BREAST CANCER RESPONSE TO NEOADJUVANT CHEMOTHERAPY QUANTIFIED BY RESIDUAL CANCER BURDEN (RCB) SCORE

Primary systemic therapy (PST) is the first weapon employed in fighting against breast cancer (BC) and the response to the numerous chemotherapy (ChT) regimens currently used is the key to the conservative surgical approach. The objective of this study was to analyse the efficiency of ChT by assessing the anatomopathological response on the surgical resection piece. 53 patients with BC have been investigated pre/post-PST within this retrospective study and the quantification of the tumour response was made using the Residual Cancer Burden Score (RCB). 6 patients achieved pathological complete response (pCR), and 13 patients presented a tumour < 2 cm. Except for the 4 patients with multiple tumours, the percentage of cases that could have benefited from post-PST conservative surgery (BCS) increased to 16.9% (9/53). 87.2% of the cases classified as RCB-III were ER+ (p = 0.005) and 82.1% PR+ (p = 0.014), while the utility of ChT in case of these BC subtypes is still in debate. The Paclitaxel (PTX) sequential administration following anthracycline-based regimens did not increase the PST response rate and was associated with significant residual disease (p = 0.027). The anthracycline-based regimens or the anti-HER2 therapy (trastuzumab) (p = 0.986) did not influence the pCR reach in a statistically significant manner. The BC low response rate to PST is associated with hormone receptor+ (HR+) subtypes with a weak response to ChT, but might also be due to malignant cells??? innate resistance to taxane therapy, presently considered as one of the cornerstones in BC treatment.

Automated summary

This study analyzed the pathological response to chemotherapy in breast cancer patients and found that some patients showed significant tumor shrinkage or complete elimination, suggesting the possibility of conservative surgery. However, certain subtypes of breast cancer had poor response to chemotherapy, and some malignant cells had intrinsic resistance to taxane therapy.