Abstract:We present the case of a 78-year-old male patient who was diagnosed with anaplastic lymphoma kinase (ALK)-negative, CC chemokine receptor 4 (CCR4)-negative, and CD30-positive anaplastic large cell lymphoma (ALCL). The patient had a past medical history of adult T-cell leukemia/lymphoma and colon cancers that had developed simultaneously approximately 2 years prior to the development of ALCL that were treated with immunochemotherapy and resection, respectively. Initial treatment for ALCL included brentuximab ve… Show more
“…Fortunately, the patient achieved CR for ALCL through treatment with romidepsin. The Tax‐specific CTLs were maintained at high percentages during the romidepsin therapy and until the last follow‐up without any relapse of ATLL and ALCL in this patient 41 . These results suggest that mogamulizumab alone is insufficient to induce adequate Tax‐specific CTLs production.…”
Section: Discussionmentioning
confidence: 68%
“…The Tax‐specific CTLs were maintained at high percentages during the romidepsin therapy and until the last follow‐up without any relapse of ATLL and ALCL in this patient. 41 These results suggest that mogamulizumab alone is insufficient to induce adequate Tax‐specific CTLs production. Herpes virus infection has been reported to activate innate and adaptive immune responses, which include the release of inflammatory cytokines and chemokines.…”
Purpose
Adult T‐cell leukemia/lymphoma (ATLL) is a relatively refractory peripheral T‐cell lymphoma caused by human T‐cell lymphotropic virus type 1 (HTLV‐1). The objective of this study was to investigate the characteristics of long‐term survivors with ATLL.
Methods
We conducted an observational study of 75 aggressive‐type ATLL patients. Flow cytometry was conducted to analyze HTLV‐1 Tax‐specific cytotoxic T‐lymphocytes (CTLs) and T‐cell receptor Vβ gene repertoire.
Results
We first evaluated six long‐term survivors among 37 patients who were newly diagnosed with ATLL and then treated with intensive chemotherapy without mogamulizumab, a monoclonal antibody for C‐C chemokine receptor four antigen. Reversal of the CD4‐to‐CD8 ratio (CD4/CD8) in peripheral mononuclear cells was observed in all six patients. Three of these six patients showed reversed CD4/CD8 immediately after herpes virus infection. Four of these six patients who could be examined demonstrated long‐term maintenance of HTLV‐1 Tax‐specific CTLs. We subsequently identified four long‐term survivors among 38 patients who were newly diagnosed with ATLL and then treated with intensive chemotherapy plus mogamulizumab. All four patients showed reversed CD4/CD8, and three of the four patients contracted herpes virus infection during immunochemotherapy. Six of the total 10 patients were subjected to CTL analyses. Tax‐specific CTLs were observed, and the CTLs that were almost entirely composed of memory CTLs in all patients were recorded. HTLV‐1 provirus was also detected in all six patients.
Conclusions
These data suggest that Tax‐specific memory CTLs probably, together with anticancer agents, eradicate ATLL cells and exhibit long‐term preventive effects from relapse ATLL. Thus, the strong activation of cellular immunity, such as herpes virus infection, seems to be necessary to induce such a potent number of Tax‐specific CTLs.
“…Fortunately, the patient achieved CR for ALCL through treatment with romidepsin. The Tax‐specific CTLs were maintained at high percentages during the romidepsin therapy and until the last follow‐up without any relapse of ATLL and ALCL in this patient 41 . These results suggest that mogamulizumab alone is insufficient to induce adequate Tax‐specific CTLs production.…”
Section: Discussionmentioning
confidence: 68%
“…The Tax‐specific CTLs were maintained at high percentages during the romidepsin therapy and until the last follow‐up without any relapse of ATLL and ALCL in this patient. 41 These results suggest that mogamulizumab alone is insufficient to induce adequate Tax‐specific CTLs production. Herpes virus infection has been reported to activate innate and adaptive immune responses, which include the release of inflammatory cytokines and chemokines.…”
Purpose
Adult T‐cell leukemia/lymphoma (ATLL) is a relatively refractory peripheral T‐cell lymphoma caused by human T‐cell lymphotropic virus type 1 (HTLV‐1). The objective of this study was to investigate the characteristics of long‐term survivors with ATLL.
Methods
We conducted an observational study of 75 aggressive‐type ATLL patients. Flow cytometry was conducted to analyze HTLV‐1 Tax‐specific cytotoxic T‐lymphocytes (CTLs) and T‐cell receptor Vβ gene repertoire.
Results
We first evaluated six long‐term survivors among 37 patients who were newly diagnosed with ATLL and then treated with intensive chemotherapy without mogamulizumab, a monoclonal antibody for C‐C chemokine receptor four antigen. Reversal of the CD4‐to‐CD8 ratio (CD4/CD8) in peripheral mononuclear cells was observed in all six patients. Three of these six patients showed reversed CD4/CD8 immediately after herpes virus infection. Four of these six patients who could be examined demonstrated long‐term maintenance of HTLV‐1 Tax‐specific CTLs. We subsequently identified four long‐term survivors among 38 patients who were newly diagnosed with ATLL and then treated with intensive chemotherapy plus mogamulizumab. All four patients showed reversed CD4/CD8, and three of the four patients contracted herpes virus infection during immunochemotherapy. Six of the total 10 patients were subjected to CTL analyses. Tax‐specific CTLs were observed, and the CTLs that were almost entirely composed of memory CTLs in all patients were recorded. HTLV‐1 provirus was also detected in all six patients.
Conclusions
These data suggest that Tax‐specific memory CTLs probably, together with anticancer agents, eradicate ATLL cells and exhibit long‐term preventive effects from relapse ATLL. Thus, the strong activation of cellular immunity, such as herpes virus infection, seems to be necessary to induce such a potent number of Tax‐specific CTLs.
“…Moreover, Romidepsin-mediated tumor suppression was abrogated by anti-PD-1 antibody treatment in colon cancer cells ( 61 ). One case report showed that romidepsin might be safe and effective for treatment of anaplastic large cell lymphoma (ALCL), which did not impair cellular immunity to HTLV-1 ( 62 ).…”
Breast cancer is one of the common malignancies with poor prognosis worldwide. The treatment of breast cancer patients includes surgery, radiation, hormone therapy, chemotherapy, targeted drug therapy and immunotherapy. In recent years, immunotherapy has potentiated the survival of certain breast cancer patients; however, primary resistance or acquired resistance attenuate the therapeutic outcomes. Histone acetyltransferases induce histone acetylation on lysine residues, which can be reversed by histone deacetylases (HDACs). Dysregulation of HDACs via mutation and abnormal expression contributes to tumorigenesis and tumor progression. Numerous HDAC inhibitors have been developed and exhibited the potent anti-tumor activity in a variety of cancers, including breast cancer. HDAC inhibitors ameliorated immunotherapeutic efficacy in cancer patients. In this review, we discuss the anti-tumor activity of HDAC inhibitors in breast cancer, including dacinostat, belinostat, abexinostat, mocetinotat, panobinostat, romidepsin, entinostat, vorinostat, pracinostat, tubastatin A, trichostatin A, and tucidinostat. Moreover, we uncover the mechanisms of HDAC inhibitors in improving immunotherapy in breast cancer. Furthermore, we highlight that HDAC inhibitors might be potent agents to potentiate immunotherapy in breast cancer.
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