Objective. Earlier research has illustrated prognostic significance of pathologic complete response (pCR) in neoadjuvant therapy (NAT) for breast cancer, whereas correlation between treatment after achieving pCR and survival improvement remains underexplored. We attempted to measure the relation between pCR achieved after NAT and breast cancer recurrence or patient’s survival. Methods. We searched PubMed, EMBASE, Web of Science, and The Cochrane Library databases to find relevant articles from their inception to November 2020. According to eligibility criteria, studies were selected and basic data were extracted. The primary endpoint was the correlation between pCR achieved after NAT and event-free survival (EFS) or overall survival (OS). The results were obtained by directly extracting specific information from the literature or estimating individual data by survival curves on DigitizeIt software, presented with HR and 95% CI. All data were processed on Stata 14.0 software. Results. Among 4338 articles, there were 25 eligible articles involving 8767 patients. The EFS of patients achieved pCR after NAT improved obviously ( HR = 0.27 ; 95% CI, 0.24-0.31), especially in triple negative ( HR = 0.17 ; 95% CI, 0.12-0.24) and HER2 positive ( HR = 0.24 ; 95% CI, 0.20-0.30) breast cancer patients. As such, pCR after NAT was implicated in significantly increased OS ( HR = 0.32 ; 95% CI, 0.27–0.37). Conclusion. Achieving pCR after NAT was notably related to the improvement of EFS and OS, especially for patients with triple-negative and HER2-positive breast cancer. pCR can be a surrogate indicator for outcome of breast cancer patients after NAT, as well as a predictor of treatment efficacy after NAT. Besides, well-designed studies are still warranted for confirmation.

The freshly detected Cuproptosis is a novel form of tumor cell death whose role in pan-cancer is still not completely unintelligible. Methods: We analyzed and assessed the Cuproptosis-related genes (FDX1, LIPT1, DLD, LIAS, DLAT, PDHA1, PDHB, MTF1, GLS and CDKN2A) conversion through the STING database and Sytoscpy software, performed functional enrichment analysis and identified the Hub genes. We extracted the expression data of Hub gene in tumor through TGCA and UCSC database, and analyzed its clinical prognosis. The cancer single-cell state atlas (CSEA) database was used to evaluate the effect of Hub genes on tumor phenotype in single cell lines. Finally, we analyzed the Hub genes mutation and evaluated its correlation with tumor immune infiltration. Results: DLD and LIAS were identified as the Hub genes of Cuproptosis, which have the same CCM score. Mutation analysis revealed that the expression of Hub genes is steady in pan-cancer, DLD and LIAS have been identified as tumor suppressor genes or oncogenes in different tumors. ROC curve analysis showed that DLD and LIAS had a very high predictive effect on survival and prognosis in LAML, and DLD also had a very high predictive effect in the other 4 tumor types. Through the expression of Hub gene in single cell lines, we found that DLD and LIAS displayed significant inhibitory and facilitative effects in different phenotypes of different tumors. Lastly, we explored the relationship between Hub genes and immune infiltration, and found that DLD was substantially associated with immune infiltration of 23 different tumors, and LIAS was significantly associated with immune infiltration of 31 different tumors. Conclusion: We preliminarily evaluated the effect of Cuproptosis on pan-cancer through the hub gene of Cuproptosis, suggesting that copper death has different effects in different tumors.