деонтология в онкологии

Регуляторная the area virus генома (upstream regulatory region, URR) settles down between the end of area of late genes and the beginning of area of early genes. Open frameworks of reading ORF генома a virus are divided{shared} on early (early, Е) and late (late, L) sites. The early fragment includes genes Е1-Е7 coding synthesis of fibers, responsible{crucial} for various functions in process репликации a virus and transformation of cells{cages}. Genes Е1 and Е2 are responsible{crucial} for репликацию a virus, and also participate in regulation of a transcription virus генома. The product of gene Е1 is responsible for maintenance персистенции virus генома in эписомальной to the form. Gene Е2 codes products which can as a trance - activate, and to suppress экспрессию early genes and энхенсерных sites URR. Трансактивирующий the factor is identified in precancer changes шейки a uterus, репрессирующий the factor in vivo is not identified [16]. Gene Е4 participates during maturing virus particles, genes Е5-Е7 possess трансформирующим potential. Genes Е6 and Е7 are always defined{determined} and экспрессируются in tumours шейки a uterus and received of tumours шейки a uterus cellular lines. The biological effect трансформирующего potential of genes Е6 and Е7 will be considered below. The late fragment генома will consist of genes L1 and L2, coding structural fibers вириона [5,21]. Подробнее...

The direction of action of fiber Е6 (супрессорное or трансактивирующее) is defined{determined} by character, position and number of sites of linkage транскрипционных factors in promotors. The promotor р97 (ВПЧ type 16) can play a role in maintenance of a latent condition of a virus infection. With онкобелком Е6 ВПЧ types 16 and 18 7 cellular fibers cooperate at least, now from them 3 cellular fibers are identified: р53, Е6-АР, Е6-ВР. The gene р53 is associated both with the control of cellular growth, and with неопластической transformation; делеции or mutations in some cases transform р53 in active онкоген. Not all malignant tumours have mutations р53, the alternative mechanism инактивации р53 however is proved by linkage with онкобелком Е6 ВПЧ types 16 and 18, that results in loss of the control for пролиферацией cells{cages}. Cellular fiber Е6-АР (Е6 associated protein) in a complex with онкобелком Е6 participates in degradation р53, and also, probably, shortens the period полужизни and reduces a level р53 in ВПЧ-иммортализованных cells{cages}. Fiber Е6-ВР (E6-binding protein) cooperates with gene Е6 ВПЧ of types 16 and 18, that in result results in inhibition of process of a differentiation of cells{cages} and, probably, creates conditions for репликации virus ДНК. Подробнее...