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Colon, Rectum & Anal Canal

C18-C21WHO Vol. 1
Digestive System

Key facts

New cases per year
~1.9 million worldwide (WHO, 2022); 158,850 estimated in the US in 2026 (SEER)
5-year relative survival
65.4% overall; 91.3% localized, 16.9% with distant metastases (SEER, 2016–2022)
Main risk factors
Older age, family history, Lynch syndrome and FAP, long-standing inflammatory bowel disease, processed and red meat, obesity, inactivity, smoking, alcohol
Screening
Stool blood tests (FIT/FOBT), sigmoidoscopy, colonoscopy; shown to reduce both incidence and mortality
Typical age at diagnosis
Median 66 years; most frequently diagnosed at ages 65–74 (SEER)

Colorectal cancer develops in the colon or rectum, the final sections of the digestive tract; this section also groups the rarer cancer of the anal canal, which is a distinct disease — most often squamous cell carcinoma, mainly caused by HPV infection. Typical signs include blood in the stool (bright red or very dark), a change in bowel habits (diarrhea, constipation, narrower stools), abdominal discomfort, unexplained weight loss and fatigue; early-stage disease often causes no symptoms at all. Risk factors include older age, a family history of colorectal cancer, inherited syndromes (Lynch syndrome, familial adenomatous polyposis), long-standing inflammatory bowel disease, and lifestyle factors such as a diet high in processed and red meat, obesity, physical inactivity, smoking and alcohol. The cancer is detected through screening — stool blood tests (FIT/FOBT), sigmoidoscopy or colonoscopy — and the diagnosis is confirmed by biopsy; screening has been shown to reduce both incidence and mortality. Worldwide it is the third most common cancer, with about 1.9 million new cases and more than 900,000 deaths per year (WHO, 2022 data).

Prognosis

Prognosis depends strongly on the stage at diagnosis. In US SEER data (2016–2022), 5-year relative survival is 65.4% overall: 91.3% when the cancer is still confined to the bowel (localized), 75.2% when it has spread to nearby structures or lymph nodes (regional), and 16.9% when distant metastases are present — and about a third of cases (34%) are currently found at the localized stage. Beyond stage, prognosis also depends on whether the tumor can be completely removed surgically, on the tumor's genetic features, and on general health. These are population statistics drawn from large groups of patients treated in the past: they cannot predict the course of any individual person's disease, and outcomes keep improving — US colorectal cancer death rates have been falling by about 1.3% per year (2015–2024).

🔬 Histological Types

📚 Latest Research

2026-09-08 • AI

From cell counts to cellular interactions: Cu-Cyto and the co-localization index as a spatial framework for the tumor immune microenvironment of rectal cancer.

Yamashita K, et al

A new deep learning framework combining Cu-Cyto image cytometry — capable of detecting and classifying approximately twenty cell types from standard immunohistochemistry whole-slide images — with a novel Co-Localization Index demonstrates that stromal, but not intratumoral, density of CD103⁺CD8⁺ tissue-resident memory-like T cells independently predicts relapse-free survival in rectal cancer patients treated with neoadjuvant chemoradiotherapy. The Cu-Cyto platform uses a bit-pattern kernel-filtering algorithm to prevent multi-counting and an off-target labeling strategy for precise nuclear-center localization, while the Co-Localization Index converts cell-classification probabilities and coordinates into a single quantitative measure of spatial co-localization between two or three cell types. This spatial framework moves beyond conventional density-based metrics such as the Immunoscore by capturing within-compartment cellular interactions, including tri-cellular relationships among CD103⁺CD8⁺ T cells, tumor cells, and stromal components. Prospective validation in independent rectal-cancer cohorts is planned to assess whether the framework can support clinical decisions on watch-and-wait organ preservation and adjuvant chemotherapy, with potential extension to other solid tumors.

International journal of clinical oncology

Source →
2026-09-08

Slap restricts oncogenic Src-family kinase signaling to maintain colonic epithelial homeostasis.

Naim D, et al

Researchers have identified SLAP (Src-like adaptor protein) as a critical tumor suppressor in the colon that restrains oncogenic signaling driven by the receptor tyrosine kinase EPHB2 and Src-family kinases (SFKs). Using mice with epithelial-specific deletion of Slap and the azoxymethane/dextran sodium sulfate colorectal cancer model, the study demonstrated that loss of SLAP increases colonic epithelial cell proliferation and accelerates tumor development, effects also observed in normal and tumor-derived colonic organoids. Mechanistically, SLAP was found to directly regulate EPHB2, with Slap deficiency leading to elevated EPHB2 protein abundance, increased tyrosine phosphorylation, and enhanced association with active SRC kinase. Crucially, pharmacological inhibition of EPHB2 suppressed SRC activation and reversed the hyperproliferative phenotype, identifying the EPHB2–SFK axis as a non-genetic driver of colonic transformation and a potential therapeutic target in colorectal cancer.

eLife

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2026-09-08

Non-coding RNA 7SK drives tumor resistance by coupling local oncogenic activation with global transcriptional repression.

Xu P, et al

A new study has uncovered a dual-axis "local activation–global suppression" mechanism by which the non-coding RNA 7SK drives therapy resistance in colorectal cancer. Using single-cell multi-omics integrated with functional assays, researchers demonstrated that 7SK selectively activates the JUN transcriptional network to fuel tumor proliferation while simultaneously reducing global transcriptional entropy to stabilize an immunosuppressive microenvironment and promote immune escape. This paradoxical mechanism is conserved across multiple cancer types, positioning 7SK as a potential pan-cancer therapeutic target and providing a new framework for understanding and combating non-coding RNA-mediated resistance.

PLoS computational biology

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💊 Therapies

Surgery
Radiation Therapy
Chemotherapy
Immunotherapy
Targeted therapies
Other local treatment methods

🥗 Diet

Mediterranean diet Nutrition in cancer cachexia Nutritional support around gastrointestinal cancer surgery Alcohol and cancer risk Red and processed meat Sugar and cancer - what the evidence shows Dietary fibre and wholegrain foods Dairy and calcium - the evidence points both ways Excess body fatness and cancer risk Oral nutritional supplements (ONS) Fibre and low-residue diets during pelvic radiotherapy

🫙 Supplements

Vitamin D St John's wort (Hypericum perforatum) Curcumin Omega-3 fatty acids (EPA and DHA) Selenium Probiotics and the gut microbiome in cancer immunotherapy American ginseng (Panax quinquefolius) for cancer-related fatigue Probiotics for diarrhoea caused by chemotherapy and radiotherapy Green tea and EGCG Laetrile (amygdalin, so-called vitamin B17) St John's wort (Hypericum perforatum) Reishi mushroom (Ganoderma lucidum) Glutamine (L-glutamine) Magnesium during cancer treatment Alpha-lipoic acid and chemotherapy-induced peripheral neuropathy Berberine Green tea and EGCG (high-dose extracts)

🧪 Tumor markers

Carcinoembryonic antigen

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🩺 Centers for this diagnosis

Show all centers for this diagnosis (36) ›
See all › Outpatient clinics for this diagnosis (24) ›

Sources

  1. NCI SEER Cancer Stat Facts: Colorectal Cancer ↗
  2. NCI PDQ: Colon Cancer Treatment (Patient Version) ↗
  3. NCI PDQ: Rectal Cancer Treatment (Patient Version) ↗
  4. WHO Fact Sheet: Colorectal Cancer ↗
  5. NCI: What Is Anal Cancer? ↗