We are analyzing https://link.springer.com/article/10.1007/s10434-999-0279-x.

Title:
Gemcitabine-Induced Programmed Cell Death (Apoptosis) of Human Pancreatic Carcinoma Is Determined by Bcl-2 Content | Annals of Surgical Oncology
Description:
Background: Gemcitabine is a new nucleoside analogue that produces a clinical response in 30% of patients with unresectable pancreatic carcinoma. The cytotoxic effects of many chemotherapeutic agents occur through induction of programmed cell death (apoptosis), which is controlled by the bcl-2 gene family. We determined whether induction of apoptosis by gemcitabine in pancreatic carcinoma is associated with cellular Bcl-2 content. Methods: Four pancreatic carcinoma cell lines (MIA-PaCa-2, AsPC-1, Panc-1, and Panc-48) were screened by Western blotting for Bcl-2 protein expression. Dose-response relationships for the cytotoxic effects of gemcitabine were determined using methylthiotetrazole assays, and induction of apoptosis was confirmed by fluorescence-activated cell sorting analysis. MIA-PaCa-2 cells transfected with human bcl-2 were also analyzed for gemcitabine-induced apoptosis. Results: Pancreatic cancer cell lines expressed varying amounts of Bcl-2, and the 50% lethal dose for gemcitabine-induced apoptosis was correlated with Bcl-2 content. Furthermore, Bcl-2 overexpression was associated with a significant increase in the 50% lethal dose for gemcitabine-induced apoptosis. Conclusions: Cellular Bcl-2 content was directly correlated with the cytotoxicity of gemcitabine in pancreatic carcinoma. Therefore, routine immunohistochemical analyses may be useful in predicting gemcitabine efficacy, and patients who would likely not benefit could be spared gemcitabine administration. Furthermore, the effectiveness of gemcitabine and other chemotherapeutic agents may be increased by gene therapy-mediated alteration of bcl-2 gene family members.
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Keywords {🔍}

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Topics {✒️}

month download article/chapter apoptosis-related factors p53 programmed cell death p53-immunopositive breast cancers gene therapy-mediated alteration cell biology mia-paca-2 cells transfected chk1 inhibitor prexasertib human pancreatic carcinoma apoptosis resistance increases unresectable pancreatic carcinoma full article pdf pancreatic cancer mortality privacy choices/manage cookies dose-response relationships pancreatic cancer cells breast ductal carcinoma resectable pancreatic adenocarcinomas related subjects gemcitabine-induced apoptosis surgical oncology aims cold spring harbor bcl-2 gene family bcl-2 family proteins davis cancer center anderson cancer center predicting gemcitabine efficacy spared gemcitabine administration gemcitabine versus 5-fu bcl-xl cellular bcl-2 content european economic area routine immunohistochemical analyses greatest oncological challenge cellular pharmacology study neuroendocrine lung tumors conserved domains important propidium iodide staining measuring thymocyte apoptosis pancreatic carcinoma conditions privacy policy article annals pancreatic cancer p53 oncoprotein expression article bold accepting optional cookies chemotherapeutic agents occur reed jc rapid colorimetric assay abbruzzese jl

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      description: Background: Gemcitabine is a new nucleoside analogue that produces a clinical response in 30% of patients with unresectable pancreatic carcinoma. The cytotoxic effects of many chemotherapeutic agents occur through induction of programmed cell death (apoptosis), which is controlled by the bcl-2 gene family. We determined whether induction of apoptosis by gemcitabine in pancreatic carcinoma is associated with cellular Bcl-2 content. Methods: Four pancreatic carcinoma cell lines (MIA-PaCa-2, AsPC-1, Panc-1, and Panc-48) were screened by Western blotting for Bcl-2 protein expression. Dose-response relationships for the cytotoxic effects of gemcitabine were determined using methylthiotetrazole assays, and induction of apoptosis was confirmed by fluorescence-activated cell sorting analysis. MIA-PaCa-2 cells transfected with human bcl-2 were also analyzed for gemcitabine-induced apoptosis. Results: Pancreatic cancer cell lines expressed varying amounts of Bcl-2, and the 50% lethal dose for gemcitabine-induced apoptosis was correlated with Bcl-2 content. Furthermore, Bcl-2 overexpression was associated with a significant increase in the 50% lethal dose for gemcitabine-induced apoptosis. Conclusions: Cellular Bcl-2 content was directly correlated with the cytotoxicity of gemcitabine in pancreatic carcinoma. Therefore, routine immunohistochemical analyses may be useful in predicting gemcitabine efficacy, and patients who would likely not benefit could be spared gemcitabine administration. Furthermore, the effectiveness of gemcitabine and other chemotherapeutic agents may be increased by gene therapy-mediated alteration of bcl-2 gene family members.
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