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22 results on '"Turke, Alexa B."'

1. Data from EGFR-Mediated Reactivation of MAPK Signaling Contributes to Insensitivity of BRAF-Mutant Colorectal Cancers to RAF Inhibition with Vemurafenib

Author

Corcoran, Ryan B., primary, Ebi, Hiromichi, primary, Turke, Alexa B., primary, Coffee, Erin M., primary, Nishino, Michiya, primary, Cogdill, Alexandria P., primary, Brown, Ronald D., primary, Della Pelle, Patricia, primary, Dias-Santagata, Dora, primary, Hung, Kenneth E., primary, Flaherty, Keith T., primary, Piris, Adriano, primary, Wargo, Jennifer A., primary, Settleman, Jeffrey, primary, Mino-Kenudson, Mari, primary, and Engelman, Jeffrey A., primary

Published
2023
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2. Supplementary Figures 1-9, Table 1, Methods from EGFR-Mediated Reactivation of MAPK Signaling Contributes to Insensitivity of BRAF-Mutant Colorectal Cancers to RAF Inhibition with Vemurafenib

Author

Corcoran, Ryan B., primary, Ebi, Hiromichi, primary, Turke, Alexa B., primary, Coffee, Erin M., primary, Nishino, Michiya, primary, Cogdill, Alexandria P., primary, Brown, Ronald D., primary, Della Pelle, Patricia, primary, Dias-Santagata, Dora, primary, Hung, Kenneth E., primary, Flaherty, Keith T., primary, Piris, Adriano, primary, Wargo, Jennifer A., primary, Settleman, Jeffrey, primary, Mino-Kenudson, Mari, primary, and Engelman, Jeffrey A., primary

Published
2023
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9. Preexistence and Clonal Selection of MET Amplification in EGFR Mutant NSCLC

Author

Turke, Alexa B., Zejnullahu, Kreshnik, Wu, Yi-Long, Song, Youngchul, Dias-Santagata, Dora, Lifshits, Eugene, Toschi, Luca, Rogers, Andrew, Mok, Tony, Sequist, Lecia, Lindeman, Neal I., Murphy, Carly, Akhavanfard, Sara, Yeap, Beow Y., Xiao, Yun, Capelletti, Marzia, Iafrate, A. John, Lee, Charles, Christensen, James G., Engelman, Jeffrey A., and Jänne, Pasi A.

Published
2010
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10. A Cross-Species Study of PI3K Protein-Protein Interactions Reveals the Direct Interaction of P85 and SHP2

Author

Breitkopf, Susanne B., primary, Yang, Xuemei, additional, Begley, Michael J., additional, Kulkarni, Meghana, additional, Chiu, Yu-Hsin, additional, Turke, Alexa B., additional, Lauriol, Jessica, additional, Yuan, Min, additional, Qi, Jie, additional, Engelman, Jeffrey A., additional, Hong, Pengyu, additional, Kontaridis, Maria I., additional, Cantley, Lewis C., additional, Perrimon, Norbert, additional, and Asara, John M., additional

Published
2016
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12. Author response: Inhibition of mutant EGFR in lung cancer cells triggers SOX2-FOXO6-dependent survival pathways

Author

Rothenberg, S Michael, primary, Concannon, Kyle, additional, Cullen, Sarah, additional, Boulay, Gaylor, additional, Turke, Alexa B, additional, Faber, Anthony C, additional, Lockerman, Elizabeth L, additional, Rivera, Miguel N, additional, Engelman, Jeffrey A, additional, Maheswaran, Shyamala, additional, and Haber, Daniel A, additional

Published
2015
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15. Abstract PR8: Insensitivity to RAF inhibition by vemurafenib in BRAF mutant colorectal cancer by EGFR-mediated reactivation of MAPK signaling

Author

Corcoran, Ryan B., primary, Hung, Kenneth E., additional, Flaherty, Keith T., additional, Piris, Adriano, additional, Wargo, Jennifer A., additional, Settleman, Jeffrey, additional, Mino-Kenudson, Mari, additional, Engelman, Jeffrey A., additional, Ebi, Hiromichi, additional, Turke, Alexa B., additional, Coffee, Erin M., additional, Nishino, Michiya, additional, Cogdill, Alexandria P., additional, Brown, Ronald D., additional, Pelle, Patricia Della, additional, and Dias-Santagata, Dora, additional

Published
2012
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16. Abstract LB-350: EGFR-mediated re-activation of MAPK signaling contributes to insensitivity ofBRAFmutant colorectal cancers to RAF inhibition by vemurafenib

Author

Corcoran, Ryan B., primary, Ebi, Hiromichi, additional, Turke, Alexa B., additional, Coffee, Erin M., additional, Nishino, Michiya, additional, Cogdill, Alexandra P., additional, Brown, Ronald D., additional, Dias-Santagata, Dora, additional, Pelle, Patricia Della, additional, Hung, Kenneth E., additional, Flaherty, Keith T., additional, Piris, Adriano, additional, Wargo, Jennifer A., additional, Settleman, Jeffrey, additional, Mino-Kenudson, Mari, additional, and Engelman, Jeffrey A., additional

Published
2012
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17. EGFR-Mediated Reactivation of MAPK Signaling Contributes to Insensitivity of BRAF-Mutant Colorectal Cancers to RAF Inhibition with Vemurafenib

Author

Corcoran, Ryan B., primary, Ebi, Hiromichi, additional, Turke, Alexa B., additional, Coffee, Erin M., additional, Nishino, Michiya, additional, Cogdill, Alexandria P., additional, Brown, Ronald D., additional, Della Pelle, Patricia, additional, Dias-Santagata, Dora, additional, Hung, Kenneth E., additional, Flaherty, Keith T., additional, Piris, Adriano, additional, Wargo, Jennifer A., additional, Settleman, Jeffrey, additional, Mino-Kenudson, Mari, additional, and Engelman, Jeffrey A., additional

Published
2012
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19. Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors

Author

Sequist, Lecia V., primary, Waltman, Belinda A., additional, Dias-Santagata, Dora, additional, Digumarthy, Subba, additional, Turke, Alexa B., additional, Fidias, Panos, additional, Bergethon, Kristin, additional, Shaw, Alice T., additional, Gettinger, Scott, additional, Cosper, Arjola K., additional, Akhavanfard, Sara, additional, Heist, Rebecca S., additional, Temel, Jennifer, additional, Christensen, James G., additional, Wain, John C., additional, Lynch, Thomas J., additional, Vernovsky, Kathy, additional, Mark, Eugene J., additional, Lanuti, Michael, additional, Iafrate, A. John, additional, Mino-Kenudson, Mari, additional, and Engelman, Jeffrey A., additional

Published
2011
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21. Using Tandem Mass Spectrometry in Targeted Mode to Identify Activators of Class IA PI3K in Cancer.

Author

Xuemei Yang, Turke, Alexa B., Jie Qi, Youngchul Song, Rexer, Brent N., Miller, Todd W., Jänne, Pasi A., Arteaga, Carlos L., Cantley, Lewis C., Engelman, Jeffrey A., and Asara, John M.

Subjects
*TANDEM mass spectrometry, *CANCER research, *PROTEIN-tyrosine kinases, *LIQUID chromatography, *SMALL cell lung cancer
Abstract

Phosphatiditylinositide-3-kinase (PI3K) is activated in some cancers by direct mutation, but it is activated more commonly in cancer by mutation of upstream acting receptor tyrosine kinases (TK). At present, there is no systematic method to determine which TK signaling cascades activate PI3K in certain cancers, despite the likely utility of such information to help guide selection of tyrosine kinase inhibitor (TKI) drug strategies for personalized therapy. Here, we present a quantitative liquid chromatography tandem mass spectrometry approach that identifies upstream activators of PI3K both in vitro and in vivo. Using non--small cell lung carcinoma to illustrate this approach, we show a correct identification of the mechanism of PI3K activation in several models, thereby identifying the most appropriate TKI to downregulate PI3K signaling. This approach also determined the molecular mechanisms and adaptors required for PI3K activation following inhibition of the mTOR kinase TORC1. We further validated the approach in breast cancer cells with mutational activation of PIK3CA, where tandem mass spectrometry detected and quantitatively measured the abundance of a helical domain mutant (E545K) of PIK3CA connected to PI3K activation. Overall, our findings establish amass spectrometric approach to identify functional interactions that govern PI3K regulation in cancer cells. Using this technique to define the pathways that activate PI3K signaling in a given tumor could help inform clinical decision making by helping guide personalized therapeutic strategies for different patients. [ABSTRACT FROM AUTHOR]

Published
2011
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22. EGFR-mediated re-activation of MAPK signaling contributes to insensitivity of BRAF mutant colorectal cancers to RAF inhibition with vemurafenib.

Author

Corcoran RB, Ebi H, Turke AB, Coffee EM, Nishino M, Cogdill AP, Brown RD, Della Pelle P, Dias-Santagata D, Hung KE, Flaherty KT, Piris A, Wargo JA, Settleman J, Mino-Kenudson M, and Engelman JA

Subjects
Animals, Cell Growth Processes drug effects, Cell Line, Tumor, Colorectal Neoplasms enzymology, Colorectal Neoplasms genetics, Colorectal Neoplasms pathology, HT29 Cells, Humans, Immunohistochemistry, Male, Mice, Mice, Nude, Vemurafenib, Xenograft Model Antitumor Assays, Colorectal Neoplasms drug therapy, ErbB Receptors metabolism, Indoles pharmacology, MAP Kinase Signaling System, Proto-Oncogene Proteins B-raf genetics, Sulfonamides pharmacology, raf Kinases antagonists & inhibitors
Abstract

Unlabelled: BRAF mutations occur in 10-15% of colorectal cancers (CRCs) and confer adverse outcome. While RAF inhibitors such as vemurafenib (PLX4032) have proven effective in BRAF mutant melanoma, they are surprisingly ineffective in BRAF mutant CRCs, and the reason for this disparity remains unclear. Compared to BRAF mutant melanoma cells, BRAF mutant CRC cells were less sensitive to vemurafenib, and P-ERK suppression was not sustained in response to treatment. Although transient inhibition of phospho-ERK by vemurafenib was observed in CRC, rapid ERK re-activation occurred through EGFR-mediated activation of RAS and CRAF. BRAF mutant CRCs expressed higher levels of phospho-EGFR than BRAF mutant melanomas, suggesting that CRCs are specifically poised for EGFR-mediated resistance. Combined RAF and EGFR inhibition blocked reactivation of MAPK signaling in BRAF mutant CRC cells and markedly improved efficacy in vitro and in vivo. These findings support evaluation of combined RAF and EGFR inhibition in BRAF mutant CRC patients., Significance: BRAF valine 600 (V600) mutations occur in 10% to 15% of colorectal cancers, yet these tumors show a surprisingly low clinical response rate (~5%) to selective RAF inhibitors such as vemurafenib, which have produced dramatic response rates (60%–80%) in melanomas harboring the identical BRAF V600 mutation. We found that EGFR-mediated MAPK pathway reactivation leads to resistance to vemurafenib in BRAF-mutant colorectal cancers and that combined RAF and EGFR inhibition can lead to sustained MAPK pathway suppression and improved efficacy in vitro and in tumor xenografts., (©2012 AACR.)

Published
2012
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