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Transformation from EGFR/PTEN co‐mutated lung adenocarcinoma to small cell carcinoma in lymph node metastasis
Author(s) -
Hayashi Takuo,
Takamochi Kazuya,
Kohsaka Shinji,
Kishikawa Satsuki,
Suehara Yoshiyuki,
Takahashi Fumiyuki,
Suzuki Kenji,
Saito Tsuyoshi,
Yao Takashi
Publication year - 2020
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/pin.12919
Subject(s) - adenocarcinoma , pten , cancer research , medicine , lymph node , lung cancer , metastasis , carcinoma , epidermal growth factor receptor , pathology , oncology , cancer , biology , pi3k/akt/mtor pathway , signal transduction , biochemistry
There is minimal evidence of EGFR ‐mutated lung adenocarcinoma transforming to small cell lung carcinoma (SCLC) without the administration of EGFR‐tyrosine kinase inhibitor (TKI). Here, we present a case of EGFR/PTEN co‐mutated lung adenocarcinoma with lymph node metastases, which comprised adenocarcinoma admixed with SCLC. EGFR L858R and PTEN R130Q mutations were shared between the primary tumor and lymph node metastasis. Additionally, EGFR I744M mutation was shared between the adenocarcinoma and SCLC components in the lymph node metastasis, confirming spontaneous transformation from adenocarcinoma to SCLC. Furthermore, TP53 and RB1 mutations were detected only in the SCLC components of the lymph node metastasis. Immunohistochemically, complete absence of Rb expression in SCLC was observed, suggesting the loss of function of RB1 . Our case clearly shows that EGFR/PTEN co‐mutated lung adenocarcinoma transformed to SCLC in the lymph node without TKI‐mediated evolutionary selection pressures.