Breast cancer bone metastasis: Difference between revisions
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==Pathogenesis== | ==Pathogenesis== | ||
The normal balance between bone resorption and deposition is significantly affected by cancer. Bone metastases due to breast cancer are mostly osteolytic lesions, though a considerable number of patients have predominant osteoblastic disease <ref name="pmid11346860">{{cite journal| author=Coleman RE, Seaman JJ| title=The role of zoledronic acid in cancer: clinical studies in the treatment and prevention of bone metastases. | journal=Semin Oncol | year= 2001 | volume= 28 | issue= 2 Suppl 6 | pages= 11-6 | pmid=11346860 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11346860 }} </ref>. | The normal balance between bone resorption and deposition is significantly affected by cancer. Bone metastases due to breast cancer are mostly osteolytic lesions, though a considerable number of patients have predominant osteoblastic disease <ref name="pmid11346860">{{cite journal| author=Coleman RE, Seaman JJ| title=The role of zoledronic acid in cancer: clinical studies in the treatment and prevention of bone metastases. | journal=Semin Oncol | year= 2001 | volume= 28 | issue= 2 Suppl 6 | pages= 11-6 | pmid=11346860 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11346860 }} </ref>. | ||
The breast cancer cells and the bone microenvironment interact extensively through many chemical mediators (pimarily osteopontin, | |||
and interleukin-11, resulting in bone destruction and tumor growth. These molecular mediators encompass exert their effect on the osteoclasts which in turn cause bone resorption. This osteoclast-mediated bone resorption is thought to be triggered by many molecules including: PTHrP (parathyroid hormone–related peptide), tumor necrosis factor α (TNF-α), and cytokines such as interleukin-1,interleukin-6, interleukin-8, and interleukin-11. These facors signal osteoblasts (the bone-building cells) to induce osteoclast differentiation through the RANKL(the ligand for the receptor activator of nuclearfactor-κB [RANK])-RANK interaction. When Osteoclasts lyse bone, they cause the release of growth factors such as bone morphogenetic proteins (BMPs), IGF-I and TGF-β from the bone matrix; which stimulate and maintain tumor cell proliferation and induce further release of PTHrP . | |||
==References== | ==References== | ||
Revision as of 17:00, 23 November 2011
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-In-Chief: Jack Khouri
Overview
Bone is the most common site of breast cancer distant spread. Bone metastases due to breast cancer cause major morbidity, decrease survival and reduce quality of life of many patients. Cancer influence on the skeleton results in two main negative consequences: pain and Skeletal-Related events (sre), defined as any of the following:
- pathologic fracture,
- a requirement for surgical intervention and palliative radiotherapy to bone lesions,
- spinal cord compression,
- hypercalcemia of malignancy.
Many disciplines should be involved in the management of breast cancer bone metastases, including medical oncology, pain and palliative care, radiation oncology and orthopedic surgery. Systemic therapy is implemented in order to delay the progression of bone metastases and may include endocrine therapy, biologic agents, chemotherapy, and bisphosphonate therapy and osteoclast inhibitors.
Pathogenesis
The normal balance between bone resorption and deposition is significantly affected by cancer. Bone metastases due to breast cancer are mostly osteolytic lesions, though a considerable number of patients have predominant osteoblastic disease [1]. The breast cancer cells and the bone microenvironment interact extensively through many chemical mediators (pimarily osteopontin, and interleukin-11, resulting in bone destruction and tumor growth. These molecular mediators encompass exert their effect on the osteoclasts which in turn cause bone resorption. This osteoclast-mediated bone resorption is thought to be triggered by many molecules including: PTHrP (parathyroid hormone–related peptide), tumor necrosis factor α (TNF-α), and cytokines such as interleukin-1,interleukin-6, interleukin-8, and interleukin-11. These facors signal osteoblasts (the bone-building cells) to induce osteoclast differentiation through the RANKL(the ligand for the receptor activator of nuclearfactor-κB [RANK])-RANK interaction. When Osteoclasts lyse bone, they cause the release of growth factors such as bone morphogenetic proteins (BMPs), IGF-I and TGF-β from the bone matrix; which stimulate and maintain tumor cell proliferation and induce further release of PTHrP .
References
- ↑ Coleman RE, Seaman JJ (2001). "The role of zoledronic acid in cancer: clinical studies in the treatment and prevention of bone metastases". Semin Oncol. 28 (2 Suppl 6): 11–6. PMID 11346860.