Suite 309
Philadelphia, PA 19107
(215) 503-9251
Most Recent Peer-reviewed Publications
- Genomewide scans in North American families reveal genetic linkage of essential tremor to a region on chromosome 6p23
- Desmin-related myopathy: Clinical, electrophysiological, radiological, neuropathological and genetic studies
- Small deletions disturb desmin architecture leading to breakdown of muscle cells and development of skeletal or cardioskeletal myopathy
- A series of West European patients with severe cardiac and skeletal myopathy associated with a de novo R406W mutation in desmin
- Expression of the intermediate filament protein synemin in myofibrillar myopathies and other muscle diseases
Medical School
MD, Mongolian National Medical University - 1991
PhD, Mongolian National Medical University, Biomedical Science
- 1999
Expertise and Research Interests
The main focus of my research is identifying the role of Prolactin (Prl)-Janus kinase 2 (Jak2)-Signal Transducer and Activator of Transcription 5 (Stat5) pathway in castration-resistant and metastatic prostate cancer cells.
I have first-authored/co-authored papers showing that 1) Autocrine prolactin promotes prostate cancer cell growth via Jak-2-Stat5a/b signaling pathway, 2) Transcription factor Stat5a/b synergizes with androgen receptor in prostate cancer cells, 3) Stat5a/b promotes growth of human prostate cancer cells in vitro and in vivo, 4) Transcription factor Stat3 stimulates metastatic behavior of human prostate cancer cells in vivo, whereas Stat5b has a preferential role in the promotion of prostate cancer cell viability and tumor growth, 5) developed a new human prostate cancer cell line, CWR22Pc, which is regulated by androgens and expresses high levels of androgen receptor and prostate specific antigen (PSA). These cells are able to form tumors in nude mice, and when androgens are withdrawn, the tumors initially shrink and then recur as castration-resistant tumors, mimicking human prostate cancer, 6) Truncation of Stat5a/b circumvents PIAS3-mediated transcriptional inhibition of Stat5 in prostate cancer cells.
Currently, I am working on a project identifying the molecular mechanism of androgen receptor dependent Stat5a/b activation in prostate cancer cells, sensitization of prostate cancer cells to radiation through Stat5a/b inhibition and genetic changes of Stat5 in prostate cancer.
Grant Support:
Principal Investigator: American Cancer Society Institutional Research Grant (IRG-08-060-04), Thomas Jefferson University; Kimmel Cancer Center.
05/01/11-04/30/12
Activation of transcription factor Stat5a/b determines the response of prostate cancer to radiation therapy via regulation of DNA damage response.
Industrial Relevance
We have established transcription factor Stat5 as a molecular target for therapy development in prostate cancer. Inhibition of Stat5a/b can be achieved by antisense oligonucleotides, RNA interference, or by development of small-molecule Stat5 inhibitors. A new androgen-regulated and tumorigenic human prostate cancer cell line, CWR22Pc, has been established.
Languages
Mongolian
English
Russian