PubMed · 8046926
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V A Almazov, B V Afanasév, Z I Podoltseva. 1993. [Multiple myeloma].. https://pubmed.ncbi.nlm.nih.gov/8046926/
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A very common metastatic site for breast carcinoma is bone. Metastatic breast carcinoma cells stimulate osteoclast-mediated bone resorption leading to osteolysis. Bisphosphonates are powerful inhibitors of osteoclast activity, and are therefore used in combination with standard chemotherapy or hormonal therapy for the treatment of cancer-associated osteolytic metastases. However, there may be an added beneficial effect of the bisphosphonates, that is, additive or synergistic activities with cytotoxic agents. Here, we investigated the effects of the bisphosphonate ibandronate in combination with taxoids (taxol and taxotere) on induction of apoptosis, invasion and adhesion of breast carcinoma cells to bone. Ibandronate did not induce apoptosis of human MDA-MB-231 breast carcinoma cells, nor did it enhance the effectiveness of taxoid-induced apoptosis in MDA-MB-231 cells. In contrast, ibandronate enhanced the antitumor activity of taxoids against invasion and cell adhesion to bone. Our findings raise the interesting possibility that the combination of bisphosphonates and taxoids may be useful for the treatment of patients with cancer types that are known to metastasize preferentially to bone.
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Molecular studies have revealed that microsatellite instability and loss of heterozygosity occurred in head-and-neck cancer, suggesting the involvement both of suppressor and of mutator pathways in head-and-neck carcinogenesis. There is evidence for relations between tumor phenotype and clinical parameters. Indeed, replication-error phenotype, characterized by microsatellite instability, was associated with decreased sensitivity to chemotherapeutic agents in cell lines. Loss of heterozygosity is a frequent mechanism of inactivation of tumor-suppressor genes, which might be implicated in resistance to chemotherapy. In head-and-neck cancer, chemosensitivity is inconstant, and no marker is available to predict response to treatment. In order to evaluate the role of tumor phenotype on resistance to chemotherapy, we analyzed 56 primary head-and-neck squamous-cell carcinomas collected at time of diagnosis and a sub-group of 23 resistant tumors collected after chemotherapy at 22 microsatellite loci. At time of diagnosis, only one tumor showed MSI-H phenotype. Loss of heterozygosity (LOH) was observed in 75% of tumors, indicating the dominant role of the suppressor in comparison with the mutator pathway in HNSCC carcinogenesis. No change in microsatellite patterns was observed after treatment, suggesting that chemotherapy did not select mismatch-repair-deficient clones. Univariate analyses showed that LOH at 9p or 17p was significantly associated with drug resistance. In a multivariate analysis, only LOH at 17p remains predictive of low response to chemotherapy, with a relative risk of 3.7 and 95% CI of 1.1-13, indicating that p53 alterations could play a role in chemotherapy resistance in HNSCC. Int. J. Cancer (Pred. Oncol.) 84:410-415, 1999.