Colorectal cancer arises in the colon or rectum, usually from benign growths called polyps that gradually accumulate genetic and epigenetic alterations. It is one of the most common cancers worldwide and a leading cause of cancer death, yet it is highly preventable and often curable if detected early.

Most cases are sporadic and linked to age, lifestyle, and environmental factors such as diets high in red and processed meat, low fiber intake, obesity, sedentary behavior, alcohol, and smoking. A smaller fraction is driven by inherited syndromes, including familial adenomatous polyposis and Lynch syndrome, which greatly increase lifetime risk. On the molecular level, colorectal tumors progress through distinct pathways characterized by chromosomal instability, microsatellite instability, or CpG island methylation, each affecting key genes such as APC, KRAS, TP53, and mismatch repair genes.

Screening is central to control. Stool tests for occult blood or tumor DNA and endoscopic methods like colonoscopy and sigmoidoscopy can detect early cancers and remove precancerous polyps. Guidelines typically recommend starting screening at midlife, earlier for high risk groups.

Treatment depends on stage and often combines surgery, radiotherapy, and systemic therapies. Traditional chemotherapy agents such as fluoropyrimidines, oxaliplatin, and irinotecan remain important. In metastatic disease, targeted therapies that inhibit EGFR or VEGF and immunotherapies that unleash T cell responses have improved outcomes, particularly for tumors with microsatellite instability. Ongoing research aims to refine molecular classification, identify predictive biomarkers, personalize therapy, and develop prevention strategies through diet, microbiome modulation, and risk adapted screening.