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Jonathan PollackAcademic Appointments
Appointment
Organization
Associate Professor
Member
Member
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Postdoctoral Advisees
Stephanie Huang,
Kevin Kwei
Web Site Links
Research/Lab website:
http://pollacklab.stanford.edu
Research Interests
Our laboratory is using DNA microarrays to systematically characterize the molecular phenotypes of tumor cells, with current efforts in leukemia, breast, prostate, lung, colon and pancreatic cancers. We have found that patterns of gene expression describe the physiologic state of tumor cells, reveal activated signal transduction pathways, and define the likely normal cell types from which tumors have arisen. Patterns of gene expression also suggest improved markers for clinical diagnosis and prognostication, which we are validating by immunohistochemistry on tissue microarrays. In concert, we are profiling gene expression in human cancer cell line model systems in which specific genes or pathways have been altered genetically or pharmacologically, in order to better understand the role of these pathways in oncogenesis.
We have also developed a novel use for cDNA microarrays in measuring gene copy number alteration. The amplification of oncogenes and deletion of tumor suppressor genes, the result of genetic instability, play a critical role in the development of cancer. Co-hybridizing differentially labeled tumor and normal genomic DNA (the principle of comparative genomic hybridization, or CGH) to DNA microarrays permits the high-resolution, genome-wide mapping of gene copy number changes in cancer. These array CGH analyses have led to the identification of numerous regions of recurrent gene amplification and deletion, harboring candidate oncogenes and tumor suppressor genes. Current efforts aim to explore the functional role and clinical significance of these gene copy number alterations in cancer.
We have also developed a novel use for cDNA microarrays in measuring gene copy number alteration. The amplification of oncogenes and deletion of tumor suppressor genes, the result of genetic instability, play a critical role in the development of cancer. Co-hybridizing differentially labeled tumor and normal genomic DNA (the principle of comparative genomic hybridization, or CGH) to DNA microarrays permits the high-resolution, genome-wide mapping of gene copy number changes in cancer. These array CGH analyses have led to the identification of numerous regions of recurrent gene amplification and deletion, harboring candidate oncogenes and tumor suppressor genes. Current efforts aim to explore the functional role and clinical significance of these gene copy number alterations in cancer.
Publications
- Lapointe J, Malhotra S, Higgins JP, Bair E, Thompson M, Salari K, Giacomini CP, Ferrari M, Montgomery K, Tibshirani R, van de Rijn M, Brooks JD, Pollack JR "hCAP-D3 Expression Marks a Prostate Cancer Subtype With Favorable Clinical Behavior and Androgen Signaling Signature." Am J Surg Pathol 2008; 32: 2: 205-209 More »
- Kwei KA, Kim YH, Girard L, Kao J, Pacyna-Gengelbach M, Salari K, Lee J, Choi YL, Sato M, Wang P, Hernandez-Boussard T, Gazdar AF, Petersen I, Minna JD, Pollack JR "Genomic profiling identifies TITF1 as a lineage-specific oncogene amplified in lung cancer." Oncogene 2008; More »
- Lapointe J, Kim YH, Miller MA, Li C, Kaygusuz G, van de Rijn M, Huntsman DG, Brooks JD, Pollack JR "A variant TMPRSS2 isoform and ERG fusion product in prostate cancer with implications for molecular diagnosis." Mod Pathol 2007; More »
- Pollack JR, "A Perspective on DNA Microarrays in Pathology Research and Practice." Am J Pathol 2007; More »
- Dumur CI, Lyons-Weiler M, Sciulli C, Garrett CT, Schrijver I, Holley TK, Rodriquez-Paris J, Pollack JR, Zehnder JL, Price M, Hagenkord JM, Rigl CT, Buturovic LJ, Anderson GG, Monzon FA "Interlaboratory Performance of a Microarray-Based Gene Expression Test to Determine Tissue of Origin in Poorly Differentiated and Undifferentiated Cancers." J Mol Diagn 2007; More »
39 publications: view full list
