Colon cancer
Colon cancer is one of the commonest cancers and also one of the most preventable. Almost all of it develops from a polyp — a benign growth that takes years to become malignant. That long interval is what makes screening effective: removing a polyp at colonoscopy prevents a cancer that would otherwise have appeared a decade later. When it is found early, it is curable in the great majority of cases, and even when it has spread to the liver, cure remains possible for a significant proportion of patients.
How it forms
Most colon cancers follow the adenoma-carcinoma sequence, one of the best-characterised progressions in cancer biology. It unfolds over ten to fifteen years through an accumulation of genetic faults, each one conferring a further growth advantage:
- Loss of the APC gene — normally a brake on the Wnt signalling pathway. Without it, β-catenin accumulates in the cell and drives continuous proliferation. This produces the initial small adenoma.
- KRAS mutation — locking a growth signalling switch permanently on, so the adenoma enlarges.
- Loss of SMAD4 and other tumour suppressor genes on chromosome 18, releasing further restraint and producing dysplasia.
- Loss of TP53 — the guardian that normally halts the cell cycle or triggers cell death in response to DNA damage. Its loss permits the accumulated abnormalities to persist, and invasion follows.
A second route, the serrated pathway, accounts for a substantial minority. Sessile serrated lesions, typically flat, subtle and in the right colon, progress through BRAF mutation and widespread methylation of gene promoters, silencing genes including the mismatch repair gene MLH1. These lesions are easier to miss at colonoscopy and progress faster than conventional adenomas, which is why bowel preparation quality and careful withdrawal technique matter so much.
A third route is mismatch repair deficiency, inherited in Lynch syndrome or acquired through methylation. The repair system that corrects errors during DNA copying fails, so mutations accumulate rapidly — producing microsatellite instability. These tumours look different under the microscope, occur more often in the right colon, and, importantly, respond very well to immunotherapy, which conventional colon cancers largely do not.
Risk factors
- age — risk rises from the fifties, though incidence in younger adults is rising and symptoms in a person under fifty should not be dismissed on age alone
- adenomatous or serrated polyps, and previous colorectal cancer
- family history; inherited syndromes — Lynch syndrome, familial adenomatous polyposis and others, covered on their own page
- inflammatory bowel disease of long duration, particularly extensive colitis
- diet high in red and processed meat, low in fibre
- obesity, physical inactivity, smoking, alcohol, type 2 diabetes
Symptoms
Early cancers cause nothing. When symptoms appear, they differ by side, which is worth understanding because right-sided cancers are the ones that present late.
Right colon — wide lumen, liquid contents. Tumours grow large before obstructing, and typically present with:
- iron-deficiency anaemia — tiredness, breathlessness, pallor, often without any bowel symptom at all
- vague abdominal discomfort
- weight loss
- a palpable mass
Left colon — narrower lumen, formed stool. Tumours obstruct earlier:
- change in bowel habit — looser, more frequent, or alternating
- rectal bleeding, often mixed with the stool
- crampy abdominal pain
- obstruction — a proportion of patients present as an emergency
Unexplained iron-deficiency anaemia in an adult requires investigation of the bowel. So does a persistent change in bowel habit, or rectal bleeding lasting more than a few weeks. Attributing rectal bleeding to haemorrhoids without examining the bowel is the commonest reason for delayed diagnosis.
How the diagnosis is made
- Colonoscopy — the definitive test. It visualises the whole colon, takes biopsies, tattoos the lesion to locate it at surgery, and detects synchronous tumours and polyps, which occur in a meaningful minority.
- CT colonography where colonoscopy is incomplete or unsuitable.
- CT of chest, abdomen and pelvis for staging — local extent, lymph nodes, liver and lung.
- MRI of the liver where lesions are seen on CT and resection may be considered.
- CEA — a baseline tumour marker, useful mainly for follow-up rather than diagnosis.
- Mismatch repair / microsatellite instability testing on all colorectal cancers — it identifies Lynch syndrome and, critically, identifies the patients for whom immunotherapy is highly effective.
- RAS and BRAF testing in advanced disease, to guide targeted treatment.
Treatment
Surgery
Surgery is the mainstay for localised disease. The operation is defined by the blood supply rather than by the tumour alone: the segment of colon is removed together with its mesentery and the lymph nodes along the feeding artery, taken at its origin. This is why a small tumour still requires removal of a substantial length of bowel.
- Right hemicolectomy — caecum and ascending colon
- Extended right hemicolectomy — hepatic flexure and transverse colon
- Left hemicolectomy — descending colon
- Sigmoid colectomy / high anterior resection — sigmoid colon
- Subtotal colectomy — for synchronous tumours, or in Lynch syndrome
A minimum of twelve lymph nodes should be examined, as this determines the accuracy of staging and therefore whether chemotherapy is offered.
Laparoscopic and robotic surgery is standard, with equivalent cancer outcomes and less pain, fewer wound complications and faster recovery. Enhanced recovery protocols — carbohydrate loading, avoiding routine drains and tubes, early feeding and early mobilisation — have shortened hospital stay substantially and are now routine.
In most cases the bowel is rejoined and no stoma is needed. A temporary stoma may be used where the join is at risk, and emergency surgery for obstruction or perforation more often requires one.
Very early cancers within a polyp may be adequately treated by complete endoscopic removal alone, where the invasion is superficial, the margin is clear, and there is no lymphovascular invasion or poor differentiation.
Chemotherapy
- Stage III (lymph node involvement) — adjuvant chemotherapy after surgery improves survival and is standard. Duration is tailored — three months rather than six for lower-risk disease, reducing nerve toxicity without loss of benefit.
- Stage II — offered selectively, where high-risk features are present: perforation, obstruction, poor differentiation, lymphovascular or perineural invasion, or fewer than twelve nodes examined. Mismatch repair-deficient stage II tumours have a good prognosis and generally do not benefit from the standard agent.
- Circulating tumour DNA testing after surgery is increasingly used to identify residual disease and refine these decisions.
Metastatic disease
This is where the outlook has changed most, and patients are often given an unduly bleak impression.
- Liver metastases can be cured. Where they are resectable, or can be made resectable by chemotherapy, resection offers long-term survival in a substantial proportion. Ablation, portal vein embolisation to grow the remaining liver, and staged operations extend what is possible. A patient with liver metastases should be assessed by a hepatobiliary surgeon, not written off.
- Lung metastases may similarly be resected.
- Chemotherapy combined with targeted agents — anti-EGFR antibodies for left-sided RAS wild-type tumours, anti-VEGF agents more broadly — prolongs survival considerably.
- Immunotherapy is highly effective for mismatch repair-deficient tumours, producing durable responses where chemotherapy would not.
- Peritoneal disease in selected patients may be treated with cytoreductive surgery and heated intraperitoneal chemotherapy in specialist centres.
Recovery
After laparoscopic colectomy with enhanced recovery, hospital stay is commonly three to five days and return to normal activity four to six weeks. Bowel function is usually looser and more frequent for some weeks to months, particularly after right hemicolectomy, and then settles. Most patients return to an unrestricted diet.
Follow-up
Surveillance aims to detect recurrence while it is still curable: clinical review, CEA measurement, CT scanning at intervals for the first few years, and colonoscopy at one year and thereafter periodically. Most recurrences occur within three years.
When to seek an opinion
Rectal bleeding lasting more than a few weeks, at any age. A persistent change in bowel habit. Unexplained iron-deficiency anaemia. Abdominal pain with weight loss. A family history of bowel cancer, particularly in a relative under fifty or in more than one relative, is a reason to ask about earlier screening.
Common questions
I have bleeding but I have piles. Is that the explanation?
It may well be, but it cannot be assumed. Haemorrhoids are common and can coexist with something else, and the commonest reason a bowel cancer is diagnosed late is that bleeding was attributed to piles without examining the bowel. Bleeding lasting more than a few weeks deserves proper assessment.
Can bowel cancer be prevented?
To a large extent, yes. Nearly all of it grows from polyps over ten years or more, and removing polyps at colonoscopy prevents the cancer forming. This is why screening works and why it is worth taking up when offered.
Will I need a bag?
In most cases, no. For cancers of the colon the bowel is usually rejoined at the same operation. A temporary stoma is sometimes used to protect the join, and is reversed after some months. Permanent stomas are much more often associated with cancers very low in the rectum than with colon cancer.
Why remove so much bowel for a small tumour?
Because the operation must remove the lymph glands that drain that part of the bowel, and those run alongside the artery supplying it. Removing the artery at its origin means removing the segment of bowel it supplies. The length removed reflects the blood supply, not the size of the tumour, and the bowel that remains works well.
Is keyhole surgery as good as open surgery for cancer?
Yes. Large trials have shown the same cancer outcomes, with less pain, fewer wound problems and a faster recovery. It is now the standard approach for most colon cancers.
It has spread to my liver. Does that mean it cannot be cured?
Not necessarily, and this is important. Bowel cancer that has spread to the liver is one of the few situations where removing the secondary deposits can cure the disease, and a significant proportion of such patients are alive and well many years later. Chemotherapy can sometimes shrink deposits enough to make surgery possible. It is worth being assessed by a liver surgeon rather than assuming the answer.
Should my children be screened?
If you have been diagnosed with bowel cancer, first-degree relatives are usually advised to begin screening earlier than the general population. If the cancer occurred young, or several family members are affected, genetic assessment is recommended, since identifying an inherited condition changes the advice for the whole family.
Does diet cause it?
Diet contributes rather than causes. Diets high in red and processed meat and low in fibre are associated with higher risk, as are obesity, inactivity, smoking and alcohol. Changing these reduces risk but does not remove it, and does not replace screening.
Related conditions
Other conditions of the colon & rectum covered on this site:
- Rectal cancer
- Bowel polyps (colorectal polyps)
- Diverticular disease and diverticulitis
- Crohn's disease — the surgical perspective
- Ulcerative colitis — the surgical perspective
- Large bowel obstruction and volvulus
- Appendicitis
- Hereditary bowel cancer syndromes (Lynch syndrome and FAP)
This page provides general information and does not replace an individual medical consultation. Assessment and treatment are decided for each patient after review of their history, examination, investigations and discussion in a multidisciplinary meeting.