Gemcitabine cytotoxicity of human malignant glioma cells: modulation by antioxidants, BCL-2 and dexamethasone.

[1]  J. Dichgans,et al.  Predicting chemoresistance in human malignant glioma cells: The role of molecular genetic analyses , 1998, International journal of cancer.

[2]  M. Weller,et al.  Dexamethasone-mediated protection from drug cytotoxicity: association with p21WAF1/CIP1 protein accumulation? , 1998, Oncogene.

[3]  S. Cory,et al.  The Bcl-2 protein family: arbiters of cell survival. , 1998, Science.

[4]  Michael Weller,et al.  Predicting response to cancer chemotherapy: the role of p53 , 1998, Cell and Tissue Research.

[5]  J. Dichgans,et al.  Topoisomerase‐I inhibitors for human malignant glioma: Differential modulation of p53, p21, bax and bcl‐2 expression and of CD95‐mediated apoptosis by camptothecin and β‐lapachone , 1997, International journal of cancer.

[6]  J. Schulz,et al.  Cooperative Interception of Neuronal Apoptosis by BCL‐2 and BAG‐1 Expression: Prevention of Caspase Activation and Reduced Production of Reactive Oxygen Species , 1997, Journal of neurochemistry.

[7]  K. Kinzler,et al.  A model for p53-induced apoptosis , 1997, Nature.

[8]  K. Goa,et al.  Gemcitabine. A review of its pharmacology and clinical potential in non-small cell lung cancer and pancreatic cancer. , 1997, Drugs.

[9]  J. Dichgans,et al.  Chemotherapy of human malignant glioma , 1997, Neurology.

[10]  F. Chen,et al.  Excision of 2',2'-difluorodeoxycytidine (gemcitabine) monophosphate residues from DNA. , 1996, Cancer research.

[11]  R. Greil,et al.  2′,2′‐Difluorodeoxycytidine (Gemcitabine) Induces Apoptosis in Myeloma Cell Lines Resistant to Steroids and 2‐Chlorodeoxyadenosine (2‐CdA) , 1996, Stem cells.

[12]  H. Klocker,et al.  Inhibitory effects of the nucleoside analogue gemcitabine on prostatic carcinoma cells , 1996, The Prostate.

[13]  R. Momparler,et al.  Comparison of the induction of apoptosis in human leukemic cell lines by 2',2'-difluorodeoxycytidine (gemcitabine) and cytosine arabinoside. , 1995, Leukemia research.

[14]  R. Larsson,et al.  Evaluation of the cytotoxic activity of gemcitabine in primary cultures of tumor cells from patients with hematologic or solid tumors. , 1995, Seminars in oncology.

[15]  V. Heinemann,et al.  Gemcitabine: metabolism, mechanisms of action, and self-potentiation. , 1995, Seminars in oncology.

[16]  T. Lawrence,et al.  Radiosensitization of human tumor cells by gemcitabine in vitro. , 1995, Seminars in oncology.

[17]  M. Weller,et al.  Protooncogene bcl-2 gene transfer abrogates Fas/APO-1 antibody-mediated apoptosis of human malignant glioma cells and confers resistance to chemotherapeutic drugs and therapeutic irradiation. , 1995, The Journal of clinical investigation.

[18]  Benjamin Rs.  Gemcitabine: a modulator of intracellular nucleotide and deoxynucleotide metabolism. , 1995 .

[19]  G. Peters,et al.  Development and molecular characterization of a 2',2'-difluorodeoxycytidine-resistant variant of the human ovarian carcinoma cell line A2780. , 1994, Cancer research.

[20]  T. Lawrence,et al.  Metabolism of 2',2'-difluoro-2'-deoxycytidine and radiation sensitization of human colon carcinoma cells. , 1994, Cancer research.

[21]  Erwin G. Van Meir,et al.  Analysis of the p53 gene and its expression in human glioblastoma cells. , 1994, Cancer research.

[22]  R. Momparler,et al.  Comparison of antineoplastic activity of 2',2'-difluorodeoxycytidine and cytosine arabinoside against human myeloid and lymphoid leukemic cells , 1991, Anti-cancer drugs.

[23]  Y Z Xu,et al.  Inhibition of ribonucleotide reduction in CCRF-CEM cells by 2',2'-difluorodeoxycytidine. , 1990, Molecular pharmacology.

[24]  M. Arning,et al.  Gemcitabine in Solid Tumors – Present Status and Further Development , 1997 .

[25]  D. Richel,et al.  Clinical, toxicological and pharmacological aspects of gemcitabine. , 1996, Cancer treatment reviews.

[26]  Y. Esumi,et al.  Disposition of gemcitabine in rat and dog after single and multiple dosings. , 1994, Xenobiotica; the fate of foreign compounds in biological systems.