We are analyzing https://link.springer.com/article/10.1186/s12967-015-0567-0.

Title:
Improved Natural Killer cell activity and retained anti-tumor CD8+ T cell responses contribute to the induction of a pathological complete response in HER2-positive breast cancer patients undergoing neoadjuvant chemotherapy | Journal of Translational Medicine
Description:
Background Locally advanced HER2-overexpressing breast cancer (BC) patients achieve a high rate of pathological complete responses (pCR) after neoadjuvant chemotherapy (NC). The apparently unaltered immune proficiency of these patients together with the immune-modulating activities of NC drugs suggest a potential contribution of host immunity in mediating clinical responses. We thus performed an extensive immunomonitoring in locally advanced BC patients undergoing NC to identify immunological correlates of pCR induction. Methods The immune profile of 40 HER2-positive and 38 HER2-negative BC patients was characterized at diagnosis and throughout NC (Paclitaxel and Trastuzumab, or Docetaxel and Epirubicin, respectively). The percentages of circulating immune cell subsets including T and B lymphocytes, Natural Killer (NK) cells, regulatory T cells, T helper 17 lymphocytes, were quantified by multiparametric flow cytometry. NK cells functional activity was evaluated through the analysis of NF-kB nuclear translocation by Multispectral flow cytometry, and with the in vitro monitoring of Trastuzumab-mediated antibody-dependent cell cytotoxicity (ADCC). CD8+ T cell responses against six different tumor-associated antigens (TAA) were characterized by IFN-γ ELISPOT and IFN-γ/IL-2 DualSpot assays. Results After NC, HER2-positive patients showed a significant increase in the number of NK cells and regulatory T cells irrespective of the pathological response, whereas patients undergoing a pCR disclosed higher percentages of T helper 17 cells. Notably, a significant increase in the number of activated NK cells was observed only in HER2-positive patients achieving a pCR. Characterization of anti-tumor T cell responses highlighted sustained levels of CD8+ T cells specific for survivin and mammaglobin-A throughout NC in patients undergoing a pCR in both arms. Moreover, HER2-positive patients achieving a pCR were characterized by a multi-epitopic and polyfunctional anti-tumor T cell response, markedly reduced in case of partial response. Conclusions These results indicate that maintenance of functional T cell responses against selected antigens and improvement of NK cell proficiency during NC are probably critical requirements for pCR induction, especially in HER2-positive BC patients. Trail registration: Trial registration number: NCT02307227, registered on ClinicalTrials.gov ( http://www.clinicaltrials.gov , November 26, 2014).
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Keywords {🔍}

cells, patients, cancer, pcr, cell, response, herpositive, pubmed, article, responses, breast, immune, google, scholar, partial, hernegative, cas, treatment, pathological, diagnosis, complete, trastuzumab, antitumor, adcc, analysis, chemotherapy, responders, neoadjuvant, tumor, figure, number, increase, data, nuclear, elispot, central, undergoing, higher, observed, achieving, therapy, ppr, immunity, clinical, performed, circulating, compared, lymphocytes, ifnγ, showed,

Topics {✒️}

cd3+cd4+cd25+cd127−/lowfoxp3+ treg cells hla-a2-restricted mammaglobin-a-derived epitopes her2/neu-overexpressing breast cancer anti-her2/neu antibody depends ifn-γ/il-2 dualspot assays ifn-γ/il-2 elispot assay taa-specific t-cell responses cd3+cd4+il17+ th17 cells human ifn-γ elispot article download pdf her2-positive breast cancer ccr7+cd45ra− central memory cd3−cd16+cd56+ nk cells α-nf-κb p65 fitc retained t-cell responses nf-kb nuclear translocation spontaneous t-cell responses ifn-γ elispot assays her2-overexpressing malignancy disclosed helper cell profiles nf-κb transcription factor ed-treated her2-negative patients anti-cd137 mab therapy computer-assisted elispot reader her2/neu kif369-377 kifgslafl her2/neu clt789-797 cltstvqlv her2/neu vlv851-859 vlvkspnhv cmv-ebv-flu-derived peptides cancer-related immune suppression nf-κb nuclear translocation her2/neu elv971-979 elvsefsrm ifn-γ elispot assay α-cd127 pe-cy5 cancer immunotherapy cd8-positive neoadjuvant anti-her2 antibodies antibody-dependent cell cytotoxicity her2-positive patients showing human breast cancer her2-positive patient achieving fluorescent-conjugated monoclonal antibodies her2-positive arm revealed nf-κb nuclear localization her2-overexpressing tumors achieving her2-overexpressing cancers her2-positive patients reaching her2-positive patients undergoing anti-tumor adaptive immunity her2-positive patients disclosed bcl-xl ria165-174 riaawmatyl stimulating her2-specific cytotoxic

Questions {❓}

Criscitiello C, Esposito A, Gelao L, Fumagalli L, Locatelli M, Minchella I et al (2014) Immune approaches to the treatment of breast cancer, around the corner?

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WebPage:
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         headline:Improved Natural Killer cell activity and retained anti-tumor CD8+ T cell responses contribute to the induction of a pathological complete response in HER2-positive breast cancer patients undergoing neoadjuvant chemotherapy
         description:Locally advanced HER2-overexpressing breast cancer (BC) patients achieve a high rate of pathological complete responses (pCR) after neoadjuvant chemotherapy (NC). The apparently unaltered immune proficiency of these patients together with the immune-modulating activities of NC drugs suggest a potential contribution of host immunity in mediating clinical responses. We thus performed an extensive immunomonitoring in locally advanced BC patients undergoing NC to identify immunological correlates of pCR induction. The immune profile of 40 HER2-positive and 38 HER2-negative BC patients was characterized at diagnosis and throughout NC (Paclitaxel and Trastuzumab, or Docetaxel and Epirubicin, respectively). The percentages of circulating immune cell subsets including T and B lymphocytes, Natural Killer (NK) cells, regulatory T cells, T helper 17 lymphocytes, were quantified by multiparametric flow cytometry. NK cells functional activity was evaluated through the analysis of NF-kB nuclear translocation by Multispectral flow cytometry, and with the in vitro monitoring of Trastuzumab-mediated antibody-dependent cell cytotoxicity (ADCC). CD8+ T cell responses against six different tumor-associated antigens (TAA) were characterized by IFN-γ ELISPOT and IFN-γ/IL-2 DualSpot assays. After NC, HER2-positive patients showed a significant increase in the number of NK cells and regulatory T cells irrespective of the pathological response, whereas patients undergoing a pCR disclosed higher percentages of T helper 17 cells. Notably, a significant increase in the number of activated NK cells was observed only in HER2-positive patients achieving a pCR. Characterization of anti-tumor T cell responses highlighted sustained levels of CD8+ T cells specific for survivin and mammaglobin-A throughout NC in patients undergoing a pCR in both arms. Moreover, HER2-positive patients achieving a pCR were characterized by a multi-epitopic and polyfunctional anti-tumor T cell response, markedly reduced in case of partial response. These results indicate that maintenance of functional T cell responses against selected antigens and improvement of NK cell proficiency during NC are probably critical requirements for pCR induction, especially in HER2-positive BC patients. Trail registration: Trial registration number: NCT02307227, registered on ClinicalTrials.gov ( http://www.clinicaltrials.gov , November 26, 2014).
         datePublished:2015-06-27T00:00:00Z
         dateModified:2015-06-27T00:00:00Z
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            Breast cancer
            Neoadjuvant chemotherapy
            Antitumor immunity
            CD8+ T lymphocytes
            NK cells
            Immunomonitoring
            Polyfunctional T cell responses
            Th17 cells
            HER2-overexpression
            Pathological complete response
            Biomedicine
            general
            Medicine/Public Health
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      headline:Improved Natural Killer cell activity and retained anti-tumor CD8+ T cell responses contribute to the induction of a pathological complete response in HER2-positive breast cancer patients undergoing neoadjuvant chemotherapy
      description:Locally advanced HER2-overexpressing breast cancer (BC) patients achieve a high rate of pathological complete responses (pCR) after neoadjuvant chemotherapy (NC). The apparently unaltered immune proficiency of these patients together with the immune-modulating activities of NC drugs suggest a potential contribution of host immunity in mediating clinical responses. We thus performed an extensive immunomonitoring in locally advanced BC patients undergoing NC to identify immunological correlates of pCR induction. The immune profile of 40 HER2-positive and 38 HER2-negative BC patients was characterized at diagnosis and throughout NC (Paclitaxel and Trastuzumab, or Docetaxel and Epirubicin, respectively). The percentages of circulating immune cell subsets including T and B lymphocytes, Natural Killer (NK) cells, regulatory T cells, T helper 17 lymphocytes, were quantified by multiparametric flow cytometry. NK cells functional activity was evaluated through the analysis of NF-kB nuclear translocation by Multispectral flow cytometry, and with the in vitro monitoring of Trastuzumab-mediated antibody-dependent cell cytotoxicity (ADCC). CD8+ T cell responses against six different tumor-associated antigens (TAA) were characterized by IFN-γ ELISPOT and IFN-γ/IL-2 DualSpot assays. After NC, HER2-positive patients showed a significant increase in the number of NK cells and regulatory T cells irrespective of the pathological response, whereas patients undergoing a pCR disclosed higher percentages of T helper 17 cells. Notably, a significant increase in the number of activated NK cells was observed only in HER2-positive patients achieving a pCR. Characterization of anti-tumor T cell responses highlighted sustained levels of CD8+ T cells specific for survivin and mammaglobin-A throughout NC in patients undergoing a pCR in both arms. Moreover, HER2-positive patients achieving a pCR were characterized by a multi-epitopic and polyfunctional anti-tumor T cell response, markedly reduced in case of partial response. These results indicate that maintenance of functional T cell responses against selected antigens and improvement of NK cell proficiency during NC are probably critical requirements for pCR induction, especially in HER2-positive BC patients. Trail registration: Trial registration number: NCT02307227, registered on ClinicalTrials.gov ( http://www.clinicaltrials.gov , November 26, 2014).
      datePublished:2015-06-27T00:00:00Z
      dateModified:2015-06-27T00:00:00Z
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      keywords:
         Breast cancer
         Neoadjuvant chemotherapy
         Antitumor immunity
         CD8+ T lymphocytes
         NK cells
         Immunomonitoring
         Polyfunctional T cell responses
         Th17 cells
         HER2-overexpression
         Pathological complete response
         Biomedicine
         general
         Medicine/Public Health
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                     type:PostalAddress
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                  name:CRO Aviano, IRCCS, National Cancer Institute
                  address:
                     name:Scientific Direction, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
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                  name:CRO Aviano, IRCCS, National Cancer Institute
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                     name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
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                  name:CRO Aviano, IRCCS, National Cancer Institute
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                     name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
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                  name:CRO Aviano, IRCCS, National Cancer Institute
                  address:
                     name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
                     type:PostalAddress
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                  name:CRO Aviano, IRCCS, National Cancer Institute
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                  name:CRO Aviano, IRCCS, National Cancer Institute
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                  name:CRO Aviano, IRCCS, National Cancer Institute
                  address:
                     name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
                     type:PostalAddress
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               name:Cancer Bio-Immunotherapy Unit, Department of Translational Research, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
               type:PostalAddress
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               name:Unit of Epidemiology and Biostatistics, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
               type:PostalAddress
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            name:CRO Aviano, IRCCS, National Cancer Institute
            address:
               name:Scientific Direction, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
               type:PostalAddress
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      name:G Miolo
      affiliation:
            name:CRO Aviano, IRCCS, National Cancer Institute
            address:
               name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
               type:PostalAddress
            type:Organization
      name:S Scalone
      affiliation:
            name:CRO Aviano, IRCCS, National Cancer Institute
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      name:L Militello
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            address:
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      name:D Lombardi
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            address:
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      name:S Spazzapan
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            name:CRO Aviano, IRCCS, National Cancer Institute
            address:
               name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
               type:PostalAddress
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      name:T Perin
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            name:CRO Aviano, IRCCS, National Cancer Institute
            address:
               name:Department of Pathology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
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      name:Riccardo Dolcetti
      affiliation:
            name:CRO Aviano, IRCCS, National Cancer Institute
            address:
               name:Cancer Bio-Immunotherapy Unit, Department of Translational Research, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:D Martorelli
      affiliation:
            name:CRO Aviano, IRCCS, National Cancer Institute
            address:
               name:Cancer Bio-Immunotherapy Unit, Department of Translational Research, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Cancer Bio-Immunotherapy Unit, Department of Translational Research, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Cancer Bio-Immunotherapy Unit, Department of Translational Research, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Unit of Epidemiology and Biostatistics, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Scientific Direction, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Department of Pathology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Division of Breast Surgical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Department of Medical Oncology, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Cancer Bio-Immunotherapy Unit, Department of Translational Research, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy
      name:Cancer Bio-Immunotherapy Unit, Department of Translational Research, CRO Aviano, IRCCS, National Cancer Institute, Aviano, Italy

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