Cancer cell cycle

Keywords Flow cytometry, BrdU, edotecarin, topoisomerase I inhibitor, irinotecan, colon cancer, cell cycle... 

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Blagosklonny, M. V., Pardee, A.B. Exploiting cancer cell cycling for selective protection of normal cells (Review). Cancer Res. 2001, 61 4301-4305. 

Sherr CJ. The Pezcoller lecture cancer cell cycles revisited. Cancer Res. 2000 60 3689-3695. 

Adler, A. S., and Chang, H. Y. (2006). From description to causality mechanisms of gene expression signatures in cancer. Cell Cycle 5(11), 1148—1151. 

Zhang, Y. W, and Vande Woude, G. F. (2007). Mig-6, signal transduction, stress response and cancer. Cell Cycle 6(5), 507-513. 

V.M., Rostad, S.W., Emerman, J.T., and Dizdaroglu, M. (2006) Oxidative changes in the DNA of stroma and epithelium from the female breast potential implications for breast cancer. Cell Cycle, 5,1629-1632. 

Mechanisms Vinblastine and vincristine are spindle poisons which, by preventing the assembly of tubulin dimers into microtubules, block the formation of the mitotic spindle. They act primarily in the M phase of the cancer cell cycle. Resistance may occur from increased efflux of the drugs from tumor cells via the membrane drug transporter. 

Lycopene-induced inhibition of cancer cell cycle was elegantly investigated and recently reported in breast and endometrial cells." The main finding was that reduction of cyclin D levels and retention of p27 " in the cycUn E-cdk2 complexes was responsible for the inhibitory effect of lycopene on cell-cycle progression. Specifically, a reduced cdk2 activity led to a reduced phosphorylation of the retinoblastoma protein, a main control protein of the G1 restriction point, leading to a delay in G1/S transition. 

Lujambio A, Esteller M 2007. CpG island hypermethylation of tumor suppressor micro-RNAs in human cancer. Cell Cycle 6(12) 1455-1459. 

Volotskova, O., et al. Targeting the cancer cell cycle by cold atmospheric plasma. Scientific Reports 2, 636 (2012)... 

Tumor suppressor genes like p53, Rb, and E2P appeared during evolution, probably to protect the integrity of the organism from uncontrolled cell proliferation within multicellular specialized tissues. This concept is supported by the observation that the respective proteins or pathways are mutated or inactivated in most human cancers. Cell cycle entry (GO-Gl- to S-phase transition) is controlled by two major pathways (1) the Rb (Rb, cy-clin Dl, and pl6 ° ) cell cycle pathway and (2) the p53/ p2iwafi Q2-S checkpoint arrest pathway. Although both pathways act largely independently, they are interconnected (Burke et al. 2005 Hsieh et al. 2002). 

Zhang, Y., J. Xuan, et al. (2010). "Reconstruction of gene regulatory modules in cancer cell cycle by multi-source data integration" PLoS One 5(4) el0268. 

Choi, Y. and Baker, J.R., Jr (2005) Targeting cancer cells with DNA-assembled dendrimers a mix and match strategy for cancer. Cell Cycle, 4, 669-71. 

Samuels, Y. and Velculescu, V.E. (2004). Oncogenic Mutations of PIK3CA in Human Cancers. Cell Cycle 3(10), 1221-1224. 

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