Stomach Cancer

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Stomach Cancer by Mind Map: Stomach Cancer

1. Pathophysiologic Etiology:

1.1. The incidence of gastric cancer represents about 2% (21,600) cases of all new cancer in the US every year. The incidence is greater in men than women. Stomach cancer contributed to 10, 990 deaths in 2013. Majority of stomach cancer cases are from adenocarcinoma.

1.2. Gastric adenocarcinoma begins in the glands of the stomach mucosa where 50% of gastric cancer develops. Atrophic gastritis and intestinal metaplasia are strongly linked to development of gastric ulcer. Lacking acid secretion by atrophic mucosa lead to alkaline environment which permits the bacteria to multiply and act on nitrates. Increasing these damages result in nitrosoamines damages and DNA of mucosal cells leading to metaplasia and neoplasia.

1.3. Gastric and duodenal carcinoma produced by severe chronic gastritis and H. pylori are responsible for stomach cancer. Both were linked in changing the mucosal cell proliferation pattern, destroy cell junctions, inhibit cell productions, and promote cell invasive ability.

1.4. Upper gastrointestinal (GI) cancers of the stomach is the sixth most common cancers worldwide, respectively, based on GLOBOCAN 2012 estimates about 2.19 million new cases of these 3 upper GI cancers were estimated to have occurred (15.5% of all cancers worldwide), and approximately 1.87 million people died from these cancers (22.8% of deaths from all cancers) in 2012. The majority of these cancers (74%) occurred in less developed countries and China alone accounted for almost half (46.7%) of these cases.

2. Pathophysiologic Factors (immunity, inflammation, infection or injury)

2.1. Infection and inflammation: Infection with H pylori and severe chronic gastritis modified the proliferation of the mucosal cell pattern that destroy the cell junction, inhibit cell production, and increased cell invasive ability, thus promote gastric and duodenal carcinoma. H pylori is a causatively linked to mucosa-associated lymphoid tissue (MALT) lymphoma that can originate in the stomach. A factor such as smoking decreases the production of prostaglandins that maintain the integrity of stomach mucosa leading to higher incidence of H. pylori infection.

2.2. Injury: Salt a caustic element to the stomach causes chronic atrophic gastritis. Hypertonic salt solution delay gastric emptying which increase the time to which carcinogenic nitrosamines can exert in their stomach mucosa. Nitrates interacts with amino acids in the stomach and form nitrosamines. The conversion of carcinogenic nitrosamines is enhanced at a low pH by iodides and thiocyanates. Nitrates become active and transform to nitrites causing stomach cancer once atrophic gastritis occurred.

3. Gene Factors:

3.1. In Kegg pathway analysis, the most significantly enriched pathway is Ribosome. Genes such as RPL11, RPL23, RPS6, and MRPS21 were enriched on this pathway. Ribosomal protein family (PRL/RPS) has been demonstrated to have a strong connection with stomach cancer (SC). For example, a recent study revealed that GLTSCR2 regulates the MDM2-TP53 pathway through RPL11, playing a key role in SC progression. Reducing the phosphorylation of RPS6 could have an influence on the sensitivity to MEK inhibition in gastric cancer cells. Another important pathway in SC is glycolysis/gluconeogenesis pathway. Reports revealed that microRNA-133b could silence PKM-splicer PTBP1, leading the inhibition of growth of human gastric cancer cells. Gene such as SIRT3 can strengthen glycolysis in SIRT3-expressing SC cells. Other pathways, like ECM-receptor interaction and metabolism of xenobiotics by cytochrome P450, have been validated to be associated with SC through bioinformatics approaches based protein-protein interaction network analysis.

4. Causative Factors:

4.1. Non-enviromental factors: 1. Family history of gastric adenocarcinoma 2. Blood type or blood group A 3. Type A atrophic gastritis 4. Pernicious anemia

4.2. Environmental Risk Factors 1. infection with H. pylori that carries cytotoxin associated antigen A (CagA) gene product 2. dietary factors such as added salt in food, nitrates, pickled foods, low intake of fruits and vegetables 3. Lifestyle including alcohol consumption and cigarette smoking 4. Diet consisting of carcinogenic substances produced in cooking (i.e, fat, meat or protein) 5. Naturally occurring carcinogen in plants including alkaloids or mold by products 6. Macronutrients consist of fat, protein, and alcohol 7. Micronutrients of folate and vitamin E which alter many micrRNA

5. Diagnostic Test

5.1. EGD - -esophagogastroduodenoscopy (EGD) for visualization and microscopic examination of exfoliated cells CT scan Barium Swallow/barium enema Positron Emission Tomography

6. Common Findings:

6.1. Earlier Findings: - Loss of appetite (specifically meat) - Malaise - Unexplained weight loss

6.2. Later Findings: - Upper abdominal pain - Vomiting - Change in bowel habits - Anemia-caused by excessive bleeding - Tumor penetrated to muscle layers of the stomach

7. Treatments:

7.1. Non-invasive Treatments: Modification of Diet: - Variety of food to improve DNA repair including kiwi, cooked carrots, coenzymeQ10, - Lycopene rich vegetable - Detoxification enzymes - Antioxidant system - Diets high in isothiocyanates - Glutathione S-transferases (GST) metabolize carcinogen

7.2. Invasive Treatments: -surgery (removing early tumor, gastrectomy, -radiotheraphy (RT) - adjuvant chemotheraphy (CRT) -combination of CRT and RT - Immunotherapy drugs - in rare cases, hemodialysis (HD) for patients with renal dysfunction

7.3. Palliative Treatment while undergoing aggressive treatments.

8. References: Chang, S., Goldstein, B. Y., Mu, L., Cai, L., You, N. Y., He, N., & ... Lu, Q. (2015). Plasma Folate, Vitamin B12, and Homocysteine and Cancers of the Esophagus, Stomach, and Liver in a Chinese Population. Nutrition & Cancer, 67(2), 212-223. doi:10.1080/01635581.2015.989375 Jiang, B., Li, S., Jiang, Z., & Shao, P. (2017). Gastric Cancer Associated Genes Identified by an Integrative Analysis of Gene Expression Data. Biomed Research International, 1-7. doi:10.1155/2017/7259097 McCance, k., Huether, S., Brashers, V., & Rote, S. (2014). Pathophysiology: The biological basis for disease in adults and children (7th Ed). St. Louis, MO: Elsevier. Silva, J. d., Maurício, S. F., Bering, T., & Correia, M. D. (2013). The Relationship Between Nutritional Status and the Glasgow Prognostic Score in Patients with Cancer of the Esophagus and Stomach. Nutrition & Cancer, 65(1), 25-33. doi:10.1080/01635581.2013.741755 Yavas, G., Elsurer, R., Yavas, C., & Ata, O. (2014). Basal renal function reserve and mean kidney dose predict future radiation-induced kidney injury in stomach cancer patients. Supportive Care In Cancer, 22(2), 445-451. doi:10.1007/s00520-013-1996-z

9. Maria Gina Agnir MSNV 605 Concept Map Case study 5