ARID1A deficiency reverses the response to anti-PD(L)1 therapy in EGFR-mutant lung adenocarcinoma by enhancing autophagy-inhibited type I interferon production.

Sun, Dantong; Qian, Haili; Wang, Jinsong; Xie, Tongji; Teng, Fei; Li, Junling; Xing, Puyuan

Sun, Dantong; Qian, Haili; Wang, Jinsong; Xie, Tongji; Teng, Fei; Li, Junling; Xing, Puyuan.

Afiliación

Sun D; Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Qian H; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Wang J; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Xie T; State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Teng F; Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Li J; Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Xing P; Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. lijunling@cicams.ac.cn.

Cell Commun Signal ; 20(1): 156, 2022 10 13.

Article en En | MEDLINE | ID: mdl-36229854

Asunto(s)

Adenocarcinoma del Pulmón; Carcinoma de Pulmón de Células no Pequeñas; Interferón Tipo I; Neoplasias Pulmonares; Adenocarcinoma del Pulmón/tratamiento farmacológico; Adenocarcinoma del Pulmón/genética; Adenocarcinoma del Pulmón/patología; Autofagia; Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico; Carcinoma de Pulmón de Células no Pequeñas/genética; Carcinoma de Pulmón de Células no Pequeñas/patología; Proteínas de Unión al ADN/genética; Receptores ErbB/metabolismo; Humanos; Inhibidores de Puntos de Control Inmunológico; Neoplasias Pulmonares/tratamiento farmacológico; Neoplasias Pulmonares/genética; Neoplasias Pulmonares/patología; Mutación/genética; Fosfatidilinositol 3-Quinasas/genética; Proteínas Proto-Oncogénicas c-akt/genética; Sirolimus; Serina-Treonina Quinasas TOR; Factores de Transcripción; Microambiente Tumoral

Palabras clave

ARID1A; Autophagy; EGFR-mutant lung adenocarcinoma; Immunotherapy; Type I interferon

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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Interferón Tipo I / Carcinoma de Pulmón de Células no Pequeñas / Adenocarcinoma del Pulmón / Neoplasias Pulmonares Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Cell Commun Signal Año: 2022 Tipo del documento: Article País de afiliación: China

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