Font Size: a A A

The Mechanism Of Regulation Of Cell Cycle And Proliferation Of Transitional Cell Carcinoma Of Bladder By Protein Kinase A

Posted on:2007-05-13Degree:DoctorType:Dissertation
Country:ChinaCandidate:D H LiuFull Text:PDF
GTID:1104360185992347Subject:Surgery
Abstract/Summary:PDF Full Text Request
Introduction and ObjectiveTransitional cell carcinoma of bladder is the most common cancer in urinary surgery, usually treated with TURBt(transurethral resection of bladder tumor) or partial resection of bladder, and is characterized by its high recurrence. Regulatory bladder instillation and followed up by cytoscope is essential. Growth factors and their receptors, the most receptable tumor markers, play an important role in regulating the proliferation of bladder cancer, including EGF and EGFR, IGF and IGFR, VEGF and VEGFR, TGF and TGFR. Cells are usually in G0 phase, when induced by some stimulus, such as growth factors, they grow from G1 phase into S phase. These tumor markers expressed higher than that in normal tissues, participating in the regulation of tumor growth and cell metabolism, and have a significant association with tumor grade, stage and prognosis.But so far, there is little known downstream these growth factors and how a-bout they regulate cell growth, we know now that protein kinase lies downstream growth factors, and takes part in the signal transduction. When activated by ex-tracelluar signals, Protein kinase cause a series of biological effects by catalyzing some enzymes. By studying protein kinase, we can know further about how growth factor regulate cell growth.There are two generally accepted restriction points in cell cycle: one is G1/ S; the other is G2/M.Protein kinase A (PKA or cyclic adenosinemonophosphate [cAMP] dependent protein kinase ) plays a critical role in numerous cellular processes including the regulation of growth, gene transcription, and metabolism. PKA is a...
Keywords/Search Tags:transitional cell carcinoma, PKA RIα, grade, stage, T24 cell line, forskolin, PKA activity, cell cycle, G1 arrest, cyclin D1, H -89, apoptosis, Bcl-2
PDF Full Text Request
Related items