Association of KRAS mutation with tumor deposit status and overall survival of colorectal cancer.


Journal

Cancer causes & control : CCC
ISSN: 1573-7225
Titre abrégé: Cancer Causes Control
Pays: Netherlands
ID NLM: 9100846

Informations de publication

Date de publication:
Jul 2020
Historique:
received: 16 12 2019
accepted: 04 05 2020
pubmed: 13 5 2020
medline: 12 9 2020
entrez: 13 5 2020
Statut: ppublish

Résumé

To examine associations of KRAS mutation with tumor deposit status and overall survival in colorectal cancer (CRC) patients. This retrospective cohort study included patients with incidental CRC diagnosed during 2010-2014 and recorded statuses of KRAS and tumor deposit in the National Cancer Database of the USA. Multivariable logistic regression and time-varying Cox regression analyses were used. We included 45,761 CRC patients with KRAS status (24,027 [52.5%] men, 24,240 [53.0%] < 65 years old, 17,338 [37.9%] with KRAS mutation). Adjusted for microsatellite instability, age, pathologic stage and tumor grade, KRAS mutation (versus wild type) was associated with tumor deposit presence (odds ratio = 1.11, 95% CI 1.02-1.20). KRAS mutation was also linked to worse overall survival of CRC patients regardless of tumor deposit status (adjusted Hazard ratio [HR] = 1.20, 95% CI 1.07-1.33 for CRC with tumor deposits, and adjusted HR = 1.24, 95% CI 1.14-1.35 or CRC without) or tumor stage (adjusted HR = 1.32, 95% CI 1.14-1.54 for early-stage and adjusted HR = 1.18, 95% CI 1.10-1.27 for late-stage). Microsatellite instability was associated with better overall survival in CRC without tumor deposit (adjusted HR = 0.89, 95% CI 0.79-0.99), but not in CRC with tumor deposit (adjusted HR = 1.12, 95% CI 0.97-1.30). KRAS mutation is independently associated with tumor deposit presence and a worse overall survival in CRC patients.

Identifiants

pubmed: 32394229
doi: 10.1007/s10552-020-01313-0
pii: 10.1007/s10552-020-01313-0
pmc: PMC7319095
mid: NIHMS1593452
doi:

Substances chimiques

KRAS protein, human 0
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

683-689

Subventions

Organisme : NCCIH NIH HHS
ID : R01 AT010243
Pays : United States
Organisme : National Natural Science Foundation of China
ID : 81872387
Organisme : NIH HHS
ID : AT010243
Pays : United States

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Auteurs

Meifang Zhang (M)

Department of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.
Department of Pathology, Princeton Medical Center, 1 Plainsboro Rd, Plainsboro, NJ, 08536, USA.

Wenwei Hu (W)

Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.

Kun Hu (K)

Department of Pathology, University at Buffalo, Buffalo, NY, USA.

Yong Lin (Y)

Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.
Department of Biostatistics, School of Public Health, Rutgers University, Piscataway, NJ, USA.

Zhaohui Feng (Z)

Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.

Jing-Ping Yun (JP)

Department of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China.

Nan Gao (N)

Department of Biological Sciences, Rutgers University, Newark, NJ, USA.

Lanjing Zhang (L)

Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA. lanjing.zhang@rutgers.edu.
Department of Pathology, Princeton Medical Center, 1 Plainsboro Rd, Plainsboro, NJ, 08536, USA. lanjing.zhang@rutgers.edu.
Department of Biological Sciences, Rutgers University, Newark, NJ, USA. lanjing.zhang@rutgers.edu.
Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, USA. lanjing.zhang@rutgers.edu.

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