Bisphosphonate risedronate reduces metastatic human breast cancer burden in bone in nude mice.

Human breast cancer frequently metastasizes to the skeleton to cause osteolysis and subsequent pain, pathological fracture, and hypercalcemia. Because bone continuously releases growth factors stored in bone matrix by bone resorption during physiological remodeling and, thus, possibly provides a favorable microenvironment for metastatic breast cancer cells to proliferate, inhibitors of bone resorption used either prophylactically or in patients with established disease, therefore, would seem likely to be useful adjuvant therapy in patients with breast cancer. However, the parameters for monitoring progressive osteolytic bone disease in humans are imprecise. We examined the effects of the third generation bisphosphonate, risedronate, which is a specific inhibitor of osteoclastic bone resorption, in a bone metastasis model in nude mice in which intracardiac injection of the human breast cancer cell line MDA-231 leads to osteolytic bone metastases. Risedronate (4 micrograms/animal/day) was given s.c. to animals (a) after radiologically small but defined osteolytic metastases were observed; (b) simultaneously with MDA-231 cell inoculation through the entire experimental period; or (c) by short-term prophylactic administration before inoculation of MDA-231 cells. In all experiments, risedronate either slowed progression or inhibited the development of bone metastases assessed radiographically. Furthermore, mice treated continuously with risedronate showed significantly longer survival than did control mice. Histomorphometrical analysis revealed that osteoclast numbers were diminished at metastatic tumor sites. Unexpectedly, there was also a marked decrease in tumor burden in bone in risedronate-treated animals. In contrast, the growth of metastatic breast cancer in soft tissues surrounding bones was not affected by risedronate. Moreover, risedronate had no effects on the local growth of s.c. implanted MDA-231 breast cancers in nude mice or on MDA-231 cell proliferation in culture. These data demonstrate that risedronate decreases metastatic MDA-231 breast cancer burden selectively in bone, as well as suppresses progression of established osteolytic lesions and prevents the development of new osteolytic lesions; thus, the data suggest that inhibition of osteoclastic bone resorption may be a useful adjunctive therapy for the treatment of cancers that have colonized in bone.

[1]  P. Kostenuik,et al.  Increased growth rate and tumor burden of spontaneously metastatic Walker 256 cancer cells in the skeleton of bisphosphonate-treated rats. , 1993, Cancer research.

[2]  H. Fleisch Bisphosphonates , 2012, Drugs.

[3]  M. Olivé,et al.  Breast tumor cell lines from pleural effusions. , 1974, Journal of the National Cancer Institute.

[4]  J. Hermans,et al.  REDUCED MORBIDITY FROM SKELETAL METASTASES IN BREAST CANCER PATIENTS DURING LONG-TERM BISPHOSPHONATE (APD) TREATMENT , 1987, The Lancet.

[5]  C. Manegold,et al.  Prophylactic treatment of skeletal metastases, tumor‐induced osteolysis, and hypercalcemia in rats with the bisphosphonate Cl2MBP , 1993, Cancer.

[6]  T. Powles,et al.  Treatment of skeletal disease in breast cancer with clodronate. , 1991, Bone.

[7]  R. Baggs,et al.  Pathogenesis of vertebral metastasis and epidural spinal cord compression , 1990, Cancer.

[8]  H J Gundersen,et al.  Direct stereological estimation of three-dimensional connectivity in rat vertebrae: effect of estrogen, etidronate and risedronate following ovariectomy. , 1995, Bone.

[9]  T. Yoneda,et al.  Facilitation and suppression of bone metastasis. , 1995, Clinical orthopaedics and related research.

[10]  T. Yoneda,et al.  Occurrence of hypercalcemia and leukocytosis with cachexia in a human squamous cell carcinoma of the maxilla in athymic nude mice: a novel experimental model of three concomitant paraneoplastic syndromes. , 1991, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[11]  M. Klagsbrun,et al.  Growth factors in bone matrix. Isolation of multiple types by affinity chromatography on heparin-Sepharose. , 1986, The Journal of biological chemistry.

[12]  S Paget,et al.  THE DISTRIBUTION OF SECONDARY GROWTHS IN CANCER OF THE BREAST. , 1889 .

[13]  A. V. van Oosterom,et al.  Osteolytic bone metastases in breast carcinoma pathogenesis, morbidity and bisphosphonate treatment. , 1986, European journal of cancer & clinical oncology.

[14]  M. Tattersall,et al.  Improving the quality of life during chemotherapy for advanced breast cancer. A comparison of intermittent and continuous treatment strategies. , 1987, The New England journal of medicine.

[15]  G. Stoica,et al.  Effect of the bisphosphonate risedronate on bone metastases in a rat mammary adenocarcinoma model system , 1994, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[16]  T. Yoneda,et al.  A synthetic antagonist to laminin inhibits the formation of osteolytic metastases by human melanoma cells in nude mice. , 1992, Cancer research.

[17]  G. Rodan,et al.  Bisphosphonate action. Alendronate localization in rat bone and effects on osteoclast ultrastructure. , 1991, The Journal of clinical investigation.

[18]  R. Baggs,et al.  A murine model of experimental metastasis to bone and bone marrow. , 1988, Cancer research.