Terapevticheskii arkhivTerapevticheskii arkhivТерапевтический архив0040-36602309-5342LLC Obyedinennaya Redaktsiya31812Editorial articleПередовая статьяReview ArticleSOCS1 gene mutations in patients with diffuse large B-cell lymphomaМутации гена SOCS1 у больных диффузной В-крупноклеточной лимфомойGavrilinaO AГаврилинаО АZvonkovE EЗвонковЕ ЕBidermanB VБидерманБ ВSeverinaN AСеверинаН АParovichnikovaE NПаровичниковаЕ Н«Гематологический научный центр» Минздрава России15072015877VOL 87, NO7 ()ТОМ 87, №7 (2015)10511110042020Copyright ©; 2015, Consilium MedicumCopyright ©; 2015, ООО "Консилиум Медикум"2015Consilium MedicumООО "Консилиум Медикум"https://creativecommons.org/licenses/by-nc-sa/4.0https://ter-arkhiv.ru/0040-3660/article/view/31812

Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous group of diseases, which accounts for 30% of all non-Hodgkin lymphomas. Current molecular studies have confirmed that there are several DLBCL subtypes characterized by different cellular origin, cytogenetic profile, molecular genetic disorders, and different pathogenesis. Impaired JAK-STAT signaling is a part of the pathogenesis of various cancers, including DLBCL. The review deals with the molecular genetic aspects of the occurrence of DLBCL and the function of the SOCS1 gene that has been proven to be responsible for the development of several cancers. Mutations of this gene result from spontaneously impaired B-cell somatic hypermutation and they are frequently inactivating. The presence of point mutations in the functionally significant region of this gene in DLBCL could identify a group of patients with poor prognosis during standard chemotherapy.

Диффузная В-крупноклеточная лимфома (ДВККЛ) — это гетерогенная группа заболеваний, составляющая 30% всех неходжкинских лимфом. Современные молекулярные исследования подтвердили существование нескольких подтипов ДВККЛ, характеризующихся различным клеточным происхождением, цитогенетическим профилем и молекулярно-генетическими нарушениями, а также различным патогенезом. Нарушение функционирования сигнального пути JAK-STAT является частью патогенеза различных онкологических заболеваний, в том числе ДВККЛ. Обзор посвящен молекулярно-генетическим аспектам возникновения ДВККЛ и функции гена SOCS1, участие которого доказано в развитии некоторых онкологических заболеваний. Мутации этого гена возникают в результате спонтанного нарушения процесса соматической гипермутации в В-клетках и часто являются инактивирующими. Наличие точечных мутаций в функционально значимой области этого гена при ДВККЛ позволило выделить группу больных с неблагоприятным прогнозом при стандартной химиотерапии.

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