Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer
Prolactin (PRL) has been reported to inhibit apoptosis in various cell types and to serve as a cofactor in the upregulation of CD25 on T cells during activation. We investigated a possible relation between prolactin receptor (PRL-R) or IL-2 receptor alpha (IL-2R α , CD25) expression on circulating T...
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| Veröffentlicht in: | British journal of cancer 2003-04, Vol.88 (8), p.1301-1309 |
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| creator | Bauernhofer, T Kuss, I Friebe-Hoffmann, U Baum, A S Dworacki, G Vonderhaar, B K Whiteside, T L |
| description | Prolactin (PRL) has been reported to inhibit apoptosis in various cell types and to serve as a cofactor in the upregulation of CD25 on T cells during activation. We investigated a possible relation between prolactin receptor (PRL-R) or IL-2 receptor alpha (IL-2R
α
, CD25) expression on circulating T lymphocytes and their apoptosis in patients with breast cancer. Peripheral blood mononuclear cells obtained from 25 patients, 25 normal controls (NC) and three cord blood samples were evaluated for Annexin V binding and expression of CD95, CD25, and PRL-R on CD3
+
T cells by multicolour flow cytometry. Plasma levels of PRL, sCD95L, and sIL-2R were determined in patients and controls and related to T-cell apoptosis. The ability of PRL to protect T cells from apoptosis induced by various agents was also studied. Expression of PRL-R on the surface of T cells was comparable in patients with breast cancer and NC, but PRL plasma levels in patients were significantly lower (
P |
| doi_str_mv | 10.1038/sj.bjc.6600860 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2747567</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>984016441</sourcerecordid><originalsourceid>FETCH-LOGICAL-c505t-5b534e046d57ba8191e3d9b2724d1f31a9b4dcea00b3d58905d7ac1308476c243</originalsourceid><addsrcrecordid>eNp1kcGL1DAUxoMo7rh69aaEBb119iVpmvayIKPuCguCrOeQpulMS5vUJHUZ8I8349QdFTyF5Pu9772XD6GXBNYEWHkZ-nXd63VRAJQFPEIrwhnNSEnFY7QCAJFBReEMPQuhT9cKSvEUnRFaVCUFWKEfX9xgsGvx5N2gdOws9kabKTqPlW3w5j3lOD0mOZokO3uAdef1PKhEb_EdHvbjtHN6H03ArXcjVpNLBqELvyoTZmwM-L6LO1x7o0LEWllt_HP0pFVDMC-W8xx9_fjhbnOT3X6-_rR5d5tpDjxmvOYsN5AXDRe1KklFDGuqmgqaN6RlRFV13mijAGrW8LIC3gilCYMyF4WmOTtHV0ffaa5Hk1AbvRrk5LtR-b10qpN_K7bbya37LqnIBS9EMni7GHj3bTYhyrEL2gyDssbNQQpGKi7IodPFP2DvZm_TcpKy9P-MVZCg9RHS3oXgTfswCQF5SFWGXqZU5ZJqKnj95_wnfIkxAW8WQAWthtan7-3CiUtb5JSzxF0euZAkuzX-NN5_W786VlgVZ28eLH_rPwEXn8an</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>230003390</pqid></control><display><type>article</type><title>Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer</title><source>MEDLINE</source><source>Nature</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Bauernhofer, T ; Kuss, I ; Friebe-Hoffmann, U ; Baum, A S ; Dworacki, G ; Vonderhaar, B K ; Whiteside, T L</creator><creatorcontrib>Bauernhofer, T ; Kuss, I ; Friebe-Hoffmann, U ; Baum, A S ; Dworacki, G ; Vonderhaar, B K ; Whiteside, T L</creatorcontrib><description>Prolactin (PRL) has been reported to inhibit apoptosis in various cell types and to serve as a cofactor in the upregulation of CD25 on T cells during activation. We investigated a possible relation between prolactin receptor (PRL-R) or IL-2 receptor alpha (IL-2R
α
, CD25) expression on circulating T lymphocytes and their apoptosis in patients with breast cancer. Peripheral blood mononuclear cells obtained from 25 patients, 25 normal controls (NC) and three cord blood samples were evaluated for Annexin V binding and expression of CD95, CD25, and PRL-R on CD3
+
T cells by multicolour flow cytometry. Plasma levels of PRL, sCD95L, and sIL-2R were determined in patients and controls and related to T-cell apoptosis. The ability of PRL to protect T cells from apoptosis induced by various agents was also studied. Expression of PRL-R on the surface of T cells was comparable in patients with breast cancer and NC, but PRL plasma levels in patients were significantly lower (
P
<0.05). In patients, 18±11% (mean±s.d.) of CD3
+
cells bound Annexin V, compared to 9±6% in NC (
P
<0.0004). Percentages of CD3
+
Fas
+
and CD3
+
CD25
+
cells were higher in the peripheral circulation of patients than NC (
P
<0.0001 and <0.04, respectively). Levels of sFasL were lowest in plasma of the patients with the highest proportions of CD3
+
Fas
+
T cells. Most T cells undergoing apoptosis were CD3
+
CD25
−
in patients, and the proportion of CD3
+
CD25
−
Annexin V
+
cells was significantly increased in patients compared to NC (
P
<0.006).
Ex vivo
PRL protected T cells from starvation-induced or anti-CD3Ab-induced but not from Fas/FasL-dependent apoptosis. These results indicate that expression of CD25 but not of PRL-R on the surface of activated T lymphocytes appears to be involved in modulating Fas/Fas – ligand interactions, which are, in part, responsible for apoptosis of T lymphocytes and excessive turnover of immune cells in the circulation of patients with breast cancer.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6600860</identifier><identifier>PMID: 12698200</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Aged ; Antigens, CD - immunology ; Apoptosis ; Apoptosis - immunology ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Breast Neoplasms - immunology ; Breast Neoplasms - pathology ; Cancer Research ; Cytokines ; Drug Resistance ; Epidemiology ; Experimental Therapeutics ; fas Receptor - immunology ; Female ; Fetal Blood ; Gynecology. Andrology. Obstetrics ; Humans ; Immune system ; Jurkat Cells ; Lymphocytes ; Mammary gland diseases ; Medical research ; Medical sciences ; Middle Aged ; Molecular Medicine ; Neoplasm Staging ; Oncology ; Receptors, Interleukin-2 - immunology ; Receptors, Prolactin - physiology ; Reference Values ; T-Lymphocytes - immunology ; Tumors</subject><ispartof>British journal of cancer, 2003-04, Vol.88 (8), p.1301-1309</ispartof><rights>The Author(s) 2003</rights><rights>2003 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 22, 2003</rights><rights>Copyright © 2003 Cancer Research UK 2003 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-5b534e046d57ba8191e3d9b2724d1f31a9b4dcea00b3d58905d7ac1308476c243</citedby><cites>FETCH-LOGICAL-c505t-5b534e046d57ba8191e3d9b2724d1f31a9b4dcea00b3d58905d7ac1308476c243</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/PMC2747567/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747567/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,2727,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14754253$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12698200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bauernhofer, T</creatorcontrib><creatorcontrib>Kuss, I</creatorcontrib><creatorcontrib>Friebe-Hoffmann, U</creatorcontrib><creatorcontrib>Baum, A S</creatorcontrib><creatorcontrib>Dworacki, G</creatorcontrib><creatorcontrib>Vonderhaar, B K</creatorcontrib><creatorcontrib>Whiteside, T L</creatorcontrib><title>Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Prolactin (PRL) has been reported to inhibit apoptosis in various cell types and to serve as a cofactor in the upregulation of CD25 on T cells during activation. We investigated a possible relation between prolactin receptor (PRL-R) or IL-2 receptor alpha (IL-2R
α
, CD25) expression on circulating T lymphocytes and their apoptosis in patients with breast cancer. Peripheral blood mononuclear cells obtained from 25 patients, 25 normal controls (NC) and three cord blood samples were evaluated for Annexin V binding and expression of CD95, CD25, and PRL-R on CD3
+
T cells by multicolour flow cytometry. Plasma levels of PRL, sCD95L, and sIL-2R were determined in patients and controls and related to T-cell apoptosis. The ability of PRL to protect T cells from apoptosis induced by various agents was also studied. Expression of PRL-R on the surface of T cells was comparable in patients with breast cancer and NC, but PRL plasma levels in patients were significantly lower (
P
<0.05). In patients, 18±11% (mean±s.d.) of CD3
+
cells bound Annexin V, compared to 9±6% in NC (
P
<0.0004). Percentages of CD3
+
Fas
+
and CD3
+
CD25
+
cells were higher in the peripheral circulation of patients than NC (
P
<0.0001 and <0.04, respectively). Levels of sFasL were lowest in plasma of the patients with the highest proportions of CD3
+
Fas
+
T cells. Most T cells undergoing apoptosis were CD3
+
CD25
−
in patients, and the proportion of CD3
+
CD25
−
Annexin V
+
cells was significantly increased in patients compared to NC (
P
<0.006).
Ex vivo
PRL protected T cells from starvation-induced or anti-CD3Ab-induced but not from Fas/FasL-dependent apoptosis. These results indicate that expression of CD25 but not of PRL-R on the surface of activated T lymphocytes appears to be involved in modulating Fas/Fas – ligand interactions, which are, in part, responsible for apoptosis of T lymphocytes and excessive turnover of immune cells in the circulation of patients with breast cancer.</description><subject>Aged</subject><subject>Antigens, CD - immunology</subject><subject>Apoptosis</subject><subject>Apoptosis - immunology</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - immunology</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Cytokines</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Experimental Therapeutics</subject><subject>fas Receptor - immunology</subject><subject>Female</subject><subject>Fetal Blood</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immune system</subject><subject>Jurkat Cells</subject><subject>Lymphocytes</subject><subject>Mammary gland diseases</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Molecular Medicine</subject><subject>Neoplasm Staging</subject><subject>Oncology</subject><subject>Receptors, Interleukin-2 - immunology</subject><subject>Receptors, Prolactin - physiology</subject><subject>Reference Values</subject><subject>T-Lymphocytes - immunology</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kcGL1DAUxoMo7rh69aaEBb119iVpmvayIKPuCguCrOeQpulMS5vUJHUZ8I8349QdFTyF5Pu9772XD6GXBNYEWHkZ-nXd63VRAJQFPEIrwhnNSEnFY7QCAJFBReEMPQuhT9cKSvEUnRFaVCUFWKEfX9xgsGvx5N2gdOws9kabKTqPlW3w5j3lOD0mOZokO3uAdef1PKhEb_EdHvbjtHN6H03ArXcjVpNLBqELvyoTZmwM-L6LO1x7o0LEWllt_HP0pFVDMC-W8xx9_fjhbnOT3X6-_rR5d5tpDjxmvOYsN5AXDRe1KklFDGuqmgqaN6RlRFV13mijAGrW8LIC3gilCYMyF4WmOTtHV0ffaa5Hk1AbvRrk5LtR-b10qpN_K7bbya37LqnIBS9EMni7GHj3bTYhyrEL2gyDssbNQQpGKi7IodPFP2DvZm_TcpKy9P-MVZCg9RHS3oXgTfswCQF5SFWGXqZU5ZJqKnj95_wnfIkxAW8WQAWthtan7-3CiUtb5JSzxF0euZAkuzX-NN5_W786VlgVZ28eLH_rPwEXn8an</recordid><startdate>20030422</startdate><enddate>20030422</enddate><creator>Bauernhofer, T</creator><creator>Kuss, I</creator><creator>Friebe-Hoffmann, U</creator><creator>Baum, A S</creator><creator>Dworacki, G</creator><creator>Vonderhaar, B K</creator><creator>Whiteside, T L</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>20030422</creationdate><title>Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer</title><author>Bauernhofer, T ; Kuss, I ; Friebe-Hoffmann, U ; Baum, A S ; Dworacki, G ; Vonderhaar, B K ; Whiteside, T L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-5b534e046d57ba8191e3d9b2724d1f31a9b4dcea00b3d58905d7ac1308476c243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Aged</topic><topic>Antigens, CD - immunology</topic><topic>Apoptosis</topic><topic>Apoptosis - immunology</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - immunology</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Cytokines</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Experimental Therapeutics</topic><topic>fas Receptor - immunology</topic><topic>Female</topic><topic>Fetal Blood</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Immune system</topic><topic>Jurkat Cells</topic><topic>Lymphocytes</topic><topic>Mammary gland diseases</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Molecular Medicine</topic><topic>Neoplasm Staging</topic><topic>Oncology</topic><topic>Receptors, Interleukin-2 - immunology</topic><topic>Receptors, Prolactin - physiology</topic><topic>Reference Values</topic><topic>T-Lymphocytes - immunology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bauernhofer, T</creatorcontrib><creatorcontrib>Kuss, I</creatorcontrib><creatorcontrib>Friebe-Hoffmann, U</creatorcontrib><creatorcontrib>Baum, A S</creatorcontrib><creatorcontrib>Dworacki, G</creatorcontrib><creatorcontrib>Vonderhaar, B K</creatorcontrib><creatorcontrib>Whiteside, T L</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>Proquest Nursing & Allied Health Source</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>Bauernhofer, T</au><au>Kuss, I</au><au>Friebe-Hoffmann, U</au><au>Baum, A S</au><au>Dworacki, G</au><au>Vonderhaar, B K</au><au>Whiteside, T L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2003-04-22</date><risdate>2003</risdate><volume>88</volume><issue>8</issue><spage>1301</spage><epage>1309</epage><pages>1301-1309</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Prolactin (PRL) has been reported to inhibit apoptosis in various cell types and to serve as a cofactor in the upregulation of CD25 on T cells during activation. We investigated a possible relation between prolactin receptor (PRL-R) or IL-2 receptor alpha (IL-2R
α
, CD25) expression on circulating T lymphocytes and their apoptosis in patients with breast cancer. Peripheral blood mononuclear cells obtained from 25 patients, 25 normal controls (NC) and three cord blood samples were evaluated for Annexin V binding and expression of CD95, CD25, and PRL-R on CD3
+
T cells by multicolour flow cytometry. Plasma levels of PRL, sCD95L, and sIL-2R were determined in patients and controls and related to T-cell apoptosis. The ability of PRL to protect T cells from apoptosis induced by various agents was also studied. Expression of PRL-R on the surface of T cells was comparable in patients with breast cancer and NC, but PRL plasma levels in patients were significantly lower (
P
<0.05). In patients, 18±11% (mean±s.d.) of CD3
+
cells bound Annexin V, compared to 9±6% in NC (
P
<0.0004). Percentages of CD3
+
Fas
+
and CD3
+
CD25
+
cells were higher in the peripheral circulation of patients than NC (
P
<0.0001 and <0.04, respectively). Levels of sFasL were lowest in plasma of the patients with the highest proportions of CD3
+
Fas
+
T cells. Most T cells undergoing apoptosis were CD3
+
CD25
−
in patients, and the proportion of CD3
+
CD25
−
Annexin V
+
cells was significantly increased in patients compared to NC (
P
<0.006).
Ex vivo
PRL protected T cells from starvation-induced or anti-CD3Ab-induced but not from Fas/FasL-dependent apoptosis. These results indicate that expression of CD25 but not of PRL-R on the surface of activated T lymphocytes appears to be involved in modulating Fas/Fas – ligand interactions, which are, in part, responsible for apoptosis of T lymphocytes and excessive turnover of immune cells in the circulation of patients with breast cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>12698200</pmid><doi>10.1038/sj.bjc.6600860</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Aged Antigens, CD - immunology Apoptosis Apoptosis - immunology Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast cancer Breast Neoplasms - immunology Breast Neoplasms - pathology Cancer Research Cytokines Drug Resistance Epidemiology Experimental Therapeutics fas Receptor - immunology Female Fetal Blood Gynecology. Andrology. Obstetrics Humans Immune system Jurkat Cells Lymphocytes Mammary gland diseases Medical research Medical sciences Middle Aged Molecular Medicine Neoplasm Staging Oncology Receptors, Interleukin-2 - immunology Receptors, Prolactin - physiology Reference Values T-Lymphocytes - immunology Tumors |
| title | Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer |
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