Richard M Neve
Affiliation: Lawrence Berkeley National Laboratory
- Identification of an epithelial-specific enhancer regulating ESX expressionRichard M Neve
Cancer Research Institute, University of California San Francisco, Box 0808, San Francisco, CA 94143 0808, USA
Gene 367:118-25. 2006..Understanding the regulation of this element will lend insight into mechanisms of epithelial differentiation and the etiology of breast cancer and may provide novel targets for cancer therapeutic intervention...
- A collection of breast cancer cell lines for the study of functionally distinct cancer subtypesRichard M Neve
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94270, USA
Cancer Cell 10:515-27. 2006..We show, 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...
- Restriction of receptor movement alters cellular response: physical force sensing by EphA2Khalid Salaita
Howard Hughes Medical Institute, Department of Chemistry, University of California, Berkeley, CA 94720, USA
Science 327:1380-5. 2010..These observations reveal a mechanism for spatio-mechanical regulation of EphA2 signaling pathways...
- Subtype and pathway specific responses to anticancer compounds in breast cancerLaura M Heiser
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
Proc Natl Acad Sci U S A 109:2724-9. 2012..These observations suggest mechanisms of response and resistance and may inform efforts to develop molecular assays that predict clinical response...
- A systems analysis of the chemosensitivity of breast cancer cells to the polyamine analogue PG-11047Wen Lin Kuo
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
BMC Med 7:77. 2009....
- Genomic and transcriptional aberrations linked to breast cancer pathophysiologiesKoei Chin
Comprehensive Cancer Center, 2340 Sutter Street, University of California, San Francisco, San Francisco, California 94143
Cancer Cell 10:529-41. 2006..Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable. Low-level CNAs appear to contribute to cancer progression by altering RNA and cellular metabolism...
- The morphologies of breast cancer cell lines in three-dimensional assays correlate with their profiles of gene expressionParaic A Kenny
Life Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720, USA
Mol Oncol 1:84-96. 2007..We further demonstrate that consistent differences in genes encoding signal transduction proteins emerge when even tumor cells are cultured in 3D microenvironments...
- Crosstalk between Aurora-A and p53: frequent deletion or downregulation of Aurora-A in tumors from p53 null miceJian Hua Mao
Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA
Cancer Cell 11:161-73. 2007..These data have implications for the design of approaches to targeted cancer therapy involving the crosstalk between Aurora-A kinase and p53 pathways...
- Basal subtype and MAPK/ERK kinase (MEK)-phosphoinositide 3-kinase feedback signaling determine susceptibility of breast cancer cells to MEK inhibitionOlga K Mirzoeva
Department of Medicine, Division of Gastroenterology, University of California, San Francisco, California 94115, USA
Cancer Res 69:565-72. 2009....
- Systems biology in cancer research: genomics to cellomicsJackie L Stilwell
Lawrence Berkeley National Laboratory, Berkeley, CA, USA
Methods Mol Biol 356:353-65. 2007....
- A conditional feedback loop regulates Ras activity through EphA2Madhu Macrae
Cancer Research Institute and Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California 94143, USA
Cancer Cell 8:111-8. 2005..Our results suggest that an escape from the negative effects of this interaction may be important in the development of cancer...
- Unraveling the biologic and clinical complexities of HER2John W Park
Comprehensive Cancer Center, University of California, San Francisco, CA 94115 1710, USA
Clin Breast Cancer 8:392-401. 2008..Other HER2-targeting strategies are also under active investigation...
- A fluid membrane-based soluble ligand-display system for live-cell assaysJwa Min Nam
Department of Chemistry, University of California and Physical Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
Chembiochem 7:436-40. 2006
- Transcriptional regulation of the murine Elf3 gene in embryonal carcinoma cells and their differentiated counterparts: requirement for a novel upstream regulatory regionJingwen Hou
Eppley Institute for Research in Cancer and Allied Diseases at the University of Nebraska Medical Center, USA
Gene 340:123-31. 2004..This region appears to be largely responsible for the increase in Elf3 promoter activity that accompanies the differentiation of embryonal carcinoma cells...
- ErbB2 activation of ESX gene expressionRichard M Neve
Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
Oncogene 21:3934-8. 2002..These results indicate that the ESX promoter represents a transcriptional target of ErbB2, and ESX expression may represent a downstream mediator of ErbB2 signaling and ErbB2-induced gene expression...
- Distinct roles for phosphoinositide 3-kinase, mitogen-activated protein kinase and p38 MAPK in mediating cell cycle progression of breast cancer cellsRichard M Neve
Department of Hematology Oncology, UCSF San Francisco and Buck Institute, Novato, California 94945, USA
Oncogene 21:4567-76. 2002..This suggests that downstream effectors of ErbB receptors represent good therapeutic targets for breast cancer...
- An integrative genomic and proteomic analysis of PIK3CA, PTEN, and AKT mutations in breast cancerKatherine Stemke-Hale
Department of Systems Biology, The University of Texas MD Anderson Cancer, Houston, Texas 77030, USA
Cancer Res 68:6084-91. 2008..The specific aberration present may have implications for the selection of PI3K-targeted therapies in hormone receptor-positive breast cancer...