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Anna C. Schinzel
Researcher at Harvard University
Publications - 33
Citations - 3177
Anna C. Schinzel is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & Transcription factor. The author has an hindex of 21, co-authored 33 publications receiving 2795 citations. Previous affiliations of Anna C. Schinzel include Massachusetts Institute of Technology & Broad Institute.
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Journal ArticleDOI
β-Catenin-Driven Cancers Require a YAP1 Transcriptional Complex for Survival and Tumorigenesis
Joseph Rosenbluh,Deepak Nijhawan,Deepak Nijhawan,Deepak Nijhawan,Andrew G. Cox,Andrew G. Cox,Xingnan Li,James T. Neal,Eric J. Schafer,Eric J. Schafer,Eric J. Schafer,Travis I. Zack,Travis I. Zack,Xiaoxing Wang,Xiaoxing Wang,Xiaoxing Wang,Aviad Tsherniak,Anna C. Schinzel,Anna C. Schinzel,Anna C. Schinzel,Diane D. Shao,Diane D. Shao,Diane D. Shao,Steven E. Schumacher,Steven E. Schumacher,Barbara A. Weir,Barbara A. Weir,Francisca Vazquez,Francisca Vazquez,Glenn S. Cowley,David E. Root,Jill P. Mesirov,Rameen Beroukhim,Rameen Beroukhim,Rameen Beroukhim,Calvin J. Kuo,Wolfram Goessling,William C. Hahn +37 more
TL;DR: It is found that β-catenin active cancers are dependent on a signaling pathway involving the transcriptional regulator YAP1 and the transcription factor TBX5, and this complex is essential to the transformation and survival of β- catenin-driven cancers.
Journal ArticleDOI
KRAS and YAP1 Converge to Regulate EMT and Tumor Survival
Diane D. Shao,Wen Xue,Elsa Beyer Krall,Elsa Beyer Krall,Arjun Bhutkar,Federica Piccioni,Xiaoxing Wang,Xiaoxing Wang,Anna C. Schinzel,Anna C. Schinzel,Sabina Sood,Joseph Rosenbluh,Joseph Rosenbluh,Jong Wook Kim,Jong Wook Kim,Yaara Zwang,Yaara Zwang,Thomas M. Roberts,David E. Root,Tyler Jacks,William C. Hahn,William C. Hahn +21 more
TL;DR: It is found that acquired resistance to Kras suppression in a Kras-driven murine lung cancer model also involved increased YAP1 signaling, which implicate transcriptional regulation of EMT by Yap1 as a significant component of oncogenic RAS signaling.
Journal ArticleDOI
An activated ErbB3/NRG1 autocrine loop supports in vivo proliferation in ovarian cancer cells
Qing Sheng,Xinggang Liu,Eleanor Fleming,Karen Yuan,Huiying Piao,Huiying Piao,Jinyun Chen,Zeinab Moustafa,Roman K. Thomas,Heidi Greulich,Anna C. Schinzel,Anna C. Schinzel,Sara Zaghlul,David Bryant Batt,Seth Ettenberg,Matthew Meyerson,Matthew Meyerson,Birgit Schoeberl,Andrew L. Kung,William C. Hahn,William C. Hahn,Ronny Drapkin,Ronny Drapkin,David M. Livingston,Joyce F. Liu +24 more
TL;DR: Perturbation of this circuit with ErbB3-directed RNAi decreased cell growth in three-dimensional culture and resulted in decreased disease progression and prolonged survival in a xenograft mouse model of ovarian cancer.
Journal ArticleDOI
Inhibition of KRAS-driven tumorigenicity by interruption of an autocrine cytokine circuit
Zehua Zhu,Amir Reza Aref,Travis J. Cohoon,Thanh U. Barbie,Yu Imamura,Shenghong Yang,Susan Moody,Rhine R. Shen,Anna C. Schinzel,Tran C. Thai,Jacob B. Reibel,Pablo Tamayo,Jason T. Godfrey,Zhi Rong Qian,Asher N. Page,Karolina Maciag,Edmond M. Chan,Whitney Silkworth,Mary T. Labowsky,Lior Rozhansky,Jill P. Mesirov,William E. Gillanders,Shuji Ogino,Nir Hacohen,Suzanne Gaudet,Michael J. Eck,Jeffrey A. Engelman,Ryan B. Corcoran,Kwok-Kin Wong,William C. Hahn,David A. Barbie +30 more
TL;DR: It is shown that the IκB kinase (IKK)-related kinases Tank-binding kinase-1 (TBK1) and IKKε promote KRAS-driven tumorigenesis by regulating autocrine CCL5 and interleukin (IL)-6 and CYT387 as a potent JAK/TBK 1/IKKε inhibitor is identified.
Journal ArticleDOI
Proteomic and Genetic Approaches Identify Syk as an AML Target
Cynthia K. Hahn,Jacob E. Berchuck,Kenneth N. Ross,Rose M. Kakoza,Karl R. Clauser,Anna C. Schinzel,Anna C. Schinzel,Linda Ross,Ilene Galinsky,Tina N. Davis,Serena J. Silver,David E. Root,Richard Stone,Daniel J. DeAngelo,Martin Carroll,William C. Hahn,William C. Hahn,Steven A. Carr,Todd R. Golub,Todd R. Golub,Todd R. Golub,Andrew L. Kung,Kimberly Stegmaier,Kimberly Stegmaier +23 more
TL;DR: This report integrated proteomic and RNAi-based strategies to identify their off-target, anti-AML mechanism and genetic and pharmacological inactivation of Syk with a drug in clinical trial for other indications promoted differentiation of AML cells and attenuated leukemia growth in vivo.