Efficacy of EGFR tyrosine kinase inhibitors in patients having EGFR-activating mutations with or without BIM polymorphisms.


Journal

Cancer chemotherapy and pharmacology
ISSN: 1432-0843
Titre abrégé: Cancer Chemother Pharmacol
Pays: Germany
ID NLM: 7806519

Informations de publication

Date de publication:
10 2020
Historique:
received: 28 05 2020
accepted: 04 09 2020
pubmed: 20 9 2020
medline: 21 5 2021
entrez: 19 9 2020
Statut: ppublish

Résumé

Patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer with BIM deletion polymorphism may have a limited response to EGFR tyrosine kinase inhibitors (EGFR-TKIs). However, some results of previous reports are discordant. It is necessary to evaluate the relationship between BIM polymorphism and the efficacy of EGFR-TKIs. We retrospectively analyzed patients treated with EGFR-TKIs. We collected serum samples from patients before EGFR-TKI administration. We analyzed BIM deletion polymorphism and BIM single nucleotide polymorphism in exon 5 c465C > T by the Invader BIM deletion polymorphism was identified in 27 of 194 patients (13.9%). BIM single nucleotide polymorphism was identified in 29 of 194 patients (14.9%). The overall response ratio was 81.5% in patients with BIM deletion polymorphism, 89.7% with BIM single nucleotide polymorphism, and 83.6% with BIM wild type. Median progression-free survival was 10.3 months with BIM deletion polymorphism, 8.5 months with BIM single nucleotide polymorphism, and 10.4 months with BIM wild type. Overall survival was 38.4 months with BIM deletion polymorphism, 29.1 months with BIM single nucleotide polymorphism, and 31.6 months with BIM wild type. There were no significant differences between the groups in overall response ratio, progression-free survival, and overall survival. BIM polymorphism does not affect EGFR-TKI efficacy.

Identifiants

pubmed: 32948919
doi: 10.1007/s00280-020-04136-7
pii: 10.1007/s00280-020-04136-7
doi:

Substances chimiques

BCL2L11 protein, human 0
Bcl-2-Like Protein 11 0
Protein Kinase Inhibitors 0
Quinazolinones 0
dacomitinib 5092U85G58
Erlotinib Hydrochloride DA87705X9K
EGFR protein, human EC 2.7.10.1
ErbB Receptors EC 2.7.10.1
Gefitinib S65743JHBS

Types de publication

Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

517-525

Auteurs

Ryo Ariyasu (R)

Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.

Noriko Yanagitani (N)

Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.

Kenichi Tadokoro (K)

BML, INC, 1361-1, Matoba, Kawagoe-shi, Saitama, 350-1101, Japan.

Toshikazu Yamaguchi (T)

BML, INC, 1361-1, Matoba, Kawagoe-shi, Saitama, 350-1101, Japan.

Ken Uchibori (K)

Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.

Satoru Kitazono (S)

Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.

Naoya Fujita (N)

Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.

Ryohei Katayama (R)

Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan. ryohei.katayama@jfcr.or.jp.

Makoto Nishio (M)

Department of Thoracic Medical Oncology, The Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan. mnishio@jfcr.or.jp.

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Classifications MeSH