The possibility of mutations of RAS signaling genes and/or TP53 in combination as a negative prognostic impact on pathological stage I non-small cell lung cancer.


Journal

Cancer medicine
ISSN: 2045-7634
Titre abrégé: Cancer Med
Pays: United States
ID NLM: 101595310

Informations de publication

Date de publication:
10 2023
Historique:
revised: 13 07 2023
received: 12 03 2023
accepted: 02 09 2023
medline: 23 10 2023
pubmed: 15 9 2023
entrez: 15 9 2023
Statut: ppublish

Résumé

The recurrence rate of non-small cell lung cancer (NSCLC) is as high as 30%, even in the cancer with pathological stage I disease. Therefore, identifying factors predictive of high-risk pathological recurrence is important. However, few studies have examined the genetic status of these tumors and its relationship to prognosis. A cohort of 328 cases of primary lung cancer that underwent complete resection at Tokyo Medical and Dental University (TMDU) was screened for 440 cancer-associated genes using panel testing. Further analyses included 92 cases of pathological stage I NSCLC who did not receive adjuvant chemotherapy. Ridge regression was performed to identify association studies mutational status and postoperative recurrence. These data were then validated using clinical and genetic data from 56 patients in The Cancer Genome Atlas (TCGA). Mutations in TP53, RAS signaling genes KRAS and HRAS, and EGFR were recurrently detected. Ridge regression analysis relevant to recurrence, as well as survival analysis, performed using data from the TMDU cohort revealed significantly shorter relapse-free survival (RFS) for patients with RAS signaling or TP53 gene mutations than for those without (log-rank test, p = 0.00090). This statistical trend was also suggested in the TCGA cohort (log-rank test, p = 0.10). Mutations in RAS signaling genes and/or TP53 could be useful for the prediction of shorter RFS of patients with stage I NSCLC.

Sections du résumé

BACKGROUND
The recurrence rate of non-small cell lung cancer (NSCLC) is as high as 30%, even in the cancer with pathological stage I disease. Therefore, identifying factors predictive of high-risk pathological recurrence is important. However, few studies have examined the genetic status of these tumors and its relationship to prognosis.
MATERIALS AND METHODS
A cohort of 328 cases of primary lung cancer that underwent complete resection at Tokyo Medical and Dental University (TMDU) was screened for 440 cancer-associated genes using panel testing. Further analyses included 92 cases of pathological stage I NSCLC who did not receive adjuvant chemotherapy. Ridge regression was performed to identify association studies mutational status and postoperative recurrence. These data were then validated using clinical and genetic data from 56 patients in The Cancer Genome Atlas (TCGA).
RESULTS
Mutations in TP53, RAS signaling genes KRAS and HRAS, and EGFR were recurrently detected. Ridge regression analysis relevant to recurrence, as well as survival analysis, performed using data from the TMDU cohort revealed significantly shorter relapse-free survival (RFS) for patients with RAS signaling or TP53 gene mutations than for those without (log-rank test, p = 0.00090). This statistical trend was also suggested in the TCGA cohort (log-rank test, p = 0.10).
CONCLUSION
Mutations in RAS signaling genes and/or TP53 could be useful for the prediction of shorter RFS of patients with stage I NSCLC.

Identifiants

pubmed: 37712717
doi: 10.1002/cam4.6535
pmc: PMC10587933
doi:

Substances chimiques

TP53 protein, human 0
Tumor Suppressor Protein p53 0
KRAS protein, human 0
HRAS protein, human EC 3.6.5.2
EGFR protein, human EC 2.7.10.1
ErbB Receptors EC 2.7.10.1
Oncogene Protein p21(ras) EC 3.6.5.2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

19406-19413

Informations de copyright

© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

Références

J Thorac Oncol. 2007 Aug;2(8):706-14
pubmed: 17762336
J Thorac Oncol. 2013 Jan;8(1):52-61
pubmed: 23242438
N Engl J Med. 2020 Aug 13;383(7):640-649
pubmed: 32786189
N Engl J Med. 2017 Jun 1;376(22):2109-2121
pubmed: 28445112
Lancet Oncol. 2022 Oct;23(10):1274-1286
pubmed: 36108662
Arch Pathol Lab Med. 2015 Feb;139(2):189-93
pubmed: 24694341
EBioMedicine. 2019 Mar;41:711-716
pubmed: 30852159
Ann Thorac Surg. 2022 May;113(5):1608-1616
pubmed: 34186090
Int J Cancer. 2019 Apr 15;144(8):1941-1953
pubmed: 30350310
J Clin Oncol. 2014 Jan 10;32(2):121-8
pubmed: 24323028
Mol Carcinog. 2017 Feb;56(2):381-388
pubmed: 27182622
Cancer Sci. 2016 Jun;107(6):713-20
pubmed: 27027665
J Mol Diagn. 2015 May;17(3):251-64
pubmed: 25801821
J Thorac Oncol. 2011 Jul;6(7):1229-35
pubmed: 21610521
Clin Cancer Res. 2017 Jun 15;23(12):3012-3024
pubmed: 28039262
Lung Cancer. 2019 Feb;128:152-157
pubmed: 30553548
Lancet. 2010 Apr 10;375(9722):1267-77
pubmed: 20338627
Lancet. 2021 Oct 9;398(10308):1344-1357
pubmed: 34555333
J Clin Oncol. 2016 May 1;34(13):1484-91
pubmed: 26926677
Nat Med. 2017 Jun;23(6):703-713
pubmed: 28481359
JAMA Oncol. 2020 Nov 01;6(11):1741-1750
pubmed: 32940636
Dis Model Mech. 2022 Feb 1;15(2):
pubmed: 35234863
Transl Lung Cancer Res. 2022 Jan;11(1):24-42
pubmed: 35242625
Nat Rev Cancer. 2016 Apr 26;16(5):319-29
pubmed: 27112209
J Thorac Oncol. 2012 Jun;7(6):963-72
pubmed: 22588152
Nature. 2020 Feb;578(7793):82-93
pubmed: 32025007
Clin Lung Cancer. 2019 May;20(3):e338-e345
pubmed: 30770327
J Thorac Oncol. 2018 Mar;13(3):323-358
pubmed: 29396253
Nature. 2017 Apr 26;545(7655):446-451
pubmed: 28445469
Cell Rep. 2022 Mar 29;38(13):110569
pubmed: 35354049
N Engl J Med. 2020 Oct 29;383(18):1711-1723
pubmed: 32955177
Cancer Med. 2023 Oct;12(19):19406-19413
pubmed: 37712717
Cell. 2018 Apr 5;173(2):321-337.e10
pubmed: 29625050
J Natl Cancer Inst. 2015 Mar 23;107(6):djv059
pubmed: 25802059
Eur Respir Rev. 2016 Dec;25(142):364-371
pubmed: 27903658
J Thorac Oncol. 2015 Sep;10(9):1243-1260
pubmed: 26291008
Ann Surg Oncol. 2012 Jul;19 Suppl 3:S347-54
pubmed: 21607772
J Thorac Oncol. 2022 Mar;17(3):362-387
pubmed: 34808341

Auteurs

Takayuki Honda (T)

Department of Respiratory Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Katsutoshi Seto (K)

Department of Thoracic Surgery, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Satoshi Endo (S)

Department of Respiratory Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.
Soka Municipal Hospital, Soka-shi, Japan.

Akira Takemoto (A)

Bioresource Research Center, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Kousuke Tanimoto (K)

Research Core, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Masashi Kobayashi (M)

Department of Thoracic Surgery, Tokyo Medical and Dental University, Bunkyo-ku, Japan.
Department of Thoracic Surgery, Kurashiki Central Hospital, Kurashiki, Japan.

Masatake Kitano (M)

Department of Respiratory Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Rie Sakakibara (R)

Department of Respiratory Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Takahiro Mitsumura (T)

Department of Respiratory Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Hironori Ishibashi (H)

Department of Thoracic Surgery, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Johji Inazawa (J)

Research Core, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Toshihiro Tanaka (T)

Bioresource Research Center, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Yasunari Miyazaki (Y)

Department of Respiratory Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

Kenichi Okubo (K)

Department of Thoracic Surgery, Tokyo Medical and Dental University, Bunkyo-ku, Japan.

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Classifications MeSH