To directly Zuchtwertsch Estimates relation between cells with H69 was H69/41d DNA isolated from both cell lines and analyzed using Affymetrix Human Genome Wide SNP Array 6.0 chips containing probes for 900 000, and a single nucleotide polymorphism Similar number of probes, in order to assess the variation in the number of copies. Figure S2 karyotypes of both cell lines from these data reconstructed. H69 cells show chromosomal aberrations than expected for cancer cells. These losses, TG100-115 gains and amplification regions GAIN / copy number variation are very Similar and H69 cells H69/41d shows clearly that they are bound by cloning. Are some obvious differences between the two cell lines. To go Removing a 4.8 Mbps rt on a copy of chromosome 2 to nineteen genes and one 9.6 Mbp deletion on one copy of chromosome 11, which contains about 83 genes Lt It is also an amplifier Gain of the long arm of chromosome 3 and a partial loss of the long arm of chromosome 15 However analysis of the mean number of SNP / copy not defined on a single genetic locus, the REN explained Why the cells can refer escape able H69/41d Hsp90 inhibitor-induced senescence.
As a second approach to the mechanism by which these cells escape senescence induced Hsp90 inhibitor to determine the cells for a number of proteins that have been shown, r have screened Important in senescence. p21 is a protein, so there of particular interest because it has Brivanib been shown to senescence in cancer cells, which do not induce p53. p21 is expressed in H69 cells, but is not detectable in cells H69/41d. Given the r In the induction and maintenance of senescence acquaintances, loss of p21 expression provides a plausible explanation: tion for the failure of cells to undergo senescence H69/41d response to Hsp90 inhibitors.
Discussion In previous studies, the most h Most common reaction described Hsp90 inhibition of cancer cells in the cell cycle. This cell cycle arrest was widely believed to be reversible in nature, although most studies have not directly addressed this variable. Growth arrest can w During the transition be made G1 / S or G2 / M, and is probably a result of dependence Dependence of the protein Hsp90 Sun CDK4, cdc2 kinase and polo-type. In a subset of types of cancer cells, Hsp90 inhibitors have been shown to induce apoptosis. That’m Ren small cell lung cancer cells and multiple myeloma cells. Of cell cycle arrest and cell death transitional cell carcinoma destiny apart a third to cancer cells senescence. In cancer cells, sometimes called premature or accelerated senescence in order to undergo differ from the replicative senescence of normal cells when they reach their Hayflick limit.
Senescence in cancer has been studied in two contexts: the first of them is senescence response observed in oncogene activation, where it plays a r security in the bodies of developing cancer can k, the second of them is as a response to the treatment of cancer. Chemotherapy, which ended DNA sch To senescence in a much gr Eren extent induce as agents that appear to microtubules. This is more likely to occur under the influence of low doses of medication, with h Heren doses to the apoptosis. Chemotherapy-induced senescence was observed both in cell culture and in animal models.