Zoledronic acid impairs myeloid differentiation to tumour-associated macrophages in mesothelioma
Background: Suppressive immune cells present in tumour microenvironments are known to augment tumour growth and hamper efficacy of antitumour therapies. The amino-bisphosphonate Zoledronic acid (ZA) is considered as an antitumour agent, as recent studies showed that ZA prolongs disease-free survival...
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| Veröffentlicht in: | British journal of cancer 2010-08, Vol.103 (5), p.629-641 |
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| container_title | British journal of cancer |
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| creator | Veltman, J D Lambers, M E H van Nimwegen, M Hendriks, R W Hoogsteden, H C Hegmans, J P J J Aerts, J G J V |
| description | Background:
Suppressive immune cells present in tumour microenvironments are known to augment tumour growth and hamper efficacy of antitumour therapies. The amino-bisphosphonate Zoledronic acid (ZA) is considered as an antitumour agent, as recent studies showed that ZA prolongs disease-free survival in cancer patients. The exact mechanism is a topic of debate; it has been suggested that ZA targets tumour-associated macrophages (TAMs).
Methods:
We investigate the role of ZA on the myeloid differentiation to TAMs in murine mesothelioma
in vivo
and
in vitro
. Mice were intraperitoneally inoculated with a lethal dose of mesothelioma tumour cells and treated with ZA to determine the effects on myeloid differentiation and survival.
Results:
We show that ZA impaired myeloid differentiation. Inhibition of myeloid differentiation led to a reduction in TAMs, but the number of immature myeloid cells with myeloid-derived suppressor cell (MDSC) characteristics was increased. In addition, ZA affects the phenotype of macrophages leading to reduced level of TAM-associated cytokines in the tumour microenvironment. No improvement of survival was observed.
Conclusion:
We conclude that ZA leads to a reduction in macrophages and impairs polarisation towards an M2 phenotype, but this was associated with an increase in the number of immature myeloid cells, which might diminish the effects of ZA on survival. |
| doi_str_mv | 10.1038/sj.bjc.6605814 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2938257</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2117921421</sourcerecordid><originalsourceid>FETCH-LOGICAL-c486t-98a184c43ca4a856deb8237da71a3b3b71394b99c919cd52e6a2111c9346d4e43</originalsourceid><addsrcrecordid>eNp1kc2LFDEQxYMo7uzq1aM0gnjq2Xx_XARZdBUWvOjFS6xO0jNpujtj0i3sf2-WGXdV8BQq9cvLq3oIvSB4SzDTl2XYdoPbSomFJvwR2hDBaEs0VY_RBmOsWmwoPkPnpQy1NFirp-iMYim50HqDvn9LY_A5zdE14KJv4nSAmEsz3YYx1drHvg85zEuEJaa5WVKzrFNacwulJFdvg28mcDkd9rALpYlzM4WSln0YY5rgGXrSw1jC89N5gb5-eP_l6mN78_n609W7m9ZxLZfWaCCaO84ccNBC-tBpypQHRYB1rFOEGd4Z4wwxzgsaJFBCiDOMS88DZxfo7VH3sHZT8K46zjDaQ44T5FubINq_O3Pc2136aalhmgpVBd6cBHL6sYay2CkWF8YR5pDWYhXXRnHBWSVf_UMOdR9zna5CUhCl2B20PUJ1M6Xk0N9bIdjeRWfLYGt09hRdffDyzwHu8d9ZVeD1CYDiYOwzzC6WB45RqrQwlbs8cqW25l3ID_b-8_Uvft60lQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>746517733</pqid></control><display><type>article</type><title>Zoledronic acid impairs myeloid differentiation to tumour-associated macrophages in mesothelioma</title><source>MEDLINE</source><source>Nature Journals Online</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>SpringerLink Journals - AutoHoldings</source><creator>Veltman, J D ; Lambers, M E H ; van Nimwegen, M ; Hendriks, R W ; Hoogsteden, H C ; Hegmans, J P J J ; Aerts, J G J V</creator><creatorcontrib>Veltman, J D ; Lambers, M E H ; van Nimwegen, M ; Hendriks, R W ; Hoogsteden, H C ; Hegmans, J P J J ; Aerts, J G J V</creatorcontrib><description>Background:
Suppressive immune cells present in tumour microenvironments are known to augment tumour growth and hamper efficacy of antitumour therapies. The amino-bisphosphonate Zoledronic acid (ZA) is considered as an antitumour agent, as recent studies showed that ZA prolongs disease-free survival in cancer patients. The exact mechanism is a topic of debate; it has been suggested that ZA targets tumour-associated macrophages (TAMs).
Methods:
We investigate the role of ZA on the myeloid differentiation to TAMs in murine mesothelioma
in vivo
and
in vitro
. Mice were intraperitoneally inoculated with a lethal dose of mesothelioma tumour cells and treated with ZA to determine the effects on myeloid differentiation and survival.
Results:
We show that ZA impaired myeloid differentiation. Inhibition of myeloid differentiation led to a reduction in TAMs, but the number of immature myeloid cells with myeloid-derived suppressor cell (MDSC) characteristics was increased. In addition, ZA affects the phenotype of macrophages leading to reduced level of TAM-associated cytokines in the tumour microenvironment. No improvement of survival was observed.
Conclusion:
We conclude that ZA leads to a reduction in macrophages and impairs polarisation towards an M2 phenotype, but this was associated with an increase in the number of immature myeloid cells, which might diminish the effects of ZA on survival.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6605814</identifier><identifier>PMID: 20664588</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/136/142 ; 631/154/436/2388 ; 692/698/690/292 ; 692/699/67/1641 ; Acids ; Angiogenesis ; Animals ; Antineoplastic Agents - pharmacology ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Bisphosphonates ; Cancer Research ; Cell Count ; Cell Differentiation - drug effects ; Cell Survival - drug effects ; Chemokines ; Cytokines - biosynthesis ; Diphosphonates - pharmacology ; Disease ; Drug Resistance ; Epidemiology ; Genotype & phenotype ; Imidazoles - pharmacology ; Macrophages - drug effects ; Medical prognosis ; Medical research ; Medical sciences ; Mesothelioma ; Mesothelioma - immunology ; Mesothelioma - pathology ; Metastasis ; Mice ; Molecular Medicine ; Myeloid Cells - drug effects ; Oncology ; Pathogens ; Phenotype ; Translational Therapeutics ; Tumors</subject><ispartof>British journal of cancer, 2010-08, Vol.103 (5), p.629-641</ispartof><rights>The Author(s) 2010</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Aug 24, 2010</rights><rights>Copyright © 2010 Cancer Research UK 2010 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-98a184c43ca4a856deb8237da71a3b3b71394b99c919cd52e6a2111c9346d4e43</citedby><cites>FETCH-LOGICAL-c486t-98a184c43ca4a856deb8237da71a3b3b71394b99c919cd52e6a2111c9346d4e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938257/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938257/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23227859$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20664588$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Veltman, J D</creatorcontrib><creatorcontrib>Lambers, M E H</creatorcontrib><creatorcontrib>van Nimwegen, M</creatorcontrib><creatorcontrib>Hendriks, R W</creatorcontrib><creatorcontrib>Hoogsteden, H C</creatorcontrib><creatorcontrib>Hegmans, J P J J</creatorcontrib><creatorcontrib>Aerts, J G J V</creatorcontrib><title>Zoledronic acid impairs myeloid differentiation to tumour-associated macrophages in mesothelioma</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Background:
Suppressive immune cells present in tumour microenvironments are known to augment tumour growth and hamper efficacy of antitumour therapies. The amino-bisphosphonate Zoledronic acid (ZA) is considered as an antitumour agent, as recent studies showed that ZA prolongs disease-free survival in cancer patients. The exact mechanism is a topic of debate; it has been suggested that ZA targets tumour-associated macrophages (TAMs).
Methods:
We investigate the role of ZA on the myeloid differentiation to TAMs in murine mesothelioma
in vivo
and
in vitro
. Mice were intraperitoneally inoculated with a lethal dose of mesothelioma tumour cells and treated with ZA to determine the effects on myeloid differentiation and survival.
Results:
We show that ZA impaired myeloid differentiation. Inhibition of myeloid differentiation led to a reduction in TAMs, but the number of immature myeloid cells with myeloid-derived suppressor cell (MDSC) characteristics was increased. In addition, ZA affects the phenotype of macrophages leading to reduced level of TAM-associated cytokines in the tumour microenvironment. No improvement of survival was observed.
Conclusion:
We conclude that ZA leads to a reduction in macrophages and impairs polarisation towards an M2 phenotype, but this was associated with an increase in the number of immature myeloid cells, which might diminish the effects of ZA on survival.</description><subject>631/136/142</subject><subject>631/154/436/2388</subject><subject>692/698/690/292</subject><subject>692/699/67/1641</subject><subject>Acids</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bisphosphonates</subject><subject>Cancer Research</subject><subject>Cell Count</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Chemokines</subject><subject>Cytokines - biosynthesis</subject><subject>Diphosphonates - pharmacology</subject><subject>Disease</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Genotype & phenotype</subject><subject>Imidazoles - pharmacology</subject><subject>Macrophages - drug effects</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Mesothelioma</subject><subject>Mesothelioma - immunology</subject><subject>Mesothelioma - pathology</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Molecular Medicine</subject><subject>Myeloid Cells - drug effects</subject><subject>Oncology</subject><subject>Pathogens</subject><subject>Phenotype</subject><subject>Translational Therapeutics</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc2LFDEQxYMo7uzq1aM0gnjq2Xx_XARZdBUWvOjFS6xO0jNpujtj0i3sf2-WGXdV8BQq9cvLq3oIvSB4SzDTl2XYdoPbSomFJvwR2hDBaEs0VY_RBmOsWmwoPkPnpQy1NFirp-iMYim50HqDvn9LY_A5zdE14KJv4nSAmEsz3YYx1drHvg85zEuEJaa5WVKzrFNacwulJFdvg28mcDkd9rALpYlzM4WSln0YY5rgGXrSw1jC89N5gb5-eP_l6mN78_n609W7m9ZxLZfWaCCaO84ccNBC-tBpypQHRYB1rFOEGd4Z4wwxzgsaJFBCiDOMS88DZxfo7VH3sHZT8K46zjDaQ44T5FubINq_O3Pc2136aalhmgpVBd6cBHL6sYay2CkWF8YR5pDWYhXXRnHBWSVf_UMOdR9zna5CUhCl2B20PUJ1M6Xk0N9bIdjeRWfLYGt09hRdffDyzwHu8d9ZVeD1CYDiYOwzzC6WB45RqrQwlbs8cqW25l3ID_b-8_Uvft60lQ</recordid><startdate>20100824</startdate><enddate>20100824</enddate><creator>Veltman, J D</creator><creator>Lambers, M E H</creator><creator>van Nimwegen, M</creator><creator>Hendriks, R W</creator><creator>Hoogsteden, H C</creator><creator>Hegmans, J P J J</creator><creator>Aerts, J G J V</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>IQODW</scope><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>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100824</creationdate><title>Zoledronic acid impairs myeloid differentiation to tumour-associated macrophages in mesothelioma</title><author>Veltman, J D ; Lambers, M E H ; van Nimwegen, M ; Hendriks, R W ; Hoogsteden, H C ; Hegmans, J P J J ; Aerts, J G J V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-98a184c43ca4a856deb8237da71a3b3b71394b99c919cd52e6a2111c9346d4e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>631/136/142</topic><topic>631/154/436/2388</topic><topic>692/698/690/292</topic><topic>692/699/67/1641</topic><topic>Acids</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bisphosphonates</topic><topic>Cancer Research</topic><topic>Cell Count</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Chemokines</topic><topic>Cytokines - biosynthesis</topic><topic>Diphosphonates - pharmacology</topic><topic>Disease</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Genotype & phenotype</topic><topic>Imidazoles - pharmacology</topic><topic>Macrophages - drug effects</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Mesothelioma</topic><topic>Mesothelioma - immunology</topic><topic>Mesothelioma - pathology</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Molecular Medicine</topic><topic>Myeloid Cells - drug effects</topic><topic>Oncology</topic><topic>Pathogens</topic><topic>Phenotype</topic><topic>Translational Therapeutics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Veltman, J D</creatorcontrib><creatorcontrib>Lambers, M E H</creatorcontrib><creatorcontrib>van Nimwegen, M</creatorcontrib><creatorcontrib>Hendriks, R W</creatorcontrib><creatorcontrib>Hoogsteden, H C</creatorcontrib><creatorcontrib>Hegmans, J P J J</creatorcontrib><creatorcontrib>Aerts, J G J V</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Veltman, J D</au><au>Lambers, M E H</au><au>van Nimwegen, M</au><au>Hendriks, R W</au><au>Hoogsteden, H C</au><au>Hegmans, J P J J</au><au>Aerts, J G J V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Zoledronic acid impairs myeloid differentiation to tumour-associated macrophages in mesothelioma</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2010-08-24</date><risdate>2010</risdate><volume>103</volume><issue>5</issue><spage>629</spage><epage>641</epage><pages>629-641</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Background:
Suppressive immune cells present in tumour microenvironments are known to augment tumour growth and hamper efficacy of antitumour therapies. The amino-bisphosphonate Zoledronic acid (ZA) is considered as an antitumour agent, as recent studies showed that ZA prolongs disease-free survival in cancer patients. The exact mechanism is a topic of debate; it has been suggested that ZA targets tumour-associated macrophages (TAMs).
Methods:
We investigate the role of ZA on the myeloid differentiation to TAMs in murine mesothelioma
in vivo
and
in vitro
. Mice were intraperitoneally inoculated with a lethal dose of mesothelioma tumour cells and treated with ZA to determine the effects on myeloid differentiation and survival.
Results:
We show that ZA impaired myeloid differentiation. Inhibition of myeloid differentiation led to a reduction in TAMs, but the number of immature myeloid cells with myeloid-derived suppressor cell (MDSC) characteristics was increased. In addition, ZA affects the phenotype of macrophages leading to reduced level of TAM-associated cytokines in the tumour microenvironment. No improvement of survival was observed.
Conclusion:
We conclude that ZA leads to a reduction in macrophages and impairs polarisation towards an M2 phenotype, but this was associated with an increase in the number of immature myeloid cells, which might diminish the effects of ZA on survival.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20664588</pmid><doi>10.1038/sj.bjc.6605814</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British journal of cancer, 2010-08, Vol.103 (5), p.629-641 |
| issn | 0007-0920 1532-1827 |
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| source | MEDLINE; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; SpringerLink Journals - AutoHoldings |
| subjects | 631/136/142 631/154/436/2388 692/698/690/292 692/699/67/1641 Acids Angiogenesis Animals Antineoplastic Agents - pharmacology Biological and medical sciences Biomedical and Life Sciences Biomedicine Bisphosphonates Cancer Research Cell Count Cell Differentiation - drug effects Cell Survival - drug effects Chemokines Cytokines - biosynthesis Diphosphonates - pharmacology Disease Drug Resistance Epidemiology Genotype & phenotype Imidazoles - pharmacology Macrophages - drug effects Medical prognosis Medical research Medical sciences Mesothelioma Mesothelioma - immunology Mesothelioma - pathology Metastasis Mice Molecular Medicine Myeloid Cells - drug effects Oncology Pathogens Phenotype Translational Therapeutics Tumors |
| title | Zoledronic acid impairs myeloid differentiation to tumour-associated macrophages in mesothelioma |
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