Background: Prosthetic reconstruction in previously irradiated breasts has been associated with a higher risk of complications. Here we describe the surgical and cosmetic outcome of our breast reconstruction process based on primary fat grafting combined with prosthetic placement. Methods: In this multicenter retrospective study, 136 patients who underwent mastectomy and external chest wall radiotherapy between 2014 and 2018 were benefited from chest wall lipofilling and silicone implant placement were chosen. Patients were assessed for skin trophicity, thickness, and mobility and were allowed to undergo several lipofilling sessions before implant placement, if required. No patient had >3 lipofilling sessions. Cosmetic outcome was evaluated by the patient, surgeon, and nurse, using a Likert-type ordinal scale. Results: We included 136 patients: 79 patients (58%) received only 1 session of lipofilling before implant placement, 33 (24.6%) had 2 sessions, and 24 (17.4%) had 3 sessions. The volume of the third lipofilling was significantly higher and the volume of the prosthesis of these patients was significantly lower than those of patients undergoing 1 or 2 lipofillings. Reconstruction failure rate was 2.2% (3 patients had explantation); however, all benefited from prosthesis reconstruction a year after the initial procedures. The average satisfaction score was 4.7 out of 5 as evaluated by patients, 4.8 out of 5 by surgeons, and 4.8 out of 5 by nurses. Conclusions: Primary lipofilling combined with prosthesis placement after radiotherapy is a reconstructive method that yields a satisfactory cosmetic outcome with a low complication rate. Such minimally invasive breast reconstruction approach can be an alternative to flap-based reconstruction.

Breast J. 2020;26:725-728. wileyonlinelibrary.com/journal/tbj | 725

Background Although autophagy plays a dual role in suppressing or promoting certain cancers, the nature of its involvement in breast cancers remains unclear. Here, we investigated the function of STXBP6, a protein regulating the autophagy‐associated SNARE complex, in triple negative breast cancer (TNBC). Results We report that STXBP6 is profoundly downregulated in TNBC specimens in association with reduced overall patient survival. Notably, we found that STXBP6 promoter was specifically hyper‐methylated in TNBC specimens. Ectopic expression of STXBP6 inhibited TNBC cell proliferation in cellular and mouse models. Mass spectrometric analysis revealed physical interactions of STXBP6 with a number of autophagy‐related proteins including SNX27, a molecule involved in endocytosis of plasma membrane receptors and protein trafficking. Overexpression of STXBP6 elicited autophagy through inhibition of mTORC1 signaling. Reciprocally, induction of autophagy rescued STXBP6 expression by inhibiting EZH2 and altering STXBP6 methylation. The mutual regulation between STXBP6 and autophagy was replicated in luminal breast cancer cells only when estrogen receptor (ER) activation was abrogated. Ectopic expression of STXBP6 significantly reduced TNBC cells’ migratory ability in vitro and tumor metastasis in vivo. Conclusions Our results unveil a role of STXBP6 in TNBC that highlights a new paradigm in autophagy regulation. Our results significantly enhance the understanding of the mechanisms of TNBC aggressiveness, which might help in designing novel therapies targeting TNBC.

Prader–Willi syndrome (PWS) is a genetic disorder caused by the lack of expression of genes on the paternally inherited chromosome region 15q11.2-q13. It is a multisystem disorder that is characterized by severe hypotonia with poor suck and feeding difficulties in early infancy, followed in early childhood by excessive eating and gradual development of morbid obesity. The incidence of type 2 diabetes mellitus is high, particularly in obese patients. Non-alcoholic fatty liver disease has also been reported in some patients with PWS. Liver adenomatosis is a benign vascular lesion of the liver, defined by the presence of >10 adenomas, in the otherwise healthy liver parenchyma. We report the first case of a patient with PWS with severe obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver who also developed liver adenomatosis, review the pediatric literature on liver adenomatosis, and discuss the potential underlying mechanisms.