Tumor Bone Diseases

  • Jean-Jacques Body


  • The propensity of breast cancer cells to metastasize in bone could notably be due to the rich supply of relevant growth factors present in the skeletal microenvironment, which increases breast cancer cell growth. Bone destruction is essentially mediated by osteoclast activation.

  • Bisphosphonates are potent inhibitors of osteoclast-mediated bone resorption that now constitute a standard non-cytotoxic treatment of bone metastases. They have become the optimal therapy for tumor-induced hypercalcemia, and at adequate doses (90 mg) the efficacy of pamidronate is not influenced significantly by the tumor type or the degree of metastatic bone involvement. Regular 90-mg pamidronate infusions can also relieve bone pain in about one-half of cases, and an objective sclerosis of osteolytic lesions can be seen in one-quarter of patients. Most importantly, the prolonged administration of oral or intravenous bisphosphonates can delay and reduce the frequency of morbid skeletal events in breast cancer metastatic to bone and in multiple myeloma by one-quarter to one-half. Intravenous bisphosphonates appear to produce larger and more rapid effects than available oral compounds.

  • Newer, more potent bisphosphonates, such as ibandronate (6 mg) and zoledronate (4 mg), appear to produce similar results to pamidronate but are more convenient to administer. They could, nevertheless, be more potent in conditions characterized by severe osteolysis. Zoledronate has thus been shown to be superior to pamidronate in moderate to severe hypercalcemia.

  • Therapy with bisphosphonates also has the advantage of preventing postmenopausal osteoporosis in women cured from breast cancer and for whom ERT is still considered to be contraindicated.


Multiple Myeloma Bone Metastasis Zoledronic Acid Intravenous Bisphosphonates Skeletal Morbidity 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

Further Reading

  1. Body JJ (2001) Bisphosphonates in the treatment of metastatic breast cancer. J Mammary Gland Biol Neoplasia 6: 477–485.PubMedCrossRefGoogle Scholar
  2. Body JJ (2000) Tumor Bone Diseases and Osteoporosis in Cancer Patients. New York, Basel: Marcel Dekker Inc.Google Scholar
  3. Body JJ, Bartl R, Burckhardt P, et al. (1998) Current use ofbisphosphonates in oncology. J Clin Oncol 16: 3890–3899.PubMedGoogle Scholar
  4. Hillner BE, Ingle IN, Berenson JR, et al. (2000) American Society of Clinical Oncology guideline on the role of bisphosphonates in breast cancer. American Society of Clinical Oncology Bisphosphonates Expert Panel. J Clin Onco 118: 1378–1391.Google Scholar
  5. Hortobagyi GN, Theriault RL, Lipton A, et al. (1998) Long-term prevention of skeletal complications of metastatic breast cancer with pamidronate. J Clin Onco 116: 2038–2044.Google Scholar
  6. McCloskey EV, MacLennan ICM, Drayson M, Chapman C, Dunn J, Kanis JA (1998) A randomized trial of the effect of clodronate on skeletal morbidity in multiple myeloma. Br J Haematol 100: 317–325.PubMedCrossRefGoogle Scholar
  7. Mundy GR (1997) Mechanisms of bone metastasis. Cancer 80: 1546–1556.PubMedCrossRefGoogle Scholar
  8. Theriault RL, Lipton A, Hortobagyi GN, et al. (1999) Pamidronate reduces skeletal morbidity in women with advanced breast cancer and lytic bone lesions: a randomized, placebo-controlled trial. J Clin Oncol 17: 846–854.PubMedGoogle Scholar

Copyright information

© Springer-Verlag London 2004

Authors and Affiliations

  • Jean-Jacques Body

There are no affiliations available

Personalised recommendations