Nakano Hirofumi, Soda Hiroshi, Takasu Mineyo, Tomonaga Nanae, Yamaguchi Hiroyuki, Nakatomi Katsumi, Fujino Satoru, Hayashi Tomayoshi, Nakamura Yoichi, Tsukamoto Kazuhiro, Kohno Shigeru
Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki 852-8501, Japan.
Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki 852-8501, Japan; Division of Respiratory Medicine, Sasebo City General Hospital, Sasebo 857-8511, Japan.
Lung Cancer. 2008 Apr;60(1):136-140. doi: 10.1016/j.lungcan.2007.08.021. Epub 2007 Sep 24.
It has been proposed that stepwise progression occurs from atypical adenomatous hyperplasia (AAH) through bronchioloalveolar carcinoma (BAC) to invasive lung adenocarcinoma. However, the underlying molecular mechanisms have not been identified. We report a patient with a mixed adenocarcinoma of the lung that had different EGFR mutations in the papillary subtype, the acinar subtype, and the surrounding AAH and BAC areas. EGFR mutations may accumulate during tumor progression and lead to heterogeneity of EGFR mutations within the tumor.
有人提出,从非典型腺瘤样增生(AAH)经细支气管肺泡癌(BAC)到浸润性肺腺癌会出现逐步进展。然而,其潜在的分子机制尚未明确。我们报告了1例肺混合性腺癌患者,其乳头状亚型、腺泡状亚型以及周围的AAH和BAC区域存在不同的表皮生长因子受体(EGFR)突变。EGFR突变可能在肿瘤进展过程中积累,并导致肿瘤内EGFR突变的异质性。