ArticlePloS one2015
c-MYC Copy-Number Gain Is an Independent Prognostic Factor in Patients with Colorectal Cancer.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Cell-free DNA copy number variations in plasma from colorectal cancer patients.Molecular oncology · 2017Trial
- Activation of Kv11.1 potassium channel suppresses non-small cell lung cancer growth by promoting c-Myc degradation.Communications biology · 2025Article
- RETRACTED: The Impact ofInternational journal of molecular sciences · 2025Review
- Establishment and validation of the prognostic risk model based on the anoikis-related genes in esophageal squamous cell carcinoma.Annals of medicine · 2024Article
- MYC upstream region orchestrates resistance to PI3K inhibitors in cancer cells through FOXO3a-mediated autophagic adaptation.Oncogene · 2024Article
- Molecular genetics of early-onset colorectal cancer.World journal of biological chemistry · 2023Review
- Article
- Copy Number Variations as Determinants of Colorectal Tumor Progression in Liquid Biopsies.International journal of molecular sciences · 2023Review
- CCAT 1- A Pivotal Oncogenic Long Non-Coding RNA in Colorectal Cancer.British journal of biomedical science · 2023Review
- Significant position of C-myc in colorectal cancer: a promising therapeutic target.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Transcriptome Analyses Identify DeregulatedBiomolecules · 2022Article
- Copy Number Alterations as Novel Biomarkers and Therapeutic Targets in Colorectal Cancer.Cancers · 2022Review
- Ailanthone suppresses the activity of human colorectal cancer cells through the STAT3 signaling pathway.International journal of molecular medicine · 2022Article
- Association between Altered Oncogenic Signaling Pathways and Overall Survival of Patients with Metastatic Colorectal Cancer.Diagnostics (Basel, Switzerland) · 2021Article
- Dihydroartemisinin is potential therapeutics for treating late-stage CRC by targeting the elevated c-Myc level.Cell death & disease · 2021Article
- Case Report: Analysis of Circulating Tumor Cells in a Triple Negative Spindle-Cell Metaplastic Breast Cancer Patient.Frontiers in medicine · 2021Article
- An Early-Onset Advanced Rectal Cancer Patient With Increased KRAS Gene Copy Number Showed A Primary Resistance to Cetuximab in Combination With Chemotherapy: A Case Report.Frontiers in oncology · 2021Article
- Article
- The prognostic role of c-MYC amplification in schistosomiasis-associated colorectal cancer.Japanese journal of clinical oncology · 2020Article
- Actionable Potentials of Less Frequently Mutated Genes in Colorectal Cancer and Their Roles in Precision Medicine.Biomolecules · 2020Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 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).
methodsThe 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.
resultsIn 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.
conclusionsc-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.
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