Colorectal cancer is a malignant tumor of the colon and rectum that originates from the epithelial cells of their inner surface. In frequency, it ranks third after lung, prostate, or breast cancer depending on sex. In Ukraine, the incidence is about 37 new cases per 100,000 population per year.
Prevalence in Europe
The highest incidence of colorectal cancer among European countries is in the Czech Republic: 60.3 cases in men and 32 in women per 100,000 population. Next are Hungary (60 and 35), Slovakia (51 and 27), and Germany (45 and 32). The lowest rates are in Greece (17.4 and 14), Romania (21.1 and 14.3), Lithuania (25 and 17), Finland (25.2 and 21.2), and Latvia (26 and 19.1).
Polyps as a precancerous stage: the molecular side
Some colorectal carcinomas arise from adenomas. Histologically, CRC is an adenocarcinoma: an epithelial tumor from the glandular epithelium of the mucosal layer that grows into the bowel wall, the submucosal and muscular layers. The transition of an adenoma to cancer is associated with the accumulation of mutations, in particular in the TP53 gene, which encodes the p53 protein and regulates cell division and apoptosis. When the Wnt signaling pathway is damaged, disruption of this regulation may accompany the transformation of an adenoma into carcinoma. A key role in the Wnt pathway is played by the APC gene: its protein restrains the accumulation of β-catenin, while mutated APC does not do this, so β-catenin accumulates, migrates to the nucleus, and activates transcription of genes that under normal conditions regulate stem cell renewal. Other mutations have also been described — in the β-catenin suppressor genes AXIN1, AXIN2, TCF7L2, NKD1, as well as increased expression of the oncogenes KRAS, C-Raf, and PI3K, which stimulate proliferation.
Signs called classic
Classic symptoms: constipation, blood and/or mucus in the stool, decreased stool caliber, loss of appetite, weight loss, nausea, vomiting. Rectal bleeding and anemia are common signs, especially in people over 50 years of age. Location changes the picture: right-sided tumors more often cause anemia and rarely obstruction, while left-sided tumors grow into the bowel lumen and can cause intestinal obstruction.
Risk factors and hereditary forms
Hereditary, sporadic, and familial forms are distinguished. The hereditary form occurs at a young age in families with a diagnosis; in it, the underlying condition is often familial adenomatous polyposis or hereditary nonpolyposis colorectal cancer. The sporadic form is diagnosed in the absence of a family history, more often after age 60, and genetic changes are present only in the tumor cells. It is considered that for the familial form the risk doubles if a first-degree relative had CRC before age 50. The absence of a family history does not exclude cancer: the sporadic form is diagnosed precisely when there are no relatives with this diagnosis.
How it is diagnosed
Diagnosis is carried out using endoscopic methods performed by an endoscopist; if a tumor is suspected, a biopsy is performed.
- colonoscopy and sigmoidoscopy — endoscopic detection of a suspicious formation;
- pathohistological analysis of the biopsy confirms the diagnosis;
- barium passage with X-ray examination — a less sensitive method;
- CT, MRI, and PET — if distant metastases are suspected.
Distant metastases most often occur in the liver and lungs, so before surgery the organs of the abdominal and thoracic cavities are examined.
Risk groups and screening
Data indicate that the risk of colorectal cancer is increased in people with the hereditary form, especially with familial adenomatous polyposis or hereditary nonpolyposis colorectal cancer. Also at increased risk are individuals whose first-degree relatives had CRC before age 50, and patients with the sporadic form, which more often occurs after age 60. Endoscopic methods are used to detect precancerous changes, in particular colonoscopy and sigmoidoscopy, during which the endoscopist can detect a suspicious formation and take a biopsy for pathohistological analysis.
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