Linked Life Data

12874704

Source:http://linkedlifedata.com/resource/pubmed/id/12874704

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-1-22
pubmed:abstractText
Bisphosphonates (BPs) suppress cancer cell colonization in bone associated with cancers such as breast cancer and multiple myeloma. The mechanism of the suppressive action of BPs is thought to be due to an inhibition of osteoclastic bone resorption which releases bone-stored growth factors that feed cancer cells colonizing bone. Recently, data are accumulating that BP suppresses growth and induces apoptosis in cancer cells in culture, suggesting that BP directly influences survival of cancer cells in an osteoclast-independent manner. These results raise the possibility that BP inhibits cancer growth in organs other than bone. However, evidence is limited that BP reduces tumor growth in non-bone sites in cancer patients. In this review, we discuss the effectiveness of BP on breast cancer colonization in non-bone sites and our results in animal models with metastases. With currently available clinical and in vivo experimental data, BPs are definitely beneficial for the treatment of cancer patients who manifest clinically detectable bone metastases. However, it is not recommended that BP be given as a preventative to patients with visceral metastases and of no evidence of bone metastases. Whether individual BP with different chemical structure has unique biological or biochemical action is an intriguing question but open at the moment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0171-967X
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
315-8
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Bisphosphonate actions on cancer.
pubmed:affiliation
Department of Biochemistry, Department of Medicine, Osaka University Graduate School of Dentistry, Japan and Endocrine Research, The University of Texas Health Science Center at San Antonio, Texas, USA. yoneda@uthscsa.edu
pubmed:publicationType
Journal Article, Review