Henderson, Laura E., additional, Damon, Leah J., additional, Timonina, Daria, additional, Sanidas, Ioannis, additional, Pinto, Christopher J., additional, Mino-Kenudson, Mari, additional, Stone, James R., additional, Dyson, Nicholas J., additional, Ellisen, Leif W., additional, Bardia, Aditya, additional, Ebi, Hiromichi, additional, Benes, Cyril H., additional, Engelman, Jeffrey A., additional, and Juric, Dejan, additional

Published
2020
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14. Assessment of ABT-263 activity across a cancer cell line collection leads to a potent combination therapy for small-cell lung cancer

Author

Koch Institute for Integrative Cancer Research at MIT, Farago, Anna, Robbins, Rebecca, Wagner, Bethany L., Rideout, William M., Elmiligy, Sarah, Malstrom, Scott E., Jacks, Tyler E., Faber, Anthony C., Costa, Carlotta, Dastur, Anahita, Gomez-Caraballo, Maria, Jakubik, Charles T., Ham, Jungoh, Edelman, Elena J., Ebi, Hiromichi, Yeo, Alan T., Hata, Aaron N., Song, Youngchul, Patel, Neha U., March, Ryan J., Tam, Ah Ting, Milano, Randy J., Boisvert, Jessica L., Hicks, Mark A., Rivera, Miguel N., Harada, Hisashi, Windle, Brad E., Ramaswamy, Sridhar, Benes, Cyril H., Engelman, Jeffrey A., Jacks, Tyler E, Koch Institute for Integrative Cancer Research at MIT, Farago, Anna, Robbins, Rebecca, Wagner, Bethany L., Rideout, William M., Elmiligy, Sarah, Malstrom, Scott E., Jacks, Tyler E., Faber, Anthony C., Costa, Carlotta, Dastur, Anahita, Gomez-Caraballo, Maria, Jakubik, Charles T., Ham, Jungoh, Edelman, Elena J., Ebi, Hiromichi, Yeo, Alan T., Hata, Aaron N., Song, Youngchul, Patel, Neha U., March, Ryan J., Tam, Ah Ting, Milano, Randy J., Boisvert, Jessica L., Hicks, Mark A., Rivera, Miguel N., Harada, Hisashi, Windle, Brad E., Ramaswamy, Sridhar, Benes, Cyril H., Engelman, Jeffrey A., and Jacks, Tyler E

Abstract

BH3 mimetics such as ABT-263 induce apoptosis in a subset of cancer models. However, these drugs have shown limited clinical efficacy as single agents in small-cell lung cancer (SCLC) and other solid tumor malignancies, and rational combination strategies remain underexplored. To develop a novel therapeutic approach, we examined the efficacy of ABT-263 across >500 cancer cell lines, including 311 for which we had matched expression data for select genes. We found that high expression of the proapoptotic gene Bcl2-interacting mediator of cell death (BIM) predicts sensitivity to ABT-263. In particular, SCLC cell lines possessed greater BIM transcript levels than most other solid tumors and are among the most sensitive to ABT-263. However, a subset of relatively resistant SCLC cell lines has concomitant high expression of the antiapoptotic myeloid cell leukemia 1 (MCL-1). Whereas ABT-263 released BIM from complexes with BCL-2 and BCL-XL, high expression of MCL-1 sequestered BIM released from BCL-2 and BCL-XL, thereby abrogating apoptosis. We found that SCLCs were sensitized to ABT-263 via TORC1/2 inhibition, which led to reduced MCL-1 protein levels, thereby facilitating BIM-mediated apoptosis. AZD8055 and ABT-263 together induced marked apoptosis in vitro, as well as tumor regressions in multiple SCLC xenograft models. In a Tp53; Rb1 deletion genetically engineered mouse model of SCLC, the combination of ABT-263 and AZD8055 significantly repressed tumor growth and induced tumor regressions compared with either drug alone. Furthermore, in a SCLC patient-derived xenograft model that was resistant to ABT-263 alone, the addition of AZD8055 induced potent tumor regression. Therefore, addition of a TORC1/2 inhibitor offers a therapeutic strategy to markedly improve ABT-263 activity in SCLC., United States. Dept. of Defense (Grant W81-XWH-13-1-0323), National Cancer Institute (U.S.) (Cancer Center Support Grant P30-CA14051)

Published
2015

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