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Comparing Copy Number Variations and SNPs

Comparing Copy Number Variations and SNPs

Sequencing of the human genome has opened up several best-kept secrets of the genome. Scientists have identified thousands of genome variations that exist within a population. These variations can be a single nucleotide or a larger chromosomal variation.
Copy number variations or CNVs are the structural variations that cover more than 1kb of DNA sequence. The single nucleotide polymorphism (SNP), on the other hand, is a single nucleotide change or a point mutation that is found in more than 1%...

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Cancer-Critical Genes I: Proto-oncogenes

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Updated: Jul 7, 2025

Comparative Lesions Analysis Through a Targeted Sequencing Approach

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Published on: November 5, 2019

Somatic Copy Number Alterations in Colorectal Cancer Lead to a Differentially Expressed ceRNA Network (ceRNet).

Héctor Herrera-Orozco^1,2, Verónica García-Castillo¹, Eduardo López-Urrutia¹

¹Laboratorio de Genómica, FES-Iztacala, Universidad Nacional Autónoma de México. Av. De los Barrios 1, Los Reyes Iztacala, Tlalnepantla 54090, Mexico.

Current Issues in Molecular Biology

|December 22, 2023

Summary

Colorectal cancer (CRC) involves chromosome instability. This study reveals how copy number alterations affect long non-coding RNAs (lncRNAs), impacting CRC and identifying key lncRNAs for patient survival.

Keywords:

colorectal cancer competitive endogenous RNA (ceRNA) network long non-coding RNAs somatic copy number alterations

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Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

Area of Science:

Genomics
Molecular Biology
Oncology

Background:

Colorectal cancer (CRC) is a leading cause of cancer death.
Chromosome instability, leading to copy number alterations, is common in CRC.
The role of copy number alterations in long non-coding RNA (lncRNA) regulation and CRC phenotype requires further investigation.

Purpose of the Study:

To investigate differentially expressed lncRNAs in copy number alteration regions in colorectal cancer.
To construct a competing endogenous RNA (ceRNA) network to understand lncRNA-mediated gene regulation.
To assess the clinical relevance of lncRNA expression in CRC patient survival.

Main Methods:

Utilized The Cancer Genome Atlas (TCGA) repository for colorectal adenocarcinoma RNA-seq and copy number alteration data.
Performed differential expression analysis for lncRNAs, miRNAs, and mRNAs.
Constructed a lncRNA-miRNA-mRNA ceRNA network and conducted KEGG/GO pathway and survival analyses.

Main Results:

Identified 78 differentially expressed lncRNAs, 410 miRNAs, and 5028 mRNAs.
Established a ceRNA network comprising 30 lncRNAs, 19 miRNAs, and 77 mRNAs, enriched in oncogenic and anti-oncogenic pathways.
Found that C5orf64, HOTAIR, and RRN3P3 lncRNA expression levels correlate with overall patient survival.

Conclusions:

lncRNAs located in somatically acquired copy number alteration regions are integral to a complex gene regulatory network in colorectal cancer.
These lncRNAs play significant roles in CRC pathogenesis and represent potential prognostic biomarkers.