English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Background  The aim of this study was to determine the incidence and clinicopathological significance of  c-MYC  gene copy-number (GCN) gain in patients with primary colorectal cancer (CRC).    Methods  The  c-MYC  GCN was investigated in 367 consecutive CRC patients (cohort 1) by using dual-color silver  in situ  hybridization. Additionally, to evaluate regional heterogeneity, we examined CRC tissue from 3 sites including the primary cancer, distant metastasis, and lymph-node metastasis in 152 advanced CRC patients (cohort 2).  KRAS  exons 2 and 3 were investigated for mutations.    Results  In cohort 1,  c-MYC  gene amplification, defined by a  c-MYC :centromere of chromosome 8 ratio ≥ 2.0, was detected in 31 (8.4%) of 367 patients. A  c-MYC  GCN gain, defined by ≥ 4.0  c-MYC  copies/nucleus, was found in 63 (17.2%) patients and was associated with poor prognosis ( P  = 0.015). Multivariate Cox regression analysis showed that the hazard ratio for  c-MYC  GCN gain was 2.35 (95% confidence interval, 1.453–3.802;  P  < 0.001). In a subgroup of stage II-III CRC patients,  c-MYC  GCN gain was significantly associated with poor prognosis by univariate ( P  = 0.034) and multivariate ( P  = 0.040) analyses.  c-MYC  protein overexpression was observed in 201 (54.8%) out of 367 patients and weakly correlated with  c-MYC  GCN gain (ρ, 0.211). In cohort 2, the  c-MYC  genetic status was heterogenous in advanced CRC patients. Discordance between GCN gain in the primary tumor and either distant or lymph-node metastasis was 25.7% and 30.4%, respectively. A similar frequency for  c-MYC  GCN gain and amplification was observed in CRC patients with both wild-type and mutated  KRAS .    Conclusions    c-MYC  GCN gain was an independent factor for poor prognosis in consecutive CRC patients and in the stage II-III subgroup. Our findings indicate that the status of  c-MYC  may be helpful in predicting the patients’ outcome and for managing CRC patients.

c-MYC Copy-Number Gain Is an Independent Prognostic Factor in Patients with Colorectal Cancer