J
Jane Fridlyand
Researcher at Genentech
Publications - 74
Citations - 19991
Jane Fridlyand is an academic researcher from Genentech. The author has contributed to research in topics: Comparative genomic hybridization & Gene. The author has an hindex of 47, co-authored 73 publications receiving 19127 citations. Previous affiliations of Jane Fridlyand include Royal Melbourne Hospital & University of California, San Francisco.
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A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes
Richard M. Neve,Richard M. Neve,Koei Chin,Jane Fridlyand,Jennifer Yeh,Frederick L. Baehner,Tea Fevr,Laura Clark,Nora Bayani,Jean-Philippe Coppe,Frances Tong,Terence P. Speed,Paul T. Spellman,Sandy DeVries,Anna Lapuk,Nicholas J. Wang,Wen-Lin Kuo,Jackie L. Stilwell,Daniel Pinkel,Donna G. Albertson,F. M. Waldman,Frank McCormick,Robert B. Dickson,Michael D. Johnson,Marc E. Lippman,Stephen P. Ethier,Adi F. Gazdar,Joe W. Gray,Joe W. Gray +28 more
TL;DR: It is shown, using Trastuzumab (Herceptin) monotherapy as an example, that the system can be used to identify molecular features that predict or indicate response to targeted therapies or other physiological perturbations.
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Comparison of discrimination methods for the classification of tumors using gene expression data
TL;DR: Different discrimination methods for the classification of tumors based on gene expression data include nearest-neighbor classifiers, linear discriminant analysis, and classification trees, which are applied to datasets from three recently published cancer gene expression studies.
Journal ArticleDOI
Distinct Sets of Genetic Alterations in Melanoma
John A. Curtin,Jane Fridlyand,Toshiro Kageshita,Hetal N. Patel,Klaus J. Busam,Heinz Kutzner,Kwang Hyun Cho,Setsuya Aiba,Eva B. Bröcker,Philip E. LeBoit,Daniel Pinkel,Boris C. Bastian +11 more
TL;DR: The genetic alterations identified in melanoma at different sites and with different levels of sun exposure indicate that there are distinct genetic pathways in the development of melanoma and implicate CDK4 and CCND1 as independent oncogenes in melanomas without mutations in BRAF or N-RAS.
Journal ArticleDOI
Genomic and transcriptional aberrations linked to breast cancer pathophysiologies.
Koei Chin,Sandy DeVries,Jane Fridlyand,Paul T. Spellman,Ritu Roydasgupta,Wen Lin Kuo,Wen Lin Kuo,Anna Lapuk,Anna Lapuk,Richard M. Neve,Richard M. Neve,Zuwei Qian,Thomas B. Ryder,Fanqing Chen,Heidi S. Feiler,Heidi S. Feiler,Taku Tokuyasu,Chris Kingsley,Shanaz H. Dairkee,Zhenhang Meng,Karen Chew,Daniel Pinkel,Ajay N. Jain,Britt-Marie Ljung,Laura J. Esserman,Donna G. Albertson,Frederic M. Waldman,Joe W. Gray,Joe W. Gray +28 more
TL;DR: It is shown that the recurrent CNAs differ between tumor subtypes defined by expression pattern and that stratification of patients according to outcome can be improved by measuring both expression and copy number, especially high-level amplification.
Journal ArticleDOI
Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors
Timothy R. Wilson,Jane Fridlyand,Yibing Yan,Elicia Penuel,Luciana Burton,Emily Chan,Jing Peng,Eva Lin,Yulei Wang,Jeffrey A. Sosman,Antoni Ribas,Jiang Li,John Moffat,Daniel P. Sutherlin,Hartmut Koeppen,Mark Merchant,Richard M. Neve,Jeff Settleman +17 more
TL;DR: It is found that most cells can be rescued from drug sensitivity by simply exposing them to one or more RTK ligands, and the observation that hepatocyte growth factor confers resistance to the BRAF inhibitor PLX4032 in BRAF-mutant melanoma cells is among the findings with clinical implications.