Anticancer research
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Anticancer research · Mar 1995
Mutant p53 expression and DNA analysis in human breast cancer comparison with conventional clinicopathological parameters.
Scientific research evaluates the prognostic importance of 53 expression and DNA flow cytometry controversially. To evaluate the prognostic relevance of mutant p53 protein overexpression and DNA flow cytometry in primary breast cancer we correlated these factors with the common prognostic parameters such as tumor size, lymph node status, grading, menopausal status and receptor status. Human breast cancer specimens from 180 previously untreated patients were collected and deep frozen. ⋯ There was a significant correlation between ploidy and the tumor grade (p = 0.003) and SPF (p 0.0001), but not correlation between ploidy and tumor size (p = 0.21), node status (p = 0.33) or receptor status (p = 0.18). A low SPF was predominantly found in tumors less than 2 cm in diameter (p 0.0001); no significant correlation was found between SPF, receptor status, tumor grade, node and menopausal status. Mutant p53 protein expression and DNA analysis in combination with common prognostic parameters might help to detect prognostically unfavourable subgroups of breast cancer patients.
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Anticancer research · Jan 1995
Comparative StudyEnhancement of radiation response of prostatic carcinoma by taxol: therapeutic potential for late-stage malignancy.
Radiation therapy for advanced prostate cancer has dose-limiting complications and often results in limited tumor control. A combination of radiation and taxol, a potential radiation sensitizer, may enhance therapeutic efficacy at currently used individual doses. Human prostatic carcinoma lines in vitro, and Dunning rat prostatic adenocarcinoma in vivo, were treated with taxol and radiation individually, and in combination. ⋯ Injection of taxol (4 mg/kg/day x 5), radiation dose fractionation (1.5 Gy/day x 5) and their combination significantly delayed Dunning tumor growth. Adverse side effects were minimal. The results imply that combination of these agents may have clinical potential in prostate cancer treatment.
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Anticancer research · May 1994
Substituted 2-acylpyridine-alpha-(N)-hetarylhydrazones as inhibitors of ribonucleotide reductase activity and L1210 cell growth.
A series of substituted 2-acylpyridine-alpha-(N)-hetarylhydrazones was prepared and studied for their effects on mammalian ribonucleotide reductase activity using a highly purified enzyme preparation from Ehrlich tumor cells and on mouse leukemia L1210 cell growth in culture. Pyridine-2-aldehyde-2-pyridylhydrazone (PH 22), ethyl-2-pyridylketone-I-phthalazinylhydrazone (PH 22-25) and pyridine-2-aldehyde-2'-quinolylhydrazone (PQ 22) inhibited purified ribonucleotide reductase activity and inhibited L1210 cell growth in culture. ⋯ There was no effect on RNA synthesis. These data indicate that these substituted hydrazones are potent inhibitors of tumor cell growth through the inhibition of ribonucleotide reductase.
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Anticancer research · May 1994
The role of glutathione (GSH) in determining sensitivity to platinum drugs in vivo in platinum-sensitive and -resistant murine leukaemia and plasmacytoma and human ovarian carcinoma xenografts.
Numerous studies performed in vitro have suggested a role for glutathione (GSH) in determining the sensitivity/resistance of tumour cells to various platinum-based drugs. Few studies have extended these findings into the in vivo setting. We have measured GSH levels in two murine (ADJ/PC6 plasmacytoma and L1210 leukaemia and their acquired platinum-drug-resistant sublines) and five human ovarian carcinoma (PXN/100, PXN/109T/C, SKOV3, HX/62 and OVCAR-3) tumour models of varying sensitivity to cisplatin. ⋯ However, in other tumours (e.g., the acquired cisplatin resistant ADJ/PC6 plasmacytoma) non-GSH mediated mechanisms of resistance (such as enhanced DNA repair) probably account for the resistance. Pretreatment of animals with oral buthionine sulfoximine (BSO), which resulted in approximately 70% depletion in tumour GSH levels, failed to potentiate the antitumour efficacy of either cisplatin (using the ADJ/PC6 and L1210 models) or the 1,2-diaminocyclohexane (DACH) platinum-drug, tetraplatin (using the ADJ/PC6 model). These BSO plus or minus cisplatin data suggest a limited role for such combinations in the clinic.
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In spite of the possibility to obtain a high percentage of objective response, the overall median survival for small cell lung cancer patients did not improve substantially in the last 10 years. Second line treatment fails to provide definitive care, however, some practical guide lines can be planned to face the problem of how and when to treat relapsed small cell lung cancer patients.