Saturday, May 16, 2020

Breast Cancer Case Study - 929 Words

Discussion In the present study, we found that rate of pCR to neoadjuvant chemotherapy was 24.7% (n=25) in the whole cohort (n=101). This finding was consistent with the range of pCR rates to prospective randomized trials of preoperative chemotherapy of 15%-40% mentioned in the literature (Burstein et al., 2008). Moreover, high Ki-67 expression (cutoff 14%) was significantly correlated with achieving a pCR in the large cohort (p=0.016). This result matched with the finding of several studies that reported that high Ki-67 expression was associated with higher response rates to neoadjuvant chemotherapy in breast cancer (Keam et al., 2011). Also, our study revealed that TNBC patients accounted for about 23% of the whole cohort of invasive†¦show more content†¦Similarly, Liu et al. (2013) gave 7 cycles of platinum-based neo-adjuvant chemotherapy in 717 patients, of whom 31% were TNBC, and found that the clinical complete response (cCR) rate and the pathological complete response (pCR) rates were significantly higher in TNBC group than in non-TNBC one. However, the low pCR rate achieved by our TNBC cases was close to that reported in a small study at Dana Farber Cancer Institute, where 26 TNBC patients received six cycles of neoadjuvant single-agent cisplatin, and only4 (15%) achieved complete response (CR), after exclusion of two cases with BRCA mutation (Silver et al., 2010). Similarly, Bidard et al., reported a pCR rate of 17% in a relatively large cohort of TNBC group (n=120) receiving a combined neoadjuvant chemotherapy regimen composed of cyclophosphamide, epirubicin and 5-fluorouracil (CEF) for 4 to 6 cycles (Bidard et al., 2008). Our low pCR rate in TNBC subgroup might be also explained by the type of chemotherapeutic agents that had been used. Rocca and colleagues conducted a retrospective analysis of core biopsies of patients with breast cancer treated with neoadjuvant cisplatin-based chemotherapy in breast cancer and showed that administration of cisplatin without anthracyclines yielded a higher rate of pCR in patients with p63-positive tumors (Rocca et al., 2008). Again, our low pCR rate in TNBC might be also explained by the heterogeneousShow MoreRelatedBreast Cancer Case Study1234 Words   |  5 Pagesultimately lead to the progression of oral cancer. (Lee et al, 2010). c‑myc was among the first oncogenes found to be amplified in breast cancer, and it can contribute to many other forms of cancer (Victoria and Michael, 2007). It is a critical downstream effector of the Wnt/TCF pathway in colon cancer and activation of Myc might play a predominant role in the pathogenesis of tumors like pediatric hepatoblastoma (Sansom et al, 2007; Cairo et al, 2008). 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