Gastrointestinal cancer
Gastrointestinal cancer | |
---|---|
Specialty | Gastroenterology oncology |
Symptoms | upper Hematemesis Melena lower Coffee ground vomiting Hematochezia |
Gastrointestinal cancer refers to
Overall, the GI tract and the accessory organs of digestion (pancreas, liver, gall bladder) are responsible for more cancers and more deaths from cancer than any other system in the body.[1][2] There is significant geographic variation in the rates of different gastrointestinal cancers.[1]
Upper digestive tract
Esophageal cancer
Esophageal cancer is the sixth-most-common cancer in the world, and its incidence is increasing.[4] Some three to five males are affected for each female.[4] An "esophageal cancer belt", in which the incidence of esophageal squamous cell carcinoma (SCC) is more than a hundred times that of adjacent areas, extends from northeastern China through central Asia to northern Iran.[1] Ethiopia also has a notably high incidence.[4] There are two main types of esophageal cancer—adenocarcinoma and squamous cell carcinoma. Worldwide, the incidence of each type is about the same, but in developed countries like North America and Europe adenocarcinoma is the more common.[4]
Cancer of the esophagus is often detected late inasmuch as there are typically no early symptoms. Nevertheless, if the cancer is caught soon enough, patients can have a five-year survival rate of 90% or above. By the time esophageal cancer is usually detected, though, it might have spread beyond the esophageal wall, and the survival rate drops significantly. In China, the overall five-year survival rate for advanced esophageal cancer is about 20%, and in the United States it is about 15%.[4]
Stomach cancer
Cancer of the
Pancreatic cancer
Pancreatic cancer is the fifth most-common cause of cancer-related deaths in the United States,[8] and the seventh most-common in Europe.[9] In 2008, globally there were 280,000 new cases of pancreatic cancer reported and 265,000 deaths.[10] These cancers are classified as endocrine or nonendocrine tumors. The most common is ductal adenocarcinoma.[1] The most significant risk factors for pancreatic cancer are advanced age (over 60) and smoking.[8] Chronic pancreatitis, diabetes or other conditions may also be involved in their development.[2] Early pancreatic cancer does not tend to result in any symptoms, but when a tumor is advanced, a patient may experience severe pain in the upper abdomen, possibly radiating to the back.[8] Another symptom might be jaundice, a yellowing of the skin and eyes.[9]
Pancreatic cancer has a poor
Liver cancer
People get liver cancer (also called hepatocellular carcinoma, HCC or hepatoma) typically from a prolonged
An attending practitioner might order a
Gallbladder cancer
Cancers of the gallbladder are typically adenocarcinomas, and are common in elderly women. Gallbladder cancer is strongly associated with
Other
- MALT lymphoma is a cancer of the mucosa-associated lymphoid tissue, usually in the stomach.
- Gastrointestinal stromal tumors represent from 1% to 3% of gastrointestinal malignancies.
- Cancers of the biliary tree, including cholangiocarcinoma.
Lower digestive tract
Colorectal cancer
Colorectal cancer is a disease of
Use of a
Anal cancer
An important anatomic landmark in anal cancer is the
Anal cancer is investigated by
Gastrointestinal carcinoid tumor
A
Field defects
A "field defect" or "field cancerization" is a region of tissue that precedes and predisposes to the development of cancer. Field defects occur in progression to gastrointestinal tract cancers.[17] These field defects may contain visible gross manifestations, epigenetic alterations and/or mutations.
Esophagus
Esophageal squamous-cell carcinomas may occur as second primary tumors associated with head and neck cancer, due to field cancerization (i.e. a regional reaction to long-term carcinogenic exposure).[20][21] A field defect associated with progression towards squamous cell carcinoma can be identified with epigenetic markers.[22]
Stomach
Gastric cancer develops within areas (field defects) of the stomach with atrophic gastritis and intestinal metaplasia: these lesions represent the cancerization field in which (intestinal-type) gastric cancers develop.[23] In one study, the field defect was clearly demonstrated in gastric carcinogenesis using miRNA high throughput data from normal gastric mucosa (from patients who had never had a gastric malignant neoplasm), non-tumor tissue adjacent to a gastric cancer, and gastric cancer tissue. Greater than five-fold reductions were found in four miRNAs in tumor-adjacent tissues and gastric cancers as compared to those miRNA levels in normal gastric tissues.[24]
Large intestine
When a segment of the large intestine, containing a cancer, is removed, the area adjacent to the cancer (and removed with it) may show additional neoplasia in the form of polyps (see image). This is visual evidence of a field defect. Some of these polyps may be premalignant neoplastic tumors. As shown by Hofstad et al.,[25] when polyps are allowed to remain in the colon and are observed for three years, about 40% of polyps are seen to grow larger, likely progressing towards cancer. Luo et al.[26] summarized the substantial body of evidence that field cancerization occurs in the colon, often due to aberrant DNA methylation.
Etiology
Bile acids are synthesized in the liver to facilitate digestion of dietary fats. High exposure of the gastrointestinal tract to bile acids can occur in several different settings, but most significantly is prevalent among individuals who have a high dietary fat intake. High bile acid exposure has been implicated in several cancers of both the upper and lower digestive tract.[27] The deleterious effects on cells of elevated bile acid exposure include induction of reactive oxygen species, induction of DNA damage leading to mutation, and induction of apoptosis in the short term and selection for apoptosis resistance over the long term.[27] High levels of bile acids also alter the microbiome and act as signaling molecules, altering the microenvironment of the colon.[28]
References
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- ^ a b Bernstein H, Bernstein C, Payne CM, Dvorak K. Bile acids as endogenous etiologic agents in gastrointestinal cancer. World J Gastroenterol. 2009 Jul 21;15(27):3329-40. doi: 10.3748/wjg.15.3329. PMID: 19610133; PMCID: PMC2712893
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