NCH Express Accounts Plus V4.59 ❎
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NCH Express Accounts Plus V4.59
NCH Express Accounts is a web-based service offered by National City Corporation to link the American Express and NCH Merchant Services computer networks. The following is NOT the NCH Merchant Services site. This site has changed and may no longer be available
We therefore depleted FGFR1 using shRNA. Cells with FGFR1 shRNA depletion expressed an average of FGFR1 protein ∼۱٫۵ fold of control cells. However, knock-down of FGFR1 exhibited no effect on the survival of cells harboring the amplification (as compared to controls or cells with WHSC1L1 or LETM2 shRNA depletion). Combined knock-down of FGFR1 with the knock-down of WHSC1L1 or LETM2 resulted in additive effects on the survival of cells harboring the amplification (as compared to controls or cells with WHSC1L1 or LETM2 shRNA depletion alone). These results indicate that FGFR1 knock-down does not result in the restoration of survival of cells with the amplification. Combined knock-down of FGFR1 with the knock-down of WHSC1L1 or LETM2 resulted in additive effects on the survival of cells harboring the amplification (as compared to controls or cells with WHSC1L1 or LETM2 shRNA depletion alone).
We therefore depleted WHSC1L1 using shRNA. Cells with WHSC1L1 shRNA depletion expressed an average of WHSC1L1 protein ∼۲ fold of control cells. However, knock-down of WHSC1L1 exhibited a modest effect on the survival of cells harboring the amplification (as compared to controls). Combined knock-down of WHSC1L1 with FGFR1 shRNA resulted in a significant additive survival effect on cells harboring the amplification (as compared to controls or cells with FGFR1 shRNA depletion alone).
From a mechanistic perspective, the phenotypic impact of FGFR1 activation appears to be relatively complex and not limited to cell survival. A clear example of this is the response to FGFR1 gain of function as seen in NCI-H1581 and NCI-H2170 cell lines expressing ectopic FGFR1. Both cell lines exhibit significant increases in proliferation in response to activation of FGFR1 (Figure 2B). FGFR1-induced mitogenic response is seen in NCI-H1581 cells infected with 3 independent FGFR1-expressing hairpins targeting FGFR1 mRNA (but not infected with a negative control hairpin), demonstrating that this increase in proliferation is independent of FGFR1 amplification. We also observed a significant increase in proliferation in response to ectopic FGFR1 expression in NCI-H2170 cells but, importantly, not in NCI-H2170 cells not harboring FGFR1 amplification (Figures 2C and 3b). These experiments suggest that FGFR1 signaling may contribute to proliferation of NCI-H2170 cells in a FGFR1-independent manner. It is possible that FGFR1 is actively involved in driving FGFR1-independent proliferation in NCI-H2170 cells, rather than being in a primary role in 8p11-12-dependent tumorigenesis.
Univariate Cox regression analyses were performed for overall survival in 3 cohorts of patients, each containing a different cohort of 103 patients treated with standard cisplatin/taxane-based chemotherapy, which included 70 patients who progressed after 4 cycles of first-line cisplatin/taxane-based chemotherapy. The survival curve was plotted using Kaplan-Meier estimates and compared using the log-rank test. Multivariate Cox regression analysis was performed in a second cohort of 103 patients who progressed after 4 cycles of first-line cisplatin/taxane-based chemotherapy, using clinicopathologic covariates and gene expression. A third cohort of 105 patients with stage IV disease from the UICC database was subjected to univariate and multivariate analysis for survival.