Effect of Neoadjuvant Chemotherapy on Immunohistochemistry in Breast Cancer

新辅助化疗对乳腺癌免疫组织化学的影响

阅读:1

Abstract

Background Neoadjuvant chemotherapy (NACT) is a key treatment strategy for locally advanced or high-risk early-stage breast cancer. This study aims to evaluate the effects of NACT on estrogen receptor (ER), progesterone receptor (PR), HER2 status, and Ki67 index, which are crucial markers for breast cancer prognosis and treatment decisions. Methods A cohort of 62 female breast cancer patients underwent NACT with varied regimens. Baseline and post-treatment data on ER, PR, HER2 status, and Ki67 were collected through immunohistochemistry and sonomammography. Statistical analysis was performed using R software, with Wilcoxon rank-sum and paired t-tests for primary and secondary outcomes, respectively. Results Significant changes were observed in receptor statuses post-NACT. Notably, 8.3% of ER-negative patients converted to ER-positive, 14.2% of PR-negative patients became PR-positive, and 16.6% of HER2-negative patients became HER2-positive. Ki67 levels decreased significantly from 51.7% to 26.28% (p < 0.001), indicating reduced tumor proliferation. Discussion The shifts in ER, PR, and HER2 status suggest the dynamic nature of breast cancer during chemotherapy, with implications for personalized treatment strategies. The reduction in Ki67 indicates a favorable tumor response, though tumor heterogeneity and treatment resistance remain challenges. These findings underscore the importance of post-treatment molecular profiling to guide therapy decisions and optimize patient outcomes. Conclusion NACT significantly alters the molecular profile of breast cancer, including receptor status and Ki67 levels, which can inform personalized treatment strategies. These findings highlight the need for post-NACT reassessment to tailor follow-up therapies and improve long-term patient outcomes.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。