Medical Oncology Unit, University Hospital, Parma 43100, Italy.
Br J Cancer. 2010 Jan 5;102(1):162-4. doi: 10.1038/sj.bjc.6605471. Epub 2009 Dec 1.
Loss of phosphatase and tensin homologue deleted in chromosome 10 (PTEN) function in advanced colorectal cancer (CRC) may represent one of the resistance mechanisms to cetuximab by interfering with the epidermal growth factor receptor signal transduction pathway.
PTEN expression tested by indirect immunofluorescence was evaluated both on primary (n=43) and on metastatic (n=24) sites in CRC patients treated with cetuximab.
The loss of PTEN expression tested on metastatic sites was negatively associated with response (100% progressive disease (PD) in PTEN-negative cases vs 30% PD in PTEN-positive cases; P<0.05), PFS (0.8 vs 8.2 months; P<0.001) and OS (2.9 vs 14.2 months; P<0.001).
A potential role of PTEN in the anti-tumour activity of cetuximab could be hypothesised.
在晚期结直肠癌(CRC)中,磷酸酶和张力蛋白同源物缺失于染色体 10(PTEN)功能的丧失可能代表了对西妥昔单抗产生耐药性的机制之一,通过干扰表皮生长因子受体信号转导通路。
通过间接免疫荧光法检测 CRC 患者接受西妥昔单抗治疗时的原发(n=43)和转移(n=24)部位的 PTEN 表达。
在转移部位检测到的 PTEN 表达缺失与反应(PTEN 阴性病例 100%进展性疾病(PD)与 PTEN 阳性病例 30% PD;P<0.05)、PFS(0.8 与 8.2 个月;P<0.001)和 OS(2.9 与 14.2 个月;P<0.001)呈负相关。
可以假设 PTEN 在西妥昔单抗的抗肿瘤活性中发挥潜在作用。