In the review risk factors which transformations chronic atrophic a gastritis in a stomach cancer promote are analyzed. The characteristic of precancer conditions as increase in risk of development of a cancer of a stomach is given. As risk factor of a cancer of a stomach definition of subtypes intestinal metaplasia is offered, dividing on full and incomplete taking into account decrease in an expression gastric mucin MUC1, MUC5AC and MUC6. The role of a genetic susceptibility of an organism to infected Н pylori, the factors of its pathogenicity promoting metaplasia epithelium is analyzed. Also role Toll-like of receptors 4 types (TLR4), participating in recognition Н. pylori is established. Development of the superfluous immune answer of the owner is connected with receptors of this type, leading to damage of a mucous membrane at Н. pylori-infected persons. In 161 particular, carriers TLR4+896А>G polymorphism have heavier atrophy of a stomach and inflammation degree, and also the raised risk a stomach cancer.
Surunkali atrofik gastritni oshqozon saratoni kasalligiga aylantiradigan xavf omillari tahlil qilingan. Oshqozon saratoni rivojlanish xavfini oshirish uchun rak oldi shartlarning xarakteristikasi berilgan. Surunkali yallig'lanish, atrofik, ichak metaplasiyasi, displaziya va oshqozon adenokarsinomasi xavfi baholangan. H. pylori infektsiyasiga genetik ta'sirga ega bo'lgan organizmning roli, uning epiteliya metaplazasiga yordam beruvchi patogenezi omillari tahlil qilingan. Mikroorganizmlarning virusli kasalligi va xo‘jayin genetik sezuvchanligining kombinatsiyasi shubhali surunkali yallig'lanish va oshqozon-ichak saratoni tez rivojlanishi, hech bo'lmasa ichak tipi uchun olib keladi. Oshqozon kantserogenezining patogenezida interleykinlarning genetik polimorfizmining roli aniqlandi. Shuningdek, H. pylori tan olinishida ishtirok etgan Toll-like 4 retseptorlari (TLR4) ning roli ham aniqlandi. Haddan tashqari xo‘jayin immunitetining rivojlanishi ushbu turdagi retseptorlari bilan bog'liq bo'lib, natijada H. pylori bilan kasallangan odamlarda shilliq qavat zararglanishiga olib keladi. Qisman, TLR4 + 896A> G polimorfizmining tashuvchilari oshqozon atrofiyasi va yallig'lanish darajasi, shuningdek, kardial bo'lmagan oshqozon saratoni xavfini oshiradi.
Проанализированы факторы риска, способствующие трансформации хронического атрофического гастрита в рак желудка. Дана характеристика предраковых состояний в порядке увеличения риска развития рака желудка. В качестве фактора риска рака желудка предложено определение подтипов кишечной метаплазии, разделяя на полную и неполную с учетом снижения экспрессии желудочных муцинов MUC1, MUC5AC и MUC6. Проанализирована роль генетической восприимчивости организма к инфицированности Н. pylori, факторы его патогенности, способствующие метаплазии эпителия. Также установлена роль Toll-like рецепторов 4 типа (TLR4), участвующих в распознавании Н. pylori. Именно с рецепторами этого типа связано развитие избыточного иммунного ответа хозяина, приводящее к повреждению слизистой оболочки у Н. pylori-инфицированных лиц. В частности, носители TLR4+896А>G полиморфизма имеют более тяжелую атрофию желудка и степень воспаления, а также повышенный риск некардиального рака желудка.
In the review risk factors which transformations chronic atrophic a gastritis in a stomach cancer promote are analyzed. The characteristic of precancer conditions as increase in risk of development of a cancer of a stomach is given. As risk factor of a cancer of a stomach definition of subtypes intestinal metaplasia is offered, dividing on full and incomplete taking into account decrease in an expression gastric mucin MUC1, MUC5AC and MUC6. The role of a genetic susceptibility of an organism to infected Н pylori, the factors of its pathogenicity promoting metaplasia epithelium is analyzed. Also role Toll-like of receptors 4 types (TLR4), participating in recognition Н. pylori is established. Development of the superfluous immune answer of the owner is connected with receptors of this type, leading to damage of a mucous membrane at Н. pylori-infected persons. In 161 particular, carriers TLR4+896А>G polymorphism have heavier atrophy of a stomach and inflammation degree, and also the raised risk a stomach cancer.
| № | Муаллифнинг исми | Лавозими | Ташкилот номи |
|---|---|---|---|
| 1 | Sobirova G. . | Senior researcher, Doctor of Medical Sciences, Republican Specialized Scientific and Practical Medical Center for Therapy and Medical Rehabilitation, | |
| 2 | Abdullaeva U.K. | Junior researcher, Bukhara State Medical Institute, | Bukhara State Medical Institute |
| № | Ҳавола номи |
|---|---|
| 1 | Prokhorov, A.V. Stomach cancer in patients younger than 30 years / A.V. Prokhorov [et al.] // Eurasian oncologist. journals - 2014. - № 2 (02). - p. 64–68. |
| 2 | Chissov, V.I. Malignant neoplasms in Russia in 2011 / V.I. Chissov. - M .: Moscow them. P.A. Herzen Ministry of Health and Social Development of Russia, 2012. - 260 p. |
| 3 | Amieva, M.R. Host-bacterial interactions in Helicobacter / M.R. Amieva, EM El-Omar // Gastroenterology. – 2008. – Vol. 134, № 1. – Р. 306–332. |