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PMID: 21200394 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Bone metastasis: mechanisms and therapeutic opportunities.

Nature reviews. Endocrinology ·Vol. 7 ·No. 4 ·2011-04-00 ·Pages 208-18

Suva LJ, Washam C, Nicholas RW, Griffin RJ

Abstract

The skeleton is one of the most common sites for metastatic cancer, and tumors arising from the breast or prostate possess an increased propensity to spread to this site. The growth of disseminated tumor cells in the skeleton requires tumor cells to inhabit the bone marrow, from which they stimulate local bone cell activity. Crosstalk between tumor cells and resident bone and bone marrow cells disrupts normal bone homeostasis, which leads to tumor growth in bone. The metastatic tumor cells have the ability to elicit responses that stimulate bone resorption, bone formation or both. The net result of these activities is profound skeletal destruction that can have dire consequences for patients. The molecular mechanisms that underlie these painful and often incurable consequences of tumor metastasis to bone are beginning to be recognized, and they represent promising new molecular targets for therapy.

MeSH Terms
Bone Neoplasms/drug therapy,metabolism,secondary Breast Neoplasms/complications,metabolism Female Humans Male Models, Biological Prostatic Neoplasms/complications,metabolism Signal Transduction
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Suva Larry J
Department of Orthopedic Surgery, Center for Orthopedic Research, Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, 4301 West Markham Street, Little Rock, AR 72205, USA. suvalarryj@uams.edu
Washam Charity
Nicholas Richard W
Griffin Robert J
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Article Info
Journal
Nature reviews. Endocrinology
Abbr.
Nat Rev Endocrinol
ISSN
1759-5037
Published
2011-04-00
Epub
2011-00-04
Pages
208-18
Language
English
Region
England
NLM ID
101500078
PMCID
PMC3134309
Subset
IM
Grants
NCI NIH HHS · R01 CA107160 · United States
NCI NIH HHS · R01 CA107160-05 · United States
NCI NIH HHS · 5R01CA107160 · United States
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