Research / Clinical
Summary
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Diseases/Research Topics
Cell Cycle Regulation, FGFRs in cancer, Growth Control, RTKs
Other Key Academic Roles:
Program Director
NIH Training Grant in Growth Regulation and Oncogenesis
Keywords: FGFR3 Signaling in Human Cancer, Cell Cycle Regulation,
PTC1 signaling, DNA Damage, Cyclin B1, RTKs
1. CELL CYCLE REGULATION - Speedy, or Spy1, is the prototpic member of a small family of proteins designated the Speedy/RINGO family. These cyclin-like proteins activate CDKs, with Spy1 particularly activating CDK2. Spy1 also stimulates the CDK2-mediated phosphorylation of the CKI, P27kip1, on T187 to stimulate its degradation, thereby regulating some aspects of cell cycle progression and DNA repair. We are continuing to investigate the importance of Spy1 in normal cell cycle regulation and in cellular responses to DNA damage.
2. SIGNALING BY PTC1 and SHH - We are continuing our studies of basic mechanisms of cell cycle regulation and control by patched1 (ptc1), a tumor suppressor frequently disrupted in both Basal Cell Carcinoma (BCC) and Nevoid Basal Cell Carcinoma Syndrome (NBCCS). These studies include an examination of the interactions between cyclin proteins and ptc1 in reglating cell cycle progression.
3. REGULATION OF RECEPTOR TYROSINE KINASES - Mutations in RTKs (receptor tyrosine kinases) contribute to significant human cancers such as multiple myeloma (FGFR3), bladder cancer (FGFR3), breast cancer (HER2), gastrointestinal stromal tumor syndrome (RET), and multiple endocrine neoplasia type 2A (RET). We are especially interested in the role of activating mutations in FGFR3 and the resulting activation of downstream sigmaling pathways that stimulate proliferation or attenuate apoptosis.
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