Advances in the biology of bone metastasis: How the skeleton affects tumor behavior

Abstract It is increasingly evident that the microenvironment of bone can influence the cancer phenotype in many ways that favor growth in bone. The ability of cancer cells to adhere to bone matrix and to promote osteoclast formation are key requirements for the establishment and growth of bone meta...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Bone (New York, N.Y.) N.Y.), 2011-01, Vol.48 (1), p.6-15
Hauptverfasser: Sterling, Julie A, Edwards, James R, Martin, T. John, Mundy, Gregory R
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 15
container_issue 1
container_start_page 6
container_title Bone (New York, N.Y.)
container_volume 48
creator Sterling, Julie A
Edwards, James R
Martin, T. John
Mundy, Gregory R
description Abstract It is increasingly evident that the microenvironment of bone can influence the cancer phenotype in many ways that favor growth in bone. The ability of cancer cells to adhere to bone matrix and to promote osteoclast formation are key requirements for the establishment and growth of bone metastases. Several cytokine products of breast cancers (e.g. PTHrP, IL-11, IL-8) have been shown to act upon host cells of the bone microenvironment to promote osteoclast formation, allowing for excessive bone resorption. The increased release of matrix-derived growth factors, especially TGF-β, acts back upon the tumor to facilitate further tumor expansion and enhance cytokine production, and also upon osteoblasts to suppress bone formation. This provides a self-perpetuating cycle of bone loss and tumor growth within the skeleton. Other contributing factors favoring tumor metastasis and colonization in bone include the unique structure and stiffness of skeletal tissue, along with the diverse cellular composition of the marrow environment (e.g. bone cells, stromal fibroblasts, immune cells), any of which can contribute to the phenotypic changes that can take place in metastatic deposits that favor their survival. Additionally, it is also apparent that breast cancer cells begin to express different bone specific proteins as well as proteins important for normal breast development and lactation that allow them to grow in bone and stimulate bone destruction. Taken together, these continually emerging areas of study suggest new potential pathways important in the pathogenesis of bone metastasis and potential areas for targeting therapeutics.
doi_str_mv 10.1016/j.bone.2010.07.015
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_893262386</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S875632821001358X</els_id><sourcerecordid>893262386</sourcerecordid><originalsourceid>FETCH-LOGICAL-c504t-480a718dced7d8b0d9faeb7dd95958ce4723d9d56adde879e87eca4487fad3a93</originalsourceid><addsrcrecordid>eNqFkcFu1DAQhi0EokvhBTgg3zhlGdtJbHNAqiqgSJV6aCtxsxx7Qr1N4mInW-3b47CFa6UZjTT65j98Q8h7BlsGrP2023Zxwi2HsgC5Bda8IBumpKi4bMVLslGyaSvBFT8hb3LeAYDQkr0mJxzaWnDRbMj1md_byWGmYaLzHdIuxCH-OtDY0zWdjjjbXCrkz_QiPv5l8j0OOMeJ2r5HN2c6L2NMtMM7uw8xvSWvejtkfPc0T8ntt6835xfV5dX3H-dnl5VroJ6rWoGVTHmHXnrVgde9xU56rxvdKIe15MJr37TWe1RSl0Zn61rJ3nphtTglH4-5Dyn-XjDPZgzZ4TDYCeOSjdKCt1yo9nmSs1ppKaCQ_Ei6FHNO2JuHFEabDoaBWa2bnVm9mNW6AWmK9XL04Sl-6Ub0_0_-aS7AlyOARcc-YDJuCFNwdrjHA-ZdXNJUTBlmMjdgrtfHrX9jAEw06qf4A1RNlKc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>821489730</pqid></control><display><type>article</type><title>Advances in the biology of bone metastasis: How the skeleton affects tumor behavior</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Sterling, Julie A ; Edwards, James R ; Martin, T. John ; Mundy, Gregory R</creator><creatorcontrib>Sterling, Julie A ; Edwards, James R ; Martin, T. John ; Mundy, Gregory R</creatorcontrib><description>Abstract It is increasingly evident that the microenvironment of bone can influence the cancer phenotype in many ways that favor growth in bone. The ability of cancer cells to adhere to bone matrix and to promote osteoclast formation are key requirements for the establishment and growth of bone metastases. Several cytokine products of breast cancers (e.g. PTHrP, IL-11, IL-8) have been shown to act upon host cells of the bone microenvironment to promote osteoclast formation, allowing for excessive bone resorption. The increased release of matrix-derived growth factors, especially TGF-β, acts back upon the tumor to facilitate further tumor expansion and enhance cytokine production, and also upon osteoblasts to suppress bone formation. This provides a self-perpetuating cycle of bone loss and tumor growth within the skeleton. Other contributing factors favoring tumor metastasis and colonization in bone include the unique structure and stiffness of skeletal tissue, along with the diverse cellular composition of the marrow environment (e.g. bone cells, stromal fibroblasts, immune cells), any of which can contribute to the phenotypic changes that can take place in metastatic deposits that favor their survival. Additionally, it is also apparent that breast cancer cells begin to express different bone specific proteins as well as proteins important for normal breast development and lactation that allow them to grow in bone and stimulate bone destruction. Taken together, these continually emerging areas of study suggest new potential pathways important in the pathogenesis of bone metastasis and potential areas for targeting therapeutics.</description><identifier>ISSN: 8756-3282</identifier><identifier>EISSN: 1873-2763</identifier><identifier>DOI: 10.1016/j.bone.2010.07.015</identifier><identifier>PMID: 20643235</identifier><language>eng</language><publisher>United States</publisher><subject>Bone and Bones - metabolism ; Bone and Bones - pathology ; Bone Neoplasms - genetics ; Bone Neoplasms - metabolism ; Bone Neoplasms - secondary ; Bone Resorption - complications ; Bone Resorption - etiology ; Bone Resorption - metabolism ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cytokines - metabolism ; Female ; Humans ; Interleukin-11 - metabolism ; Interleukin-8 - metabolism ; Neoplasms - complications ; Neoplasms - metabolism ; Orthopedics ; Osteoblasts - metabolism ; Osteoblasts - pathology ; Osteoclasts - metabolism ; Osteoclasts - pathology ; Osteogenesis ; Parathyroid Hormone-Related Protein - metabolism ; Transforming Growth Factor beta - metabolism</subject><ispartof>Bone (New York, N.Y.), 2011-01, Vol.48 (1), p.6-15</ispartof><rights>Copyright © 2010. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-480a718dced7d8b0d9faeb7dd95958ce4723d9d56adde879e87eca4487fad3a93</citedby><cites>FETCH-LOGICAL-c504t-480a718dced7d8b0d9faeb7dd95958ce4723d9d56adde879e87eca4487fad3a93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20643235$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sterling, Julie A</creatorcontrib><creatorcontrib>Edwards, James R</creatorcontrib><creatorcontrib>Martin, T. John</creatorcontrib><creatorcontrib>Mundy, Gregory R</creatorcontrib><title>Advances in the biology of bone metastasis: How the skeleton affects tumor behavior</title><title>Bone (New York, N.Y.)</title><addtitle>Bone</addtitle><description>Abstract It is increasingly evident that the microenvironment of bone can influence the cancer phenotype in many ways that favor growth in bone. The ability of cancer cells to adhere to bone matrix and to promote osteoclast formation are key requirements for the establishment and growth of bone metastases. Several cytokine products of breast cancers (e.g. PTHrP, IL-11, IL-8) have been shown to act upon host cells of the bone microenvironment to promote osteoclast formation, allowing for excessive bone resorption. The increased release of matrix-derived growth factors, especially TGF-β, acts back upon the tumor to facilitate further tumor expansion and enhance cytokine production, and also upon osteoblasts to suppress bone formation. This provides a self-perpetuating cycle of bone loss and tumor growth within the skeleton. Other contributing factors favoring tumor metastasis and colonization in bone include the unique structure and stiffness of skeletal tissue, along with the diverse cellular composition of the marrow environment (e.g. bone cells, stromal fibroblasts, immune cells), any of which can contribute to the phenotypic changes that can take place in metastatic deposits that favor their survival. Additionally, it is also apparent that breast cancer cells begin to express different bone specific proteins as well as proteins important for normal breast development and lactation that allow them to grow in bone and stimulate bone destruction. Taken together, these continually emerging areas of study suggest new potential pathways important in the pathogenesis of bone metastasis and potential areas for targeting therapeutics.</description><subject>Bone and Bones - metabolism</subject><subject>Bone and Bones - pathology</subject><subject>Bone Neoplasms - genetics</subject><subject>Bone Neoplasms - metabolism</subject><subject>Bone Neoplasms - secondary</subject><subject>Bone Resorption - complications</subject><subject>Bone Resorption - etiology</subject><subject>Bone Resorption - metabolism</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cytokines - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Interleukin-11 - metabolism</subject><subject>Interleukin-8 - metabolism</subject><subject>Neoplasms - complications</subject><subject>Neoplasms - metabolism</subject><subject>Orthopedics</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoblasts - pathology</subject><subject>Osteoclasts - metabolism</subject><subject>Osteoclasts - pathology</subject><subject>Osteogenesis</subject><subject>Parathyroid Hormone-Related Protein - metabolism</subject><subject>Transforming Growth Factor beta - metabolism</subject><issn>8756-3282</issn><issn>1873-2763</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi0EokvhBTgg3zhlGdtJbHNAqiqgSJV6aCtxsxx7Qr1N4mInW-3b47CFa6UZjTT65j98Q8h7BlsGrP2023Zxwi2HsgC5Bda8IBumpKi4bMVLslGyaSvBFT8hb3LeAYDQkr0mJxzaWnDRbMj1md_byWGmYaLzHdIuxCH-OtDY0zWdjjjbXCrkz_QiPv5l8j0OOMeJ2r5HN2c6L2NMtMM7uw8xvSWvejtkfPc0T8ntt6835xfV5dX3H-dnl5VroJ6rWoGVTHmHXnrVgde9xU56rxvdKIe15MJr37TWe1RSl0Zn61rJ3nphtTglH4-5Dyn-XjDPZgzZ4TDYCeOSjdKCt1yo9nmSs1ppKaCQ_Ei6FHNO2JuHFEabDoaBWa2bnVm9mNW6AWmK9XL04Sl-6Ub0_0_-aS7AlyOARcc-YDJuCFNwdrjHA-ZdXNJUTBlmMjdgrtfHrX9jAEw06qf4A1RNlKc</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Sterling, Julie A</creator><creator>Edwards, James R</creator><creator>Martin, T. John</creator><creator>Mundy, Gregory R</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7QP</scope></search><sort><creationdate>20110101</creationdate><title>Advances in the biology of bone metastasis: How the skeleton affects tumor behavior</title><author>Sterling, Julie A ; Edwards, James R ; Martin, T. John ; Mundy, Gregory R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-480a718dced7d8b0d9faeb7dd95958ce4723d9d56adde879e87eca4487fad3a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Bone and Bones - metabolism</topic><topic>Bone and Bones - pathology</topic><topic>Bone Neoplasms - genetics</topic><topic>Bone Neoplasms - metabolism</topic><topic>Bone Neoplasms - secondary</topic><topic>Bone Resorption - complications</topic><topic>Bone Resorption - etiology</topic><topic>Bone Resorption - metabolism</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cytokines - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Interleukin-11 - metabolism</topic><topic>Interleukin-8 - metabolism</topic><topic>Neoplasms - complications</topic><topic>Neoplasms - metabolism</topic><topic>Orthopedics</topic><topic>Osteoblasts - metabolism</topic><topic>Osteoblasts - pathology</topic><topic>Osteoclasts - metabolism</topic><topic>Osteoclasts - pathology</topic><topic>Osteogenesis</topic><topic>Parathyroid Hormone-Related Protein - metabolism</topic><topic>Transforming Growth Factor beta - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sterling, Julie A</creatorcontrib><creatorcontrib>Edwards, James R</creatorcontrib><creatorcontrib>Martin, T. John</creatorcontrib><creatorcontrib>Mundy, Gregory R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><jtitle>Bone (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sterling, Julie A</au><au>Edwards, James R</au><au>Martin, T. John</au><au>Mundy, Gregory R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Advances in the biology of bone metastasis: How the skeleton affects tumor behavior</atitle><jtitle>Bone (New York, N.Y.)</jtitle><addtitle>Bone</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>48</volume><issue>1</issue><spage>6</spage><epage>15</epage><pages>6-15</pages><issn>8756-3282</issn><eissn>1873-2763</eissn><abstract>Abstract It is increasingly evident that the microenvironment of bone can influence the cancer phenotype in many ways that favor growth in bone. The ability of cancer cells to adhere to bone matrix and to promote osteoclast formation are key requirements for the establishment and growth of bone metastases. Several cytokine products of breast cancers (e.g. PTHrP, IL-11, IL-8) have been shown to act upon host cells of the bone microenvironment to promote osteoclast formation, allowing for excessive bone resorption. The increased release of matrix-derived growth factors, especially TGF-β, acts back upon the tumor to facilitate further tumor expansion and enhance cytokine production, and also upon osteoblasts to suppress bone formation. This provides a self-perpetuating cycle of bone loss and tumor growth within the skeleton. Other contributing factors favoring tumor metastasis and colonization in bone include the unique structure and stiffness of skeletal tissue, along with the diverse cellular composition of the marrow environment (e.g. bone cells, stromal fibroblasts, immune cells), any of which can contribute to the phenotypic changes that can take place in metastatic deposits that favor their survival. Additionally, it is also apparent that breast cancer cells begin to express different bone specific proteins as well as proteins important for normal breast development and lactation that allow them to grow in bone and stimulate bone destruction. Taken together, these continually emerging areas of study suggest new potential pathways important in the pathogenesis of bone metastasis and potential areas for targeting therapeutics.</abstract><cop>United States</cop><pmid>20643235</pmid><doi>10.1016/j.bone.2010.07.015</doi><tpages>10</tpages></addata></record>
fulltext fulltext
identifier ISSN: 8756-3282
ispartof Bone (New York, N.Y.), 2011-01, Vol.48 (1), p.6-15
issn 8756-3282
1873-2763
language eng
recordid cdi_proquest_miscellaneous_893262386
source MEDLINE; Access via ScienceDirect (Elsevier)
subjects Bone and Bones - metabolism
Bone and Bones - pathology
Bone Neoplasms - genetics
Bone Neoplasms - metabolism
Bone Neoplasms - secondary
Bone Resorption - complications
Bone Resorption - etiology
Bone Resorption - metabolism
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Cytokines - metabolism
Female
Humans
Interleukin-11 - metabolism
Interleukin-8 - metabolism
Neoplasms - complications
Neoplasms - metabolism
Orthopedics
Osteoblasts - metabolism
Osteoblasts - pathology
Osteoclasts - metabolism
Osteoclasts - pathology
Osteogenesis
Parathyroid Hormone-Related Protein - metabolism
Transforming Growth Factor beta - metabolism
title Advances in the biology of bone metastasis: How the skeleton affects tumor behavior
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T21%3A10%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Advances%20in%20the%20biology%20of%20bone%20metastasis:%20How%20the%20skeleton%20affects%20tumor%20behavior&rft.jtitle=Bone%20(New%20York,%20N.Y.)&rft.au=Sterling,%20Julie%20A&rft.date=2011-01-01&rft.volume=48&rft.issue=1&rft.spage=6&rft.epage=15&rft.pages=6-15&rft.issn=8756-3282&rft.eissn=1873-2763&rft_id=info:doi/10.1016/j.bone.2010.07.015&rft_dat=%3Cproquest_cross%3E893262386%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=821489730&rft_id=info:pmid/20643235&rft_els_id=1_s2_0_S875632821001358X&rfr_iscdi=true