Background Skin‐sparing mastectomy (SSM) and nipple‐sparing mastectomy (NSM) are the standard techniques for achieving a cosmetic outcome, but necrosis of a cutaneous flap including the nipple–areolar complex (NAC) is a serious complication. To analyze the risk factors for skin flap necrosis, we retrospectively evaluated a clinical database of breast cancer patients treated with mastectomy followed by immediate breast reconstruction. Methods Four hundred and twelve cases were consecutively recorded between 2006 and 2016. Body weight (BW), body mass index (BMI), distance from NAC to referent tumor, distance from overlying skin to the tumor and weight of breast resection (WBR) as measured in the operating theater were included in the statistical analysis. Results NSM, SSM and total mastectomy were performed in 123 (30%), 96 (23%) and 193 cases (47%), respectively. A tissue expander was used in 379 cases (92%), a silicone implant in 8 (2%) and autologous breast reconstruction in 25 (6%). Skin flap necrosis was found in 7% of all cases and NAC necrosis in 13% of NSM cases. In a univariate analysis, BW, NSM and WBR were risk factors for skin flap necrosis, and BW, BMI and WBR were risk factors for NAC necrosis. In a multivariate analysis, NSM and WBR remained significant risk factors for skin flap necrosis, and WBR was a significant risk factor for NAC necrosis. Conclusions WBR is an important risk factor for skin flap necrosis. Especially, NAC necrosis should be considered for patients with large‐volume breasts who undergo NSM and immediate breast reconstruction.

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Background: Triple-negative breast cancer (TNBC) includes heterogenous molecular subtypes, e.g., basal-like, immunomodulatory, mesenchymal, mesenchymal stem cell and luminal androgen receptor subtypes. Chemotherapy is the standard care for patients with early TNBC, but advanced or metastatic disease has unfavorable prognosis. PARP inhibitors and immune checkpoint inhibitors are effective for patients with BRCA gene mutation and PD-L1-positive TNBC, respectively. However, their clinical benefits seem to be limited. Thus, we are investigating new therapy targeted on immune modulation in TNBC. Materials and methods: First, we performed microarray expression analysis (Agilent Technologies, Inc.) of small RNA extracted from 11 breast cancer specimens. Second, miRNA subset was compared in TNBC and non-TNBC, and several genes were identified as predicted targets for interaction of miRNA in TNBC. Third, we examined a targeted gene and protein expressions in cancer tissues by real-time qPCR and immunohistochemical staining. Tissues samples were obtained from breast cancer patients with TNBC and non-TNBC, who were scheduled to receive neoadjuvant chemotherapy (NAC). Statistical significance is evaluated by chi-squared test. This study is approved at IRB in Kyorin University School of Medicine and also supported by Grant-in-Aid for Scientific Research C of Japan Society for the Promotion of Science. Results: From comprehensive analysis, SOCS1 (suppressor of cytokine signaling 1), IL-13 and several genes were predicted as interactive targets of miRNA in TNBC. We focused on SOCS1 gene amplification and its protein overexpression in breast cancer. Most patients were treated with NAC of anthracycline- and/or taxane-based regimens. Their pathological response was graded in surgical specimens according to classification of the Japanese Breast Cancer Society. From 55 tissue specimens stained by anti-SOCS1 antibody, there was no difference among staining intensity graded at score 0-3 and pathological response of chemotherapy. However, gene amplification of SOCS1 was not statistically different but relatively lower in 6 cases with pathologically partial or complete response (grade 2 or 3) than in 11 cases with no pathological response (grade 1a or 1b). Discussions: SOCS1 is well known as a negative regulator of JAK-STAT pathway. SOCS1 is also related to suppression of T cell activation and modulation of M1 macrophage. Our data suggest that down regulation of SOCS1 gene influences clinical benefit of chemotherapy as well as host immune response like tumor-infiltrating lymphocytes (TIL). We will examine relationship between SOCS1 protein expression and TIL in breast cancer and also examine cell proliferation and T cell activation in TNBC and non-TNBC cell lines under presence and absence of SOCS1 gene expression. Conclusion: SOCS1 is a promising molecular target to modulate immune editing in TNBC. Citation Format: Shigeru Imoto, Tomohiro Chiba, Sota Asaga, Hirotsugu Isaka, Shigehiro Yokoi, Yoshiharu Ishizaka, Ai Tsuchiya, Hiroshi Kamma. New targeted therapy on SOCS1-related immune-response in triple-negative breast cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1709.

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We report a case of giant breast angiosarcoma. A 20-year-old woman noticed enlargement of her rightbreastandconsultedherfamilydoctor.Thesymptomhadbeenstablefor4months.Granulomatous mastitiswassuspected.However,shecomplainedthattheenlargementhadbecomerapid,andshewas referredtoourhospital.Herrightbreastwasfoundtohaveswollento20cmindiameterandhadsubcutaneous hemorrhages. Breast ultrasound revealed a tumor in the entire right breast, with a heterogeneousechoiclesionandinternalbloodflowsignals.ContrastCTandMRIimagesdemonstratedatumor shadowwithpartialcontrasteffectoccupyingtheentirerightmammarygland.Therewasnodistantorganmetastasis.Basedoncarefulcoreneedlebiopsy,thetumorwasdiagnosedasanangiosarcoma.She underwenttotalmastectomywithexcisionoftheoverlyingskinandthepectoralismajormuscle,anddissectionoftheaxillarylymphnodes.Theskindefectwasreconstructedwithalatissimusdorsimyocutaneous flap. Post-mastectomy radiation therapy was performed on the chest wall, and no other adjuvant therapywasscheduled.Approximately2yearsaftertreatment,shewasfreeofrecurrence.Herein,we reportacaseofbreastangiosarcoma,discussit,andreviewtheliterature.