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An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis
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| Zeitschriftentitel: | Cancer Research |
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| Personen und Körperschaften: | , , , , , , , , , , , , , |
| In: | Cancer Research, 75, 2015, 16, S. 3246-3254 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Association for Cancer Research (AACR)
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| Schlagwörter: |
| author_facet |
Katayama, Hiroyuki Boldt, Clayton Ladd, Jon J. Johnson, Melissa M. Chao, Timothy Capello, Michela Suo, Jinfeng Mao, Jianning Manson, JoAnn E. Prentice, Ross Esteva, Francisco Wang, Hong Disis, Mary L. Hanash, Samir Katayama, Hiroyuki Boldt, Clayton Ladd, Jon J. Johnson, Melissa M. Chao, Timothy Capello, Michela Suo, Jinfeng Mao, Jianning Manson, JoAnn E. Prentice, Ross Esteva, Francisco Wang, Hong Disis, Mary L. Hanash, Samir |
|---|---|
| author |
Katayama, Hiroyuki Boldt, Clayton Ladd, Jon J. Johnson, Melissa M. Chao, Timothy Capello, Michela Suo, Jinfeng Mao, Jianning Manson, JoAnn E. Prentice, Ross Esteva, Francisco Wang, Hong Disis, Mary L. Hanash, Samir |
| spellingShingle |
Katayama, Hiroyuki Boldt, Clayton Ladd, Jon J. Johnson, Melissa M. Chao, Timothy Capello, Michela Suo, Jinfeng Mao, Jianning Manson, JoAnn E. Prentice, Ross Esteva, Francisco Wang, Hong Disis, Mary L. Hanash, Samir Cancer Research An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis Cancer Research Oncology |
| author_sort |
katayama, hiroyuki |
| spelling |
Katayama, Hiroyuki Boldt, Clayton Ladd, Jon J. Johnson, Melissa M. Chao, Timothy Capello, Michela Suo, Jinfeng Mao, Jianning Manson, JoAnn E. Prentice, Ross Esteva, Francisco Wang, Hong Disis, Mary L. Hanash, Samir 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-15-0248 <jats:title>Abstract</jats:title> <jats:p>The repertoire of antigens associated with the development of an autoimmune response in breast cancer has relevance to detection and treatment strategies. We have investigated the occurrence of autoantibodies associated with the development of triple-negative breast cancer (TNBC) in the before diagnosis setting and in samples collected at the time of diagnosis of TNBC. Lysate arrays containing protein fractions from the TNBC MDA-MB-231 cell line were hybridized with TNBC plasmas from the Women's Health Initiative cohort, collected before clinical diagnosis and with plasmas from matched controls. An immune response directed against spliceosome and glycolysis proteins was observed with case plasmas as previously reported in estrogen receptor+ breast cancer. Importantly, autoantibodies directed against networks involving BRCA1, TP53, and cytokeratin proteins associated with a mesenchymal/basal phenotype were distinct to TNBC before diagnosis samples. Concordant autoantibody findings were observed with mouse plasma samples collected before occurrence of palpable tumors from a C3(1)-T triple negative mouse model. Plasma samples collected at the time of diagnosis of stage II TNBC and from matched healthy controls were subjected to proteomic analysis by mass spectrometry to identify Ig-bound proteins yielding a predominance of cytokeratins, including several associated with a mesenchymal/basal phenotype among cases compared with controls. Our data provide evidence indicative of a dynamic repertoire of antigens associated with a humoral immune response reflecting disease pathogenesis in TNBC. Cancer Res; 75(16); 3246–54. ©2015 AACR.</jats:p> An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis Cancer Research |
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| title |
An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_unstemmed |
An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_full |
An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_fullStr |
An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_full_unstemmed |
An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_short |
An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_sort |
an autoimmune response signature associated with the development of triple-negative breast cancer reflects disease pathogenesis |
| topic |
Cancer Research Oncology |
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http://dx.doi.org/10.1158/0008-5472.can-15-0248 |
| publishDate |
2015 |
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3246-3254 |
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<jats:title>Abstract</jats:title>
<jats:p>The repertoire of antigens associated with the development of an autoimmune response in breast cancer has relevance to detection and treatment strategies. We have investigated the occurrence of autoantibodies associated with the development of triple-negative breast cancer (TNBC) in the before diagnosis setting and in samples collected at the time of diagnosis of TNBC. Lysate arrays containing protein fractions from the TNBC MDA-MB-231 cell line were hybridized with TNBC plasmas from the Women's Health Initiative cohort, collected before clinical diagnosis and with plasmas from matched controls. An immune response directed against spliceosome and glycolysis proteins was observed with case plasmas as previously reported in estrogen receptor+ breast cancer. Importantly, autoantibodies directed against networks involving BRCA1, TP53, and cytokeratin proteins associated with a mesenchymal/basal phenotype were distinct to TNBC before diagnosis samples. Concordant autoantibody findings were observed with mouse plasma samples collected before occurrence of palpable tumors from a C3(1)-T triple negative mouse model. Plasma samples collected at the time of diagnosis of stage II TNBC and from matched healthy controls were subjected to proteomic analysis by mass spectrometry to identify Ig-bound proteins yielding a predominance of cytokeratins, including several associated with a mesenchymal/basal phenotype among cases compared with controls. Our data provide evidence indicative of a dynamic repertoire of antigens associated with a humoral immune response reflecting disease pathogenesis in TNBC. Cancer Res; 75(16); 3246–54. ©2015 AACR.</jats:p> |
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| author | Katayama, Hiroyuki, Boldt, Clayton, Ladd, Jon J., Johnson, Melissa M., Chao, Timothy, Capello, Michela, Suo, Jinfeng, Mao, Jianning, Manson, JoAnn E., Prentice, Ross, Esteva, Francisco, Wang, Hong, Disis, Mary L., Hanash, Samir |
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| description | <jats:title>Abstract</jats:title> <jats:p>The repertoire of antigens associated with the development of an autoimmune response in breast cancer has relevance to detection and treatment strategies. We have investigated the occurrence of autoantibodies associated with the development of triple-negative breast cancer (TNBC) in the before diagnosis setting and in samples collected at the time of diagnosis of TNBC. Lysate arrays containing protein fractions from the TNBC MDA-MB-231 cell line were hybridized with TNBC plasmas from the Women's Health Initiative cohort, collected before clinical diagnosis and with plasmas from matched controls. An immune response directed against spliceosome and glycolysis proteins was observed with case plasmas as previously reported in estrogen receptor+ breast cancer. Importantly, autoantibodies directed against networks involving BRCA1, TP53, and cytokeratin proteins associated with a mesenchymal/basal phenotype were distinct to TNBC before diagnosis samples. Concordant autoantibody findings were observed with mouse plasma samples collected before occurrence of palpable tumors from a C3(1)-T triple negative mouse model. Plasma samples collected at the time of diagnosis of stage II TNBC and from matched healthy controls were subjected to proteomic analysis by mass spectrometry to identify Ig-bound proteins yielding a predominance of cytokeratins, including several associated with a mesenchymal/basal phenotype among cases compared with controls. Our data provide evidence indicative of a dynamic repertoire of antigens associated with a humoral immune response reflecting disease pathogenesis in TNBC. Cancer Res; 75(16); 3246–54. ©2015 AACR.</jats:p> |
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| spelling | Katayama, Hiroyuki Boldt, Clayton Ladd, Jon J. Johnson, Melissa M. Chao, Timothy Capello, Michela Suo, Jinfeng Mao, Jianning Manson, JoAnn E. Prentice, Ross Esteva, Francisco Wang, Hong Disis, Mary L. Hanash, Samir 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-15-0248 <jats:title>Abstract</jats:title> <jats:p>The repertoire of antigens associated with the development of an autoimmune response in breast cancer has relevance to detection and treatment strategies. We have investigated the occurrence of autoantibodies associated with the development of triple-negative breast cancer (TNBC) in the before diagnosis setting and in samples collected at the time of diagnosis of TNBC. Lysate arrays containing protein fractions from the TNBC MDA-MB-231 cell line were hybridized with TNBC plasmas from the Women's Health Initiative cohort, collected before clinical diagnosis and with plasmas from matched controls. An immune response directed against spliceosome and glycolysis proteins was observed with case plasmas as previously reported in estrogen receptor+ breast cancer. Importantly, autoantibodies directed against networks involving BRCA1, TP53, and cytokeratin proteins associated with a mesenchymal/basal phenotype were distinct to TNBC before diagnosis samples. Concordant autoantibody findings were observed with mouse plasma samples collected before occurrence of palpable tumors from a C3(1)-T triple negative mouse model. Plasma samples collected at the time of diagnosis of stage II TNBC and from matched healthy controls were subjected to proteomic analysis by mass spectrometry to identify Ig-bound proteins yielding a predominance of cytokeratins, including several associated with a mesenchymal/basal phenotype among cases compared with controls. Our data provide evidence indicative of a dynamic repertoire of antigens associated with a humoral immune response reflecting disease pathogenesis in TNBC. Cancer Res; 75(16); 3246–54. ©2015 AACR.</jats:p> An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis Cancer Research |
| spellingShingle | Katayama, Hiroyuki, Boldt, Clayton, Ladd, Jon J., Johnson, Melissa M., Chao, Timothy, Capello, Michela, Suo, Jinfeng, Mao, Jianning, Manson, JoAnn E., Prentice, Ross, Esteva, Francisco, Wang, Hong, Disis, Mary L., Hanash, Samir, Cancer Research, An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis, Cancer Research, Oncology |
| title | An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_full | An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_fullStr | An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_full_unstemmed | An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_short | An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| title_sort | an autoimmune response signature associated with the development of triple-negative breast cancer reflects disease pathogenesis |
| title_unstemmed | An Autoimmune Response Signature Associated with the Development of Triple-Negative Breast Cancer Reflects Disease Pathogenesis |
| topic | Cancer Research, Oncology |
| url | http://dx.doi.org/10.1158/0008-5472.can-15-0248 |