Molecular Subtypes Are Frequently Discordant Between Lesions in Patients With Synchronous Colorectal Cancer: Molecular Analysis of 59 Patients.
Adult
Aged
Aged, 80 and over
Colorectal Neoplasms
/ genetics
DNA Methylation
Female
Humans
Male
Microsatellite Instability
Middle Aged
MutL Protein Homolog 1
/ metabolism
Proto-Oncogene Proteins B-raf
/ genetics
Proto-Oncogene Proteins p21(ras)
/ genetics
Tumor Suppressor Protein p53
/ genetics
beta Catenin
/ genetics
BRAF
Colorectal cancer
MLH1 methylation
MSI
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
Mar 2019
Mar 2019
Historique:
received:
22
01
2019
revised:
18
02
2019
accepted:
21
02
2019
entrez:
8
3
2019
pubmed:
8
3
2019
medline:
12
3
2019
Statut:
ppublish
Résumé
We aimed to investigate the molecular features of synchronous colorectal cancer (CRC). Out of 1,262 patients with CRC, 130 lesions in 59 patients with synchronous CRC were retrospectively analyzed. Microsatellite, v-Ki-Ras2 Kristen rat sarcoma viral oncogene homolog (KRAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), tumor protein 53 (TP53) and β-catenin status were evaluated and compared between synchronous CRC lesions in each patient. The subtypes of instability, BRAF and β-catenin subtypes was significant but low. Patients with discordant KRAS and TP53 were not concordant between lesions in the same patient, and concordance of microsatellite KRAS/BRAF subtypes comprised 50.8% of those with synchronous CRC. The rate of patients with lesions containing both mutL homolog 1 (MLH1) methylation and microsatellite stable status was 66.7% in those with synchronous CRC, with at least one lesion with high microsatellite instability. The present study on synchronous CRC demonstrated a low concordance of molecular subtypes between lesions in the same patient. A molecular analysis of metastatic lesions is warranted for molecular targeted therapy of metastatic synchronous CRC.
Sections du résumé
BACKGROUND
BACKGROUND
We aimed to investigate the molecular features of synchronous colorectal cancer (CRC).
MATERIALS AND METHODS
METHODS
Out of 1,262 patients with CRC, 130 lesions in 59 patients with synchronous CRC were retrospectively analyzed. Microsatellite, v-Ki-Ras2 Kristen rat sarcoma viral oncogene homolog (KRAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), tumor protein 53 (TP53) and β-catenin status were evaluated and compared between synchronous CRC lesions in each patient.
RESULTS
RESULTS
The subtypes of instability, BRAF and β-catenin subtypes was significant but low. Patients with discordant KRAS and TP53 were not concordant between lesions in the same patient, and concordance of microsatellite KRAS/BRAF subtypes comprised 50.8% of those with synchronous CRC. The rate of patients with lesions containing both mutL homolog 1 (MLH1) methylation and microsatellite stable status was 66.7% in those with synchronous CRC, with at least one lesion with high microsatellite instability.
CONCLUSION
CONCLUSIONS
The present study on synchronous CRC demonstrated a low concordance of molecular subtypes between lesions in the same patient. A molecular analysis of metastatic lesions is warranted for molecular targeted therapy of metastatic synchronous CRC.
Identifiants
pubmed: 30842178
pii: 39/3/1425
doi: 10.21873/anticanres.13258
doi:
Substances chimiques
CTNNB1 protein, human
0
KRAS protein, human
0
MLH1 protein, human
0
Tumor Suppressor Protein p53
0
beta Catenin
0
BRAF protein, human
EC 2.7.11.1
Proto-Oncogene Proteins B-raf
EC 2.7.11.1
MutL Protein Homolog 1
EC 3.6.1.3
Proto-Oncogene Proteins p21(ras)
EC 3.6.5.2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1425-1432Informations de copyright
Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.