Описание
COLON CANCER: OVERVIEW
Disease Types & Epidemiology
How common is the disease?
Colorectal or colon cancer is a disease in which cells in the large intestine grow out of control. Regardless of where the cancer started – in the colon or the rectum – tumors in these locations share a lot in common, which is why they’re together known as colorectal cancer. Colorectal cancer (CRC) predominantly develops as malignant tumors where cells are at first dividing on-site and then spreading in different tissues out of the intestine [cdc.gov]
The variety of abnormal cells defines the colorectal cancer type. The most common – 95% - are adenocarcinomas, which arise from glandular epithelial cells. Typical adenocarcinoma takes at least ten years to develop from benign adenoma [Hossain et al., 2022]. However, about 15% of adenocarcinomas are more aggressive in two cases: mucinous adenocarcinoma – 10% of CRC – and signet ring cell adenocarcinoma – 1% of CRC. These tumors may spread rapidly within 2-3 years after appearing and are more challenging to treat.
Rare CRC types – less than 1 % of each kind – are:
1) neurons-derived carcinoid tumors called Neuroendocrine Tumors (NET);
2) lymphocyte-derived Non-Hodgkin Lymphoma;
3) intestinal “pacemaker” cells of Cajal produce rare Gastrointestinal Stromal Tumors (GIST);
4) “cancer of smooth muscle in rectum or colon” - Leiomyosarcoma;
5) colon and rectal Melanomas from pigmental epithelial cells;
6) colorectal squamous cell carcinoma;
7) Familial Adenomatous Polyposis (FAP) – a specific inherited condition associated with massive large intestine polyposis from 10-12 years of age.
In the United States, there are 36.6 new cases of CRC per 100,000 men and women per year. According to the National Cancer Institute, about 4.1% of adults will be diagnosed with colorectal cancer at some point in their lifetime [National Cancer Institute].
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Causes & Risk Factors
What is the primary issue of colon cancer?
CRC includes 20-30% hereditary (FAP and Lynch syndrome) and 70-80% spontaneous cases.
The most common scenario for adenocarcinoma CRC development is when epithelial cells undergo a series of genetic or epigenetic changes that enable them to be hyperproliferative – grow fast and spread far. The cancer begins from a tiny benign adenoma in the colorectal segment of the intestine. During the next 10-15 years, under the influence of persistent chronic inflammation from carcinogens and mechanical defects, the adenoma may acquire some cellular damage via pathways of microsatellite instability (MSI) – in 20% of cases - and chromosomal instability (CIN) – 80%. That is a transformation caused by the loss of the tumor suppressor gene APC, which leads tiny adenoma to grow into large but still benign one. Consequently, the activation of KRAS/ BRAF oncogenes and loss of tumor suppressor genes DCC and p53 open a gate of adenoma-to-adenocarcinoma transition through early and late adenoma stages to malignant tumor.
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