Colorectal Neoplasms

The supplied grounding supports a multifactorial etiology rather than a single cause. Reported causes or associated etiologic factors include chronic ulcerative colitis, familial polyposis coli, asbestos exposure, and irradiation of the cervix uteri, along with mutations affecting oncogenes, tumor suppressor genes, and DNA repair pathways.

The disease is linked to mutations in genes involved in oncogenic signaling, tumor suppression, and DNA repair, including DNA mismatch repair and microsatellite repeat instability. The literature also emphasizes chronic inflammation, tumor microenvironment effects, cytokine signaling, dysregulated gene expression, and microbiome-associated dysbiosis as contributors to malignant transformation, progression, angiogenesis, and metastasis.

Supported risk factors include chronic ulcerative colitis, familial polyposis coli, asbestos exposure, and prior irradiation of the cervix uteri. Review literature also identifies obesity, lack of physical exercise, smoking, ageing, and dietary habits associated with high-income countries as factors that increase risk.

Treatment is described at the modality level as a combination of endoscopic and surgical local excision, preoperative radiotherapy for downstaging, systemic therapy, extensive surgery for locoregional or metastatic disease, local ablative therapies for metastases, and palliative chemotherapy. Drug classes and targeted approaches mentioned in the grounding include fluoropyrimidines, irinotecan, oxaliplatin-based chemotherapy, anti-EGFR therapy, anti-angiogenesis therapy, immune checkpoint inhibitors, and other targeted therapies.