the survival of patients with breast cancer has remarkably improved. In particular, oncoplastic breast surgery has gained momentum due to its positive impact on patients' quality of life. Oncoplastic breast conservation surgery and postmastectomy breast reconstruction are the two main branches of this frontier discipline. Although oncoplastic breast surgery gained scholarly attention in China later than in Western countries, considerable development and progress has been made over the last few decades. Here, we aimed to summarize the academic achievements of Chinese oncoplastic surgeons in implant-based breast reconstruction, autologous tissue breast reconstruction, mammoplasty by lipofilling, endoscope-assisted breast reconstruction, and nipple-areola reconstruction. we also summarized patient-reported outcomes. The drawbacks of the current investigations will be discussed along with the directions for future clinical practice and research.

Objective To investigate the effect of cancer-associated fibroblasts (CAFs)-derived chemokine ligands 7 (CCL7) on the proliferation and invasion of triple-negative breast cancer (TNBC) cells. Methods The mRNA expression level and protein level of CCL7 in CAFs and paracancerous fibroblasts were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western Blot respectively. To confirm the paracrine level of CCL7 in CAFs and paracancerous fibroblasts, the protein levels of CCL7 in the corresponding conditional medium were detected through enzyme-linked immunosorbent assay (ELISA). The effect of CCL7 on the proliferation and invasion of MDA-MB-231 (TNBC cell line) was investigated by MTS assay and Transwell assay, respectively. Results In comparison with paracancerous fibroblasts, the mRNA expression level and protein level of CCL7 in CAFs were significantly increased (both P<0.01). There was an obviously increase of paracrine level of CCL7 in CAFs-conditional medium (P<0.01). The MTS assay and Transwell assay results indicated that CCL7 was more able to promote the proliferation and invasion of MDA-MB-231. Conclusion CAFs in the TNBC stroma can produce more chemokine CCL7, and CCL7 can promote the proliferation and invasion of TNBC cells

Objective: Ischemia-reperfusion (IR) injury is a leading cause of flap compromise and organ dysfunction during free-tissue transfer, and remains a great challenge for plastic surgeons. Thioredoxin-1 (Trx-1) was proved to protect the IR flap by mitigating the oxidative stress, and inhibiting the activation of apoptosis signal-regulating kinase-1 (ASK-1) and mitogen-activated protein kinase (MAPK) pathway. The aim of this study is to investigate the distinction of Trx-1 expression, apoptosis indices in different layers of IR flaps, and the feasibility of tissue-layer-specific administration of Trx-1. Methods: Ten patients′ specimens of IR flaps for DIEP breast reconstruction were collected and assessed for apoptosis and Trx-1 expression. Twenty mice were used to establish the IR flap model. The mice were sacrificed twenty-four hours after reperfusion. The flap tissues were harvested and tested by immunohistochemistry staining and TUNEL assay. The tissue-layer-specific dermoprotective effect of Trx-1 and the molecular mechanisms were assessed by an in vitro epithelial skin cell hypoxia-reoxygenation model. The statistics were conducted by t test and ANOVA using SPSS 20.0. Results: Trx-1 expression and apoptotic cells were observed mainly located in the basal layer of epidermis and the papillary layer of dermis in human IR flaps and mice models. Trx-1 depletion was 24.19 %± 2.23% in the basal layer of epidermis and the papillary layer of dermis of patient IR flaps, decreasing significantly compared with 70.71% ± 6.38% in control group (t = 27.54, P< 0.001). Similar tissue-layer-specific down regulation of Trx-1 also displayed in mice IR flap models (19.83% ± 2.34% vs. 76.59% ± 4.88%; t = 34.71, P<0.001). The apoptotic index in human samples significantly increased from 1.32% ± 1.52% in control group to 43.71 %± 3.17% in IR group (t =38.23, P<0.001); while it was proved to be dramatically raised in mice models from 0.86% ± 1.15% in control group to 41.14 %± 4.21% in IR group (t= 36.96, P < 0.001). Western Blot analysis revealed Trx-1 down regulation and a significant increase in ASK-1, p-p38, and c-PARP abundance in the hypoxia-reoxygenation-treated HaCaT cells (P < 0.01). Supplementation of recombinant human Trx-1 significantly reduced the apoptosis-related protein expression. Conclusions The basal layer of epidermis and the papillary layer of dermis are the main damaged tissue layers in the early stage of skin flap ischemia-reperfusion injury. The IR flap can be protected by precisely replenishing the vulnerable layers with Trx-1.