. The practicability t of this approach assumes homogeneity t of gene expression in different tumor nodules in a patient. Recently, our group has tested whether the gene expression differed between the individual tumor nodules Nutlin-3 in one patient with a gene expression analysis in 55 L Sions in 29 patients. Patterns of gene expression were highly Similar in L Emissions from pre-treatment of a patient compared to the very different patterns of patients.143 seen whether gene expression profiling, the sensitivity of melphalan and temozolomide in melanoma predicted for transit continues to be an area of active investigation. Temozolomide is for O6 methylguanine DNA methyltransferase to be seen by many as the prime Re mechanism of resistance of melanoma cells.
We found a quantified and correlated expression of MGMT activity by the 26 melanoma cell lines with strong temozolomide sensitivity. 95 Still other studies that have attempted activity144 MGMT 145, correlate MK-2866 expression and promoter methylation147 146 to temozolomide resistance produced mixed results. For several cellular Re events have the potential of Chemosensitivit t of tumor cells, large scale gene expression profiling, as the only path analysis as opposed to Ver countries too, k nnten more insight into the differential Chemosensitivit offer t temozolomide. In this context, the re-examine whether the signature gene g in the analysis of one eren Ma derived bar gene serves a robust Pr predictor of resistance to temozolomide in MGMT activity t and generating expression.
With 60 cell lines NCI 60 panel of cancer cell lines, 45 genes as Pr Identified predictors for resistance or sensitivity to temozolomide and used to generate a genetic signature of temozolomide resistance. If validated in a separate set of 26 melanoma cell lines, the genetic fingerprint temozolomide resistance are significantly correlated with the measured resistance temozolomide. This correlation was lower than that of a single analysis of the expression of MGMT in the same cell lines.95 used to decide whether a genetic signature of temozolomide or the expression of MGMT single best response of the patient ahead of melanoma in transit temozolomide infusion require validation in a clinical study. Create a melphalan-based signature SG was more difficult.
The first attempts to develop a pr Diktiven gene signature of RNA from different melanoma cell lines extracted to create challenging and do not have a signature that can produce validated k. Recent experiments using RNA from samples obtained from patients were more fruitful. With tissue samples that we have 100 genes in response to ILI with melphalan and correlates are currently in the process of validating this gene signature as Pr Predictor for response to therapy regional melphalan. Implications for regional chemotherapy in melanoma transit is an effective treatment for melanoma at the end of isolation with response rates well above those observed with systemictherapy power. SG is a well tolerated Gliches regional chemotherapy, and is considered less technically demanding to perform, depending on Hilp. Complete response rates are the same for ILI and Hilp, but the trends Hilp an hour Response here and become more sustainable and