The recurrence, that could be observed after publicity or gene transfer alone was slowed down if they were connected. More over, these results weren’t seen when Hedgehog agonist reporter gene transfer was used in the place of bcl xs gene in combination with cisplatin, this control combination outstanding only cytostatic. Recurrence and purchase of chemoresistance are responsible for the failure occurring in about 70% of ovarian carcinoma cases. Although in about 25% of the patients, disease early grows under chemotherapy, showing intrinsic chemoresistance, clinical response to platinum/taxanes based program is observed in most of cases. But, recurrence and associated acquisition of chemoresistance usually happen then among these performing people, nearly all of which eventually die from disease, ultimately causing a 5-year survival rate of about thirty days. Planning to study the mechanisms involved with resistance to cisplatin in-vitro, we labored on four ovarian carcinoma cell lines and first recognized their short and long term response to the drug. OAW42 and igrov1 cell lines seemed to be sensitive and painful, as cells died without repeating after treatment to C20. On the other hand, cisplatin failed to induce apoptosis in SKOV3 cell line. In IGROV1 R10 cells, while cell death was seen in response to treatment, it was accompanied with a recurrence. Ergo, SKOV3 cell line appeared as Infectious causes of cancer a model of intrinsic resistance, as a of acquired resistance, which represents probably the most frequent clinical condition although IGROV1 R10 cell line, which was obtained after successive exposures of IGROV1 cell line to cisplatin, appeared. In lots of treatment conditions of our research, it could be pointed out that although apoptosis occurred, a little proportion of cells was preserved in a state, before recovering a normal growth within a variable delay. This presupposes these surviving cells are transiently protected in the drug induced apoptosis. Mechanisms that interrupt AP26113 apoptosis might ergo contribute to cisplatin resistance as well as to repeat. Anti apoptotic members of Bcl 2 family, the expression that is frequently changed during carcinogenesis in various cancers including ovarian carcinoma, have already been shown to be involved with cisplatin resistance. We progressively focused our study on Bcl xL anti apoptotic protein. Indeed, ribonuclease protection assay unmasked that bcl xL displayed different degrees of mRNA expression in response to cisplatin among cell lines, whereas, for example, no relationship might be established between bcl 2 expression and cellular response to cisplatin. A few information have suggested that Bcl 2 family members could be differentially regulated according to the tissue, and that some members could overcome the part of the others in a tissue specific manner.