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      Effect of cisplatin on metastatic castration-resistant prostate cancer with BRCA2 mutation: A case report

      case-report

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          Abstract

          Poly (ADP-ribose) polymerase inhibitors exhibit strong activity for treating the DNA damage repair defect in patients with prostate carcinoma (PCa). Although conventional DNA-damaging agents can theoretically lead to synthetic antitumoral effects, no report has clearly mentioned the clinical use of cisplatin for treating PCa patients with the breast cancer gene (BRCA)2 mutation. We administered 80 mg/m 2 cisplatin triweekly to a patient with metastatic castration-resistant PCa (mCRPC) with the BRCA2 mutation, and after ten cycles, the prostate-specific antigen was dramatically decreased. We suggest that BRCA2 mutations may indicate the use of cisplatin for treating patients with mCRPC.

          Highlights

          • •

            DNA damage repair defect may be a key as a treatment target for prostate carcinoma.

          • •

            No clear report of cisplatin-use in prostate carcinoma with BRCA2 mutation.

          • •

            Cisplatin was effective in a patient with prostate carcinoma with BRCA2 mutation.

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          Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups: the TNT Trial

          Cheryl E. Gillett, Judith M Bliss, Sarah E. Pinder … (2018)
          BRCA1/2 germline mutations predispose to breast cancer (gBRCA-BC) by impairing homologous recombination (HR) causing genomic instability. HR also repairs DNA lesions caused by platinums and PARP inhibitors. Triple Negative Breast Cancers (TNBC) harbour sub-populations with BRCA1/2 mutations, hypothesised to be especially platinum sensitive. Putative “BRCAness” subgroups may also be especially platinum sensitive. We assessed carboplatin and mechanistically distinct docetaxel in a phase-III trial in unselected advanced TNBC. A pre-specified programme enabled biomarker-treatment interaction analyses in gBRCA-BC and “BRCAness” subgroups: tumour BRCA1 methylation; BRCA1 mRNA-low; HR deficiency mutational signatures and basal phenotypes. Primary endpoint was objective response rate (ORR). In the unselected population (376 patients; 188 carboplatin, 188 docetaxel) carboplatin was not more active than docetaxel (ORR: 31.4v34.0; p=0.66). In contrast in patients with gBRCA-BC carboplatin had double the ORR compared to docetaxel (68%v33%), test for biomarker-treatment interaction (p=0.01). No treatment interaction was observed for BRCA1 methylation, BRCA1 mRNA-low status or a Myriad-HRD mutation signature assay. Significant treatment interaction with basal-like subtype was driven by high docetaxel response in the non-basal subgroup. Patients with advanced TNBC benefit from BRCA1/2 mutation characterization, but not BRCA1 methylation or Myriad-HRD analysis, informing platinum choices. Basal-like gene expression analysis may also influence treatment choices.
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            The association between germline BRCA2 variants and sensitivity to platinum-based chemotherapy among men with metastatic prostate cancer

            Mark M. Pomerantz, Sándor Spisák, Li Jia … (2017)
            Background BRCA2-associated breast and ovarian cancers are sensitive to platinum-based chemotherapy. It is unknown whether BRCA2-associated prostate cancer responds favorably to such treatment. Methods Retrospective analysis of a single-institution cohort of men with castration-resistant metastatic prostate cancer was performed to determine the association between carrier status of pathogenic BRCA2 germline variants and prostate-specific antigen response to carboplatin-based chemotherapy. From 2001-2015, 8,081 adult men with prostate cancer seen in consultation and/or treated at Dana-Farber Cancer Institute provided blood samples and consented to analysis of biological material and clinical records. A subgroup of 141 received at least two doses of carboplatin and docetaxel for castration-resistant disease (94% were also taxane refractory). These subjects were categorized according to absence or presence of pathogenic germline mutations in BRCA2, based on DNA sequencing from whole blood. Primary outcome was response rate to carboplatin/docetaxel chemotherapy as defined by decline in prostate-specific antigen exceeding 50% within 12 weeks of initiating this regimen. Association between BRCA2 mutation status and response to carboplatin-based chemotherapy was tested, using Fisher’s exact test, with a two-sided p-value of <0.05 as threshold for significance. Results Pathogenic germline BRCA2 variants were observed in 8/141 (5.7%; 95% CI=2.5%-10.9%) participants. Six of eight (75%) BRCA2 carriers experienced prostate-specific antigen decline >50% within 12 weeks, compared to 23 of 133 (17%) non-carriers (absolute difference 58%; 95% CI=27%-88%; P<0.001). Prostate cancer cell lines functionally corroborate these clinical findings. Conclusions BRCA2-associated castration-resistant prostate cancer is associated with higher likelihood of response to carboplatin-based chemotherapy than non-BRCA2 associated prostate cancer.
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              Activity of Platinum-Based Chemotherapy in Patients With Advanced Prostate Cancer With and Without DNA Repair Gene Aberrations

              Sabine Schmid, Aurelius Omlin, Celestia Higano … (2020)
              Key Points Question Is there a role for platinum-based treatment in molecularly selected patients with advanced prostate cancer? Findings In a case series of 508 patients, platinum-based therapy was associated with antitumor activity, especially among patients with known DNA repair gene aberrations. In patients with DNA repair gene aberrations, nearly half had a decrease in prostate-specific antigen levels of at least 50% and experienced soft tissue responses. Meaning In patients with prostate cancer and DNA repair gene aberrations, platinum-based therapy may be considered a treatment option.
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                Author and article information

                Contributors
                Ken-ichi Tabata
                Journal
                Journal ID (nlm-ta): Urol Case Rep
                Journal ID (iso-abbrev): Urol Case Rep
                Title: Urology Case Reports
                Publisher: Elsevier
                ISSN (Electronic): 2214-4420
                Publication date PMC-release: 17 May 2021
                Publication date Collection: September 2021
                Publication date (Electronic): 17 May 2021
                Volume: 38
                Electronic Location Identifier: 101712
                Affiliations
                [a ]Department of Urology, Yokosuka General Hospital Uwamachi, Kanagawa, Japan
                [b ]Department of Urology, Kitasato University School of Medicine, Kanagawa, Japan
                Author notes
                [∗ ]Corresponding author. Ken-ichi Tabata Department of Urology, Kitasato University School of Medicine, 1-15-1 Kitasato Minami-ku Sagamihara, Kanagawa, 252-0374, Japan. ktabata@ 123456med.kitasato-u.ac.jp
                Article
                Publisher Item ID: S2214-4420(21)00152-2 Publisher ID: 101712
                DOI: 10.1016/j.eucr.2021.101712
                PMC ID: 8175266
                SO-VID: e78dee87-9555-4b84-b093-ad5fb0c15249
                Copyright © © 2021 Published by Elsevier Inc.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 20 April 2021
                Date revision received : 5 May 2021
                Date accepted : 10 May 2021
                Categories
                Subject: Oncology

                Keywords: prostate cancer,dna damage repair defect,brca2 mutation,cisplatin
                Data availability:
                Keywords: prostate cancer, dna damage repair defect, brca2 mutation, cisplatin

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