Colorectal Cancer Screening & Polyps
When to start, which test, how often to return, and how CRC is treated
Average-risk screening
Start at 45. For average-risk adults, colorectal cancer screening begins at age 45 (USPSTF 2021, ACS), lowered from 50 because early-onset colorectal cancer is rising. Screen routinely through 75, selectively from 76 to 85 based on health and prior screening, and generally not after 85.
| Test | Interval | Key points |
|---|---|---|
| Colonoscopy | Every 10 years | Gold standard; finds and removes polyps in one procedure |
| Fecal immunochemical test (FIT) | Every year | Detects human globin; single sample; no diet or drug restrictions |
| Multitarget stool DNA-FIT (Cologuard) | Every 3 years | More sensitive but less specific than FIT alone |
| CT colonography | Every 5 years | Needs bowel prep; cannot remove polyps |
| Flexible sigmoidoscopy | Every 5 years | Examines only the distal colon |
FIT beats guaiac. Because FIT detects human globin, it needs no dietary or medication restrictions and is more specific for lower-GI bleeding than older guaiac cards (gFOBT), which react to dietary peroxidases and upper-GI blood.
Higher-risk groups
| Group | Start colonoscopy | Repeat |
|---|---|---|
| One first-degree relative with CRC or advanced adenoma | Age 40, or 10 years before the youngest relative's diagnosis, whichever is earlier | Every 5 years |
| Ulcerative colitis or Crohn colitis | 8 years after diagnosis; at diagnosis if PSC coexists | Every 1–3 years with biopsies for dysplasia (yearly with PSC) |
| Lynch syndrome | Age 20–25, or 2–5 years before the earliest family case | Every 1–2 years |
| Familial adenomatous polyposis | Age 10–12 | Yearly sigmoidoscopy or colonoscopy until colectomy |
PSC plus IBD is the highest-risk combination for colorectal cancer, so surveillance starts at the moment IBD is diagnosed.
Lynch syndrome. An autosomal dominant germline mismatch-repair mutation (MLH1, MSH2, MSH6, PMS2) causes microsatellite instability (MSI) and fast adenoma-to-cancer progression, hence the short interval. Cancers are often right-sided and early; endometrial cancer is the most common extracolonic tumor, with ovarian, gastric, small-bowel, and urinary tract cancers also increased. Suspect it with Amsterdam or Bethesda criteria and confirm with tumor MSI testing or immunohistochemistry for mismatch-repair proteins, followed by germline testing.
FAP. An autosomal dominant APC mutation produces hundreds to thousands of adenomas starting in adolescence. Cancer risk approaches 100%, so prophylactic colectomy is required. Duodenal and periampullary adenomas need upper endoscopy; desmoid tumors and osteomas (Gardner variant) and retinal pigment epithelial hypertrophy are extracolonic clues. Attenuated FAP has fewer polyps and later onset.
Polyps and post-polypectomy surveillance
Polyp risk. Small hyperplastic polyps in the rectosigmoid have negligible malignant potential. Adenomas are the classic precursor: tubular carries the least risk, villous the most. Sessile serrated lesions, often flat and right-sided, are also precancerous. An advanced adenoma is ≥10 mm, has villous histology, or has high-grade dysplasia.
Repeat colonoscopy after a complete exam:
- 10 years: normal exam, or small hyperplastic rectosigmoid polyps
- 7–10 years: 1–2 tubular adenomas <10 mm
- 3–5 years: 3–4 small adenomas
- 3 years: an advanced adenoma, or 5–10 adenomas
- 1 year: more than 10 adenomas (and consider genetic testing for a polyposis syndrome)
- About 6 months: piecemeal removal of a lesion ≥20 mm, to check for residual tissue
Presentation, diagnosis, and staging
Right bleeds, left obstructs. Screening finds most cancers before symptoms. Symptomatic tumors behave according to the caliber of the colon and consistency of the stool around them.
| Feature | Right-sided (cecum, ascending) | Left-sided (sigmoid, rectum) |
|---|---|---|
| Growth | Bulky exophytic mass in a wide lumen with liquid stool | Infiltrating, circumferential ("apple-core") lesion in a narrow lumen |
| Presentation | Occult bleeding: iron-deficiency anemia and fatigue, normal bowel habits | Obstruction: change in stool caliber, constipation, hematochezia |
Iron-deficiency anemia in a man or a postmenopausal woman is GI blood loss until proven otherwise. Streptococcus gallolyticus (bovis) bacteremia or endocarditis also warrants colonoscopy to hunt for occult colon cancer.
Diagnosis and staging. Colonoscopy with biopsy establishes the diagnosis. Stage with CT of the chest, abdomen, and pelvis and a baseline CEA; rectal cancer adds pelvic MRI (and endorectal ultrasound) to assess T stage. Staging is TNM: stages I–II are node-negative, stage III is node-positive, and stage IV has distant spread, most often to the liver through the portal vein. Nodal involvement drives adjuvant therapy.
Treatment and follow-up
Colon cancer: surgery first. Resect with regional lymphadenectomy. Add adjuvant FOLFOX (5-FU, leucovorin, oxaliplatin) for stage III (node-positive) and high-risk stage II disease; stage I needs surgery alone.
Rectal cancer: shrink first. Stage II/III rectal cancer receives neoadjuvant chemoradiation to downstage the tumor, followed by total mesorectal excision.
Metastatic disease. Chemotherapy plus biologics: bevacizumab (anti-VEGF), and cetuximab (anti-EGFR) only if the tumor is RAS wild-type. MSI-high tumors respond to checkpoint inhibitors, and limited liver metastases can be resected.
CEA monitors, never screens. CEA is nonspecific (also raised by smoking, cirrhosis, and other cancers), so it is not a screening test. After curative resection, surveillance uses CEA every 3–6 months, periodic CT, and colonoscopy at 1 year to detect recurrence or metachronous tumors.