Villa Celina, Cagle Philip T, Johnson Melissa, Patel Jyoti D, Yeldandi Anjana V, Raj Rishi, DeCamp Malcolm M, Raparia Kirtee
From the Department of Pathology (Drs Villa, Yeldandi, and Raparia), the Division of Medical Oncology, and Robert H. Lurie Comprehensive Cancer Center (Drs Johnson and Patel), the Division of Pulmonary, and Critical Care Medicine (Dr Raj); and the Division of Thoracic Surgery, and Robert H. Lurie Comprehensive Cancer Center (Dr DeCamp), Northwestern University Feinberg School of Medicine, Chicago, Illinois; and the Department of Pathology & Genomic Medicine, The Methodist Hospital, Houston, Texas (Dr Cagle).
Arch Pathol Lab Med. 2014 Oct;138(10):1353-7. doi: 10.5858/arpa.2013-0376-OA. Epub 2014 Feb 26.
Epidermal growth factor receptor (EGFR) mutations have been identified as predictors of response to EGFR tyrosine kinase inhibitors in non-small cell lung cancer.
To investigate the relationship of EGFR mutation status to the histologic subtype of adenocarcinoma according to the new International Association for the Study of Lung Cancer (IASLC)/American Thoracic Society (ATS)/European Respiratory Society (ERS) classification.
We screened EGFR mutation in 200 consecutive lung adenocarcinoma resection specimens diagnosed between 2008 and 2011.
Among 200 lung adenocarcinomas, EGFR mutations were identified in 41 tumors (20.5%). The mean age in the EGFR-mutant group was 64.8 years and this group consisted of 78% females and 22% males. Most patients with EGFR-positive lung cancers were never-smokers (51%) as compared to 8% with EGFR-negative cancers (P < .001). The most common mutations identified in our population were deletions in exon 19 (22 patients) and L858R in exon 21 (12 patients). Five patients had double mutations. The predominant pattern of adenocarcinoma was lepidic (44%) in EGFR-mutant lung cancers as compared to 69% with acinar pattern in EGFR wild-type lung cancers (P < .001). Of 22 minimally invasive adenocarcinomas, 8 (36%) had EGFR mutations, accounting for 20% of adenocarcinomas with EGFR mutations (P < .05).
Based on the new IASLC/ATS/ERS classification, the predominant subtype of adenocarcinoma was lepidic (44%) in EGFR-mutant lung cancers (P < .001). However, histologic subtype should not be used to exclude patients from tyrosine kinase inhibitor therapy, since EGFR mutations are found in lung adenocarcinomas of other subtypes.
表皮生长因子受体(EGFR)突变已被确定为非小细胞肺癌中EGFR酪氨酸激酶抑制剂反应的预测指标。
根据国际肺癌研究协会(IASLC)/美国胸科学会(ATS)/欧洲呼吸学会(ERS)的新分类,研究EGFR突变状态与腺癌组织学亚型之间的关系。
我们对2008年至2011年间诊断的200例连续肺腺癌切除标本进行了EGFR突变筛查。
在200例肺腺癌中,41例肿瘤(20.5%)检测到EGFR突变。EGFR突变组的平均年龄为64.8岁,该组女性占78%,男性占22%。EGFR阳性肺癌患者大多从不吸烟(51%),而EGFR阴性肺癌患者中这一比例为8%(P <.001)。在我们的研究人群中,最常见的突变是19外显子缺失(22例患者)和21外显子L858R(12例患者)。5例患者有双重突变。EGFR突变型肺癌中腺癌的主要模式是鳞屑样生长型(44%),而EGFR野生型肺癌中腺泡型的比例为69%(P <.001)。在22例微浸润腺癌中,8例(36%)有EGFR突变,占EGFR突变腺癌的20%(P <.05)。
根据新的IASLC/ATS/ERS分类,EGFR突变型肺癌中腺癌的主要亚型是鳞屑样生长型(44%)(P <.001)。然而,组织学亚型不应被用于排除酪氨酸激酶抑制剂治疗的患者,因为在其他亚型的肺腺癌中也发现了EGFR突变。