Drug resistance mechanisms in Japanese anaplastic lymphoma kinase-positive non-small cell lung cancer and the clinical responses based on the resistant mechanisms.
Aminopyridines
Anaplastic Lymphoma Kinase
/ genetics
Asian People
Carbazoles
/ therapeutic use
Carcinoma, Non-Small-Cell Lung
/ drug therapy
Crizotinib
/ therapeutic use
Drug Resistance, Neoplasm
/ genetics
Humans
Lactams
Lactams, Macrocyclic
/ therapeutic use
Lung Neoplasms
/ drug therapy
Mutation
/ genetics
Piperidines
/ therapeutic use
Protein Kinase Inhibitors
/ therapeutic use
Pyrazoles
Pyrimidines
/ therapeutic use
Recombinant Proteins
/ genetics
Sulfones
/ therapeutic use
anaplastic lymphoma kinase
mutation
progression-free survival
resistance mechanism
tyrosine kinase inhibitor
Journal
Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776
Informations de publication
Date de publication:
Mar 2020
Mar 2020
Historique:
received:
25
11
2019
revised:
05
01
2020
accepted:
08
01
2020
pubmed:
22
1
2020
medline:
17
3
2020
entrez:
22
1
2020
Statut:
ppublish
Résumé
The treatment for anaplastic lymphoma kinase (ALK)-positive lung cancer has been rapidly evolving since the introduction of several ALK tyrosine kinase inhibitors (ALK-TKI) in clinical practice. However, the acquired resistance to these drugs has become an important issue. In this study, we collected a total of 112 serial biopsy samples from 32 patients with ALK-positive lung cancer during multiple ALK-TKI treatments to reveal the resistance mechanisms to ALK-TKI. Among 32 patients, 24 patients received more than two ALK-TKI. Secondary mutations were observed in 8 of 12 specimens after crizotinib failure (G1202R, G1269A, I1171T, L1196M, C1156Y and F1245V). After alectinib failure, G1202R and I1171N mutations were detected in 7 of 15 specimens. G1202R, F1174V and G1202R, and P-gp overexpression were observed in 3 of 7 samples after ceritinib treatment. L1196M + G1202R, a compound mutation, was detected in 1 specimen after lorlatinib treatment. ALK-TKI treatment duration was longer in the on-target treatment group than that in the off-target group (13.0 vs 1.2 months). In conclusion, resistance to ALK-TKI based on secondary mutation in this study was similar to that in previous reports, except for crizotinib resistance. Understanding the appropriate treatment matching resistance mechanisms contributes to the efficacy of multiple ALK-TKI treatment strategies.
Identifiants
pubmed: 31961053
doi: 10.1111/cas.14314
pmc: PMC7060465
doi:
Substances chimiques
Aminopyridines
0
Carbazoles
0
Lactams
0
Lactams, Macrocyclic
0
Piperidines
0
Protein Kinase Inhibitors
0
Pyrazoles
0
Pyrimidines
0
Recombinant Proteins
0
Sulfones
0
Crizotinib
53AH36668S
ALK protein, human
EC 2.7.10.1
Anaplastic Lymphoma Kinase
EC 2.7.10.1
ceritinib
K418KG2GET
alectinib
LIJ4CT1Z3Y
lorlatinib
OSP71S83EU
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
932-939Subventions
Organisme : Nippon Foundation
ID : N/A
Organisme : Japan Agency for Medical Research and Development
ID : JP19ck0106472h0001
Organisme : Japan Agency for Medical Research and Development
ID : JP19cm0106203h0004
Organisme : Japan Society for the Promotion of Science
ID : JP15H02368
Organisme : Japan Society for the Promotion of Science
ID : JP16H04715
Organisme : Japan Society for the Promotion of Science
ID : JP17H06327
Organisme : Japan Society for the Promotion of Science
ID : JP19H03524
Informations de copyright
© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
Références
EBioMedicine. 2015 Dec 12;3:54-66
pubmed: 26870817
J Exp Med. 2019 Apr 1;216(4):982-1000
pubmed: 30872362
Cancer Discov. 2014 Jun;4(6):662-673
pubmed: 24675041
Cancer Discov. 2018 Jun;8(6):714-729
pubmed: 29650534
Cancer Sci. 2020 Mar;111(3):932-939
pubmed: 31961053
Lancet Oncol. 2017 Dec;18(12):1590-1599
pubmed: 29074098
J Clin Oncol. 2018 Apr 20;36(12):1199-1206
pubmed: 29373100
Lancet Oncol. 2017 Jul;18(7):874-886
pubmed: 28602779
J Thorac Oncol. 2016 Jun;11(6):e67-72
pubmed: 26751586
Cancer Res. 2011 Sep 15;71(18):6051-60
pubmed: 21791641
N Engl J Med. 2014 Dec 4;371(23):2167-77
pubmed: 25470694
Clin Cancer Res. 2012 Mar 1;18(5):1472-82
pubmed: 22235099
N Engl J Med. 2010 Oct 28;363(18):1734-9
pubmed: 20979473
Cancer Sci. 2013 Nov;104(11):1396-400
pubmed: 23991695
Lancet. 2017 Mar 4;389(10072):917-929
pubmed: 28126333
Lancet Oncol. 2016 Feb;17(2):234-242
pubmed: 26708155
Lung Cancer. 2015 Nov;90(2):255-60
pubmed: 26395848
N Engl J Med. 2017 Aug 31;377(9):829-838
pubmed: 28586279
EBioMedicine. 2019 Mar;41:105-119
pubmed: 30662002
Cancer Sci. 2016 Aug;107(8):1117-23
pubmed: 27270784
Lancet. 2017 Jul 1;390(10089):29-39
pubmed: 28501140
N Engl J Med. 2016 Jan 7;374(1):54-61
pubmed: 26698910
N Engl J Med. 2013 Jun 20;368(25):2385-94
pubmed: 23724913
Nature. 2007 Aug 2;448(7153):561-6
pubmed: 17625570
Cancer Res. 2010 Dec 15;70(24):10038-43
pubmed: 21030459
Cancer Discov. 2016 Oct;6(10):1118-1133
pubmed: 27432227
Proc Natl Acad Sci U S A. 2015 Mar 17;112(11):3493-8
pubmed: 25733882
Lancet Oncol. 2018 Dec;19(12):1654-1667
pubmed: 30413378
Sci Transl Med. 2012 Feb 8;4(120):120ra17
pubmed: 22277784
N Engl J Med. 2010 Oct 28;363(18):1693-703
pubmed: 20979469