CIRCUMVENTION OF CISPLATIN RESISTANCE IN H-RAS TRANSFORMED-NIH/3T3 CELLS BY SUPPRESSOR MUTANT OF H-RAS
The expression of H-ras oncogene, it has been shown, induces cisplatin resistance in vitro. Using two types of flat revertants (R1, F32/F33) which lost the transformed phenotypes, we studied the mechanism of the cisplatin resistance. R1 cells, which expressed an activated c-H-ras oncogene,
exhibited increased cisplatin resistance. Further, F32/F33 cell lines, which were suppressed the H-ras function by a suppressor mutant of H-ras, restored the cisplatin sensitivity. These results implicate that the cisplatin resistance was directly related to the expression of H-ras and can
be circumvented by suppression of the H-ras functions.
Document Type: Research Article
Affiliations: HOKKAIDO UNIV,SCH MED,INST CANC,MOLEC GENET LAB,SAPPORO,HOKKAIDO 060,JAPAN.
Publication date: 01 June 1992
- The International Journal of Oncology provides an international forum for the publication of the latest, cutting-edge research in the broad area of oncology and cancer treatment. The journal accepts original high quality works and reviews on all aspects of oncology research including carcinogenesis, metastasis, epidemiology, chemotherapy and viral oncology. Through fair and efficient peer review, the journal is dedicated to publishing top tier research in the field, offering authors rapid publication as well as high standards of copy-editing and production. The International Journal of Oncology is published on a monthly basis in both print and early online.
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