Department of Internal Medicine, Chungbuk National University College of Medicine, Cheongju, Korea.
Clin Lung Cancer. 2011 Nov;12(6):380-6. doi: 10.1016/j.cllc.2011.02.006. Epub 2011 May 20.
We evaluated EGFR and KRAS mutations between 37 paired primary tumors and corresponding metastases in lung adenocarcinoma. A substantial discordance was found in EGFR mutation status between primary tumors and corresponding metastases including pleural metastases. Moreover, the responsiveness to EGFR tyrosine kinase inhibitors tend to be correlated with EGFR mutation status in metastatic lesions than in primary tumors.
The aim of this study was to compare epidermal growth factor receptor (EGFR) and KRAS mutations between primary tumors and corresponding metastases including pleural metastases in lung adenocarcinoma.
Thirty-seven paired primary lung adenocarcinomas and corresponding metastatic tumors were analyzed for EGFR and KRAS mutations. In addition, 21 pleural metastases including malignant pleural effusion or pleural biopsy were used in performing these mutation analyses.
EGFR mutations were detected in 18 primary lung adenocarcinomas (48.6%) and in 16 corresponding metastases (43.2%). EGFR mutations showed a discordance rate of 16.2% (6 of 37 patients) between primary lung adenocarcinomas and corresponding metastases. Among 21 pleural metastases, 3 patients (14.3%) showed that the EGFR mutation was discordant. KRAS mutations were detected in one primary tumor and in two metastatic tumors. Eighteen patients were treated with EGFR tyrosine kinase inhibitors. One of seven patients who experienced partial response had EGFR mutations only in the metastasis, and two of seven patients who experienced progressive disease carried wild-type EGFR only in the metastasis.
EGFR mutations were discordant between primary tumors and corresponding metastases in a significant portion of lung adenocarcinomas. Furthermore, these discordance was also observed in metastases to the pleura, the nearest metastatic site.
我们评估了肺腺癌中 37 对原发性肿瘤和相应转移灶的 EGFR 和 KRAS 突变。在原发性肿瘤和相应转移灶(包括胸膜转移灶)之间,我们发现 EGFR 突变状态存在实质性差异。此外,EGFR 酪氨酸激酶抑制剂的反应性似乎与转移灶中的 EGFR 突变状态相关,而不是与原发性肿瘤相关。
本研究旨在比较肺腺癌中原发性肿瘤和相应转移灶(包括胸膜转移灶)之间的表皮生长因子受体(EGFR)和 KRAS 突变。
分析了 37 对原发性肺腺癌和相应转移灶的 EGFR 和 KRAS 突变。此外,还对 21 例包括恶性胸腔积液或胸膜活检的胸膜转移灶进行了这些突变分析。
18 例原发性肺腺癌(48.6%)和 16 例相应转移灶(43.2%)中检测到 EGFR 突变。原发性肺腺癌和相应转移灶之间的 EGFR 突变存在 16.2%(37 例患者中的 6 例)的不一致率。在 21 例胸膜转移灶中,3 例(14.3%)显示 EGFR 突变不一致。KRAS 突变在 1 例原发性肿瘤和 2 例转移性肿瘤中被检测到。18 例患者接受了 EGFR 酪氨酸激酶抑制剂治疗。7 例部分缓解的患者中,1 例只有转移灶存在 EGFR 突变,7 例进展性疾病的患者中,2 例只有转移灶存在野生型 EGFR。
在相当一部分肺腺癌中,原发性肿瘤和相应转移灶之间的 EGFR 突变存在不一致。此外,这种不一致性也存在于最接近的转移部位——胸膜转移灶中。