ATM kinase regulates tumor immunoreactions in lymphocyte-predominant breast cancer through modulation of NKG2D ligand and TNF cytokines on tumor cells
To explore impact of Ataxia telangiectasia mutated (ATM) kinase on immunoreactions in lymphocyte-predominant breast cancer (LPBC), particularly its role in triple negative breast cancer (TNBC), 194 cases of LPBC were identified with pertinent clinical information retrieved. The expressions of ATM, a...
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| Veröffentlicht in: | Medical molecular morphology 2020-12, Vol.53 (4), p.210-220 |
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| creator | Xu, Peng Sun, Yuanyuan Song, Yuanming Jiao, Jiao Shen, Beibei Li, Weidong Jiang, Chengying Li, Yaqing Zhang, Xinmin Yu, Jinpu Fu, Li Guo, Xiaojing |
| description | To explore impact of Ataxia telangiectasia mutated (ATM) kinase on immunoreactions in lymphocyte-predominant breast cancer (LPBC), particularly its role in triple negative breast cancer (TNBC), 194 cases of LPBC were identified with pertinent clinical information retrieved. The expressions of ATM, activated ATM (P-ATM), Fas ligand (FASL), tumor necrosis factor-related apoptosis-induced ligand (TRAIL), major histocompatibility complex class I chain-related protein A (MICA), CD8, and Forkhead box P3 (FOXP3) were assessed by immunohistochemically. We found that ATM expressed on tumor cells was correlated with upregulated expression of P-ATM and MICA (
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| doi_str_mv | 10.1007/s00795-020-00247-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2357459476</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2473786020</sourcerecordid><originalsourceid>FETCH-LOGICAL-c399t-84acb1a2578173276bf98e2baf97f21671745e53d9e874cad804954c904ca5c33</originalsourceid><addsrcrecordid>eNp9kctu3CAUhlHVqrm0L9BFhNRNN065GGOWUdpclDTdTNcIYzzjxMAE8GJepM-bM3WaSF10wU18__8fOAh9ouSUEiK_ZpiUqAgjFSGslpV4gw5p25CK1kq9fdm35AAd5XxPCJcNE-_RAWekkZTSQ_T7bPUDP4zBZIeTW8-TKS7jMvuY8Oj9HGJyxpYxhozHgKed326i3RVXbZProwdlKLgDKBdsTbAu4bJJcV5vsI_93g-0OA747uaSfcPTuDahx_uxurvA4BQhHSIBWlKtm6b8Ab0bzJTdx-f1GP26-L46v6puf15en5_dVpYrVaq2NrajhgnZUsmZbLpBtY51ZlByYBTeKGvhBO-Va2VtTd-SWonaKgIHYTk_Rl8W322Kj7PLRfsx7yswwcU5a8YFOKhaNoB-_ge9j3MKUJ2Gv-cS_poRoNhC2RRzTm7Q2zR6k3aaEr3vml66pgHWf7qmBYhOnq3nzrv-RfK3TQDwBchwFdYuvWb_x_YJvWyj2w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2473786020</pqid></control><display><type>article</type><title>ATM kinase regulates tumor immunoreactions in lymphocyte-predominant breast cancer through modulation of NKG2D ligand and TNF cytokines on tumor cells</title><source>Springer Nature - Complete Springer Journals</source><creator>Xu, Peng ; Sun, Yuanyuan ; Song, Yuanming ; Jiao, Jiao ; Shen, Beibei ; Li, Weidong ; Jiang, Chengying ; Li, Yaqing ; Zhang, Xinmin ; Yu, Jinpu ; Fu, Li ; Guo, Xiaojing</creator><creatorcontrib>Xu, Peng ; Sun, Yuanyuan ; Song, Yuanming ; Jiao, Jiao ; Shen, Beibei ; Li, Weidong ; Jiang, Chengying ; Li, Yaqing ; Zhang, Xinmin ; Yu, Jinpu ; Fu, Li ; Guo, Xiaojing</creatorcontrib><description><![CDATA[To explore impact of Ataxia telangiectasia mutated (ATM) kinase on immunoreactions in lymphocyte-predominant breast cancer (LPBC), particularly its role in triple negative breast cancer (TNBC), 194 cases of LPBC were identified with pertinent clinical information retrieved. The expressions of ATM, activated ATM (P-ATM), Fas ligand (FASL), tumor necrosis factor-related apoptosis-induced ligand (TRAIL), major histocompatibility complex class I chain-related protein A (MICA), CD8, and Forkhead box P3 (FOXP3) were assessed by immunohistochemically. We found that ATM expressed on tumor cells was correlated with upregulated expression of P-ATM and MICA (
P
< 0.05), down-regulated expression of FASL and TRAIL (
P
< 0.01), and decreased Ki-67 tumor labeling (
P
< 0.05). However, within the TNBC group, only a negative correlation with FASL expression was found (
P
= 0.001). ATM and MICA expressions were significantly down -regulated in TNBC (
P
< 0.01) compared to non-TNBC, while TRAIL was significantly upregulated (
P
< 0.01). Tregs were increased in TNBC (
P
< 0.05), with CD8 + TILs decreased (
P
< 0.01). Ki-67 index was higher in TNBC than in non-TNBC (
P
< 0.01). ATM may play an important role in immunoreaction of LPBC, probably through upregulation of MICA and down-regulation of FASL and TRAIL. The down-regulated ATM expression in TNBC might be responsible for impaired tumor immunoactivity, rapid tumor growth, and aggressive clinical course.]]></description><identifier>ISSN: 1860-1480</identifier><identifier>EISSN: 1860-1499</identifier><identifier>DOI: 10.1007/s00795-020-00247-5</identifier><identifier>PMID: 32067111</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Anatomy ; Apoptosis ; Ataxia telangiectasia ; Ataxia telangiectasia mutated protein ; Breast cancer ; CD8 antigen ; FasL protein ; Forkhead protein ; Foxp3 protein ; Information processing ; Ligands ; Lymphocytes ; Major histocompatibility complex ; Medicine ; Medicine & Public Health ; Molecular Medicine ; Original Paper ; Pathology ; TRAIL protein ; Tumor cells ; Tumor necrosis factor ; Tumor necrosis factor-TNF</subject><ispartof>Medical molecular morphology, 2020-12, Vol.53 (4), p.210-220</ispartof><rights>The Japanese Society for Clinical Molecular Morphology 2020</rights><rights>The Japanese Society for Clinical Molecular Morphology 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-84acb1a2578173276bf98e2baf97f21671745e53d9e874cad804954c904ca5c33</citedby><cites>FETCH-LOGICAL-c399t-84acb1a2578173276bf98e2baf97f21671745e53d9e874cad804954c904ca5c33</cites><orcidid>0000-0003-3753-2900</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00795-020-00247-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00795-020-00247-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32067111$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Peng</creatorcontrib><creatorcontrib>Sun, Yuanyuan</creatorcontrib><creatorcontrib>Song, Yuanming</creatorcontrib><creatorcontrib>Jiao, Jiao</creatorcontrib><creatorcontrib>Shen, Beibei</creatorcontrib><creatorcontrib>Li, Weidong</creatorcontrib><creatorcontrib>Jiang, Chengying</creatorcontrib><creatorcontrib>Li, Yaqing</creatorcontrib><creatorcontrib>Zhang, Xinmin</creatorcontrib><creatorcontrib>Yu, Jinpu</creatorcontrib><creatorcontrib>Fu, Li</creatorcontrib><creatorcontrib>Guo, Xiaojing</creatorcontrib><title>ATM kinase regulates tumor immunoreactions in lymphocyte-predominant breast cancer through modulation of NKG2D ligand and TNF cytokines on tumor cells</title><title>Medical molecular morphology</title><addtitle>Med Mol Morphol</addtitle><addtitle>Med Mol Morphol</addtitle><description><![CDATA[To explore impact of Ataxia telangiectasia mutated (ATM) kinase on immunoreactions in lymphocyte-predominant breast cancer (LPBC), particularly its role in triple negative breast cancer (TNBC), 194 cases of LPBC were identified with pertinent clinical information retrieved. The expressions of ATM, activated ATM (P-ATM), Fas ligand (FASL), tumor necrosis factor-related apoptosis-induced ligand (TRAIL), major histocompatibility complex class I chain-related protein A (MICA), CD8, and Forkhead box P3 (FOXP3) were assessed by immunohistochemically. We found that ATM expressed on tumor cells was correlated with upregulated expression of P-ATM and MICA (
P
< 0.05), down-regulated expression of FASL and TRAIL (
P
< 0.01), and decreased Ki-67 tumor labeling (
P
< 0.05). However, within the TNBC group, only a negative correlation with FASL expression was found (
P
= 0.001). ATM and MICA expressions were significantly down -regulated in TNBC (
P
< 0.01) compared to non-TNBC, while TRAIL was significantly upregulated (
P
< 0.01). Tregs were increased in TNBC (
P
< 0.05), with CD8 + TILs decreased (
P
< 0.01). Ki-67 index was higher in TNBC than in non-TNBC (
P
< 0.01). ATM may play an important role in immunoreaction of LPBC, probably through upregulation of MICA and down-regulation of FASL and TRAIL. The down-regulated ATM expression in TNBC might be responsible for impaired tumor immunoactivity, rapid tumor growth, and aggressive clinical course.]]></description><subject>Anatomy</subject><subject>Apoptosis</subject><subject>Ataxia telangiectasia</subject><subject>Ataxia telangiectasia mutated protein</subject><subject>Breast cancer</subject><subject>CD8 antigen</subject><subject>FasL protein</subject><subject>Forkhead protein</subject><subject>Foxp3 protein</subject><subject>Information processing</subject><subject>Ligands</subject><subject>Lymphocytes</subject><subject>Major histocompatibility complex</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular Medicine</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>TRAIL protein</subject><subject>Tumor cells</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><issn>1860-1480</issn><issn>1860-1499</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kctu3CAUhlHVqrm0L9BFhNRNN065GGOWUdpclDTdTNcIYzzjxMAE8GJepM-bM3WaSF10wU18__8fOAh9ouSUEiK_ZpiUqAgjFSGslpV4gw5p25CK1kq9fdm35AAd5XxPCJcNE-_RAWekkZTSQ_T7bPUDP4zBZIeTW8-TKS7jMvuY8Oj9HGJyxpYxhozHgKed326i3RVXbZProwdlKLgDKBdsTbAu4bJJcV5vsI_93g-0OA747uaSfcPTuDahx_uxurvA4BQhHSIBWlKtm6b8Ab0bzJTdx-f1GP26-L46v6puf15en5_dVpYrVaq2NrajhgnZUsmZbLpBtY51ZlByYBTeKGvhBO-Va2VtTd-SWonaKgIHYTk_Rl8W322Kj7PLRfsx7yswwcU5a8YFOKhaNoB-_ge9j3MKUJ2Gv-cS_poRoNhC2RRzTm7Q2zR6k3aaEr3vml66pgHWf7qmBYhOnq3nzrv-RfK3TQDwBchwFdYuvWb_x_YJvWyj2w</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Xu, Peng</creator><creator>Sun, Yuanyuan</creator><creator>Song, Yuanming</creator><creator>Jiao, Jiao</creator><creator>Shen, Beibei</creator><creator>Li, Weidong</creator><creator>Jiang, Chengying</creator><creator>Li, Yaqing</creator><creator>Zhang, Xinmin</creator><creator>Yu, Jinpu</creator><creator>Fu, Li</creator><creator>Guo, Xiaojing</creator><general>Springer Singapore</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3753-2900</orcidid></search><sort><creationdate>20201201</creationdate><title>ATM kinase regulates tumor immunoreactions in lymphocyte-predominant breast cancer through modulation of NKG2D ligand and TNF cytokines on tumor cells</title><author>Xu, Peng ; Sun, Yuanyuan ; Song, Yuanming ; Jiao, Jiao ; Shen, Beibei ; Li, Weidong ; Jiang, Chengying ; Li, Yaqing ; Zhang, Xinmin ; Yu, Jinpu ; Fu, Li ; Guo, Xiaojing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-84acb1a2578173276bf98e2baf97f21671745e53d9e874cad804954c904ca5c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Anatomy</topic><topic>Apoptosis</topic><topic>Ataxia telangiectasia</topic><topic>Ataxia telangiectasia mutated protein</topic><topic>Breast cancer</topic><topic>CD8 antigen</topic><topic>FasL protein</topic><topic>Forkhead protein</topic><topic>Foxp3 protein</topic><topic>Information processing</topic><topic>Ligands</topic><topic>Lymphocytes</topic><topic>Major histocompatibility complex</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular Medicine</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>TRAIL protein</topic><topic>Tumor cells</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Peng</creatorcontrib><creatorcontrib>Sun, Yuanyuan</creatorcontrib><creatorcontrib>Song, Yuanming</creatorcontrib><creatorcontrib>Jiao, Jiao</creatorcontrib><creatorcontrib>Shen, Beibei</creatorcontrib><creatorcontrib>Li, Weidong</creatorcontrib><creatorcontrib>Jiang, Chengying</creatorcontrib><creatorcontrib>Li, Yaqing</creatorcontrib><creatorcontrib>Zhang, Xinmin</creatorcontrib><creatorcontrib>Yu, Jinpu</creatorcontrib><creatorcontrib>Fu, Li</creatorcontrib><creatorcontrib>Guo, Xiaojing</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Medical molecular morphology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Peng</au><au>Sun, Yuanyuan</au><au>Song, Yuanming</au><au>Jiao, Jiao</au><au>Shen, Beibei</au><au>Li, Weidong</au><au>Jiang, Chengying</au><au>Li, Yaqing</au><au>Zhang, Xinmin</au><au>Yu, Jinpu</au><au>Fu, Li</au><au>Guo, Xiaojing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ATM kinase regulates tumor immunoreactions in lymphocyte-predominant breast cancer through modulation of NKG2D ligand and TNF cytokines on tumor cells</atitle><jtitle>Medical molecular morphology</jtitle><stitle>Med Mol Morphol</stitle><addtitle>Med Mol Morphol</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>53</volume><issue>4</issue><spage>210</spage><epage>220</epage><pages>210-220</pages><issn>1860-1480</issn><eissn>1860-1499</eissn><abstract><![CDATA[To explore impact of Ataxia telangiectasia mutated (ATM) kinase on immunoreactions in lymphocyte-predominant breast cancer (LPBC), particularly its role in triple negative breast cancer (TNBC), 194 cases of LPBC were identified with pertinent clinical information retrieved. The expressions of ATM, activated ATM (P-ATM), Fas ligand (FASL), tumor necrosis factor-related apoptosis-induced ligand (TRAIL), major histocompatibility complex class I chain-related protein A (MICA), CD8, and Forkhead box P3 (FOXP3) were assessed by immunohistochemically. We found that ATM expressed on tumor cells was correlated with upregulated expression of P-ATM and MICA (
P
< 0.05), down-regulated expression of FASL and TRAIL (
P
< 0.01), and decreased Ki-67 tumor labeling (
P
< 0.05). However, within the TNBC group, only a negative correlation with FASL expression was found (
P
= 0.001). ATM and MICA expressions were significantly down -regulated in TNBC (
P
< 0.01) compared to non-TNBC, while TRAIL was significantly upregulated (
P
< 0.01). Tregs were increased in TNBC (
P
< 0.05), with CD8 + TILs decreased (
P
< 0.01). Ki-67 index was higher in TNBC than in non-TNBC (
P
< 0.01). ATM may play an important role in immunoreaction of LPBC, probably through upregulation of MICA and down-regulation of FASL and TRAIL. The down-regulated ATM expression in TNBC might be responsible for impaired tumor immunoactivity, rapid tumor growth, and aggressive clinical course.]]></abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>32067111</pmid><doi>10.1007/s00795-020-00247-5</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-3753-2900</orcidid></addata></record> |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Anatomy Apoptosis Ataxia telangiectasia Ataxia telangiectasia mutated protein Breast cancer CD8 antigen FasL protein Forkhead protein Foxp3 protein Information processing Ligands Lymphocytes Major histocompatibility complex Medicine Medicine & Public Health Molecular Medicine Original Paper Pathology TRAIL protein Tumor cells Tumor necrosis factor Tumor necrosis factor-TNF |
| title | ATM kinase regulates tumor immunoreactions in lymphocyte-predominant breast cancer through modulation of NKG2D ligand and TNF cytokines on tumor cells |
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