ОБЗОРЫ

История вопроса о роли биопсии костного мозга в системе стадирования классической лимфомы Ходжкина и современный взгляд в эру ПЭТ-КТ (обзор литературы)

ОБЗОРЫ , ,

А.А. Даниленко, Н.А. Фалалеева, С.В. Шахтарина

Медицинский радиологический научный центр им. А.Ф. Цыба — филиал ФГБУ «НМИЦ радиологии» Минздрава России, ул. Королева, д. 4, Обнинск, Калужская область, Российская Федерация, 249036

Для переписки: Анатолий Александрович Даниленко, д-р мед. наук, ул. Королева, д. 4, Обнинск, Российская Федерация, 249036; тел.: +7(909)250-18-10; e-mail: danilenkoanatol@mail.ru

Для цитирования: Даниленко А.А., Фалалеева Н.А., Шахтарина С.В. История вопроса о роли биопсии костного мозга в системе стадирования классической лимфомы Ходжкина и современный взгляд в эру ПЭТ-КТ (обзор литературы). Клиническая онкогематология. 2023;16(4):351–60.

DOI: 10.21320/2500-2139-2023-16-4-351-360

РЕФЕРАТ

Стадирование лимфомы Ходжкина представляет собой основу для выбора оптимальной программы лечения. Неотъемлемой частью стадирования в течение долгого времени оставалась оценка костного мозга. Исследование вовлеченности костного мозга в опухолевый процесс включает в себя применение методов лучевой диагностики и морфологического исследования его образцов, получаемых методом трепанобиопсии. На протяжении пяти десятилетий использования трепанобиопсии отношение онкологов и гематологов к этой инвазивной и болезненной манипуляции остается противоречивым — от полного отрицания до необходимости проведения ее каждому или большинству пациентов. Данный обзор посвящен истории вопроса и целесообразности применения трепанобиопсии у больных классической лимфомой Ходжкина.

Ключевые слова: лимфома Ходжкина, костный мозг, трепанобиопсия.

Получено: 26 марта 2023 г.

Принято в печать: 2 сентября 2023 г.

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Роль лейкоцитов в формировании нейтрофильных внеклеточных ловушек и тромбообразовании при Ph-негативных миелопролиферативных новообразованиях (обзор литературы)

ОБЗОРЫ , ,

Б.Т. Джумабаева

ФГБУ «НМИЦ гематологии» Минздрава России, Новый Зыковский пр-д, д. 4, Москва, Российская Федерация, 125167

Для переписки: Болдукыз Толгонбаевна Джумабаева, д-р мед. наук, Новый Зыковский пр-д, д. 4, Москва, Российская Федерация, 125167; тел.: +7(495)612-64-63, +7(926)271-92-82; e-mail: bola.blood@yandex.ru

Для цитирования: Джумабаева Б.Т. Роль лейкоцитов в формировании нейтрофильных внеклеточных ловушек и тромбообразовании при Ph-негативных миелопролиферативных новообразованиях (обзор литературы). Клиническая онкогематология. 2023;16(3):263–7.

DOI: 10.21320/2500-2139-2023-16-3-263-267

РЕФЕРАТ

Тромботические осложнения нередко служат причиной смерти пациентов с хроническими Ph-негативными миелопролиферативными новообразованиями (МПН). Несмотря на многочисленные исследования, патогенез тромбообразования при МПН остается неясным. Его механизм сложный, многофакторный. Один из основных этапов тромбогенеза характеризуется активацией клеточных механизмов и образованием нейтрофильных внеклеточных ловушек (neutrophil extracellular traps — NET). NET состоят из нитей ДНК, гистонов, гранулярных белков и наряду с уничтожением патогенов обеспечивают идеальную матрицу для активации тромбоцитов и механизмов коагуляции.

Ключевые слова: миелопролиферативные новообразования, нейтрофилы, тромбоз, нейтрофильные внеклеточные ловушки (NET).

Получено: 14 декабря 2022 г.

Принято в печать: 29 мая 2023 г.

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ЛИТЕРАТУРА

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Классическая лимфома Ходжкина: структура опухоли и прогностическое значение иммунного микроокружения

ОБЗОРЫ , , ,

А.А. Гусак, К.В. Лепик, Л.В. Федорова, В.В. Маркелов, В.В. Байков

НИИ детской онкологии, гематологии и трансплантологии им. Р.М. Горбачевой, ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет им. акад. И.П. Павлова» Минздрава России, ул. Льва Толстого, д. 6/8, Санкт-Петербург, Российская Федерация, 197022

Для переписки: Артем Александрович Гусак, ул. Льва Толстого, д. 6/8, Санкт-Петербург, Российская Федерация, 197022; e-mail: artemgusak@yandex.ru

Для цитирования: Гусак А.А., Лепик К.В., Федорова Л.В., Маркелов В.В., Байков В.В. Классическая лимфома Ходжкина: структура опухоли и прогностическое значение иммунного микроокружения. Клиническая онкогематология. 2023;16(3):242–62.

DOI: 10.21320/2500-2139-2023-16-3-242-262

РЕФЕРАТ

Классическая лимфома Ходжкина (ЛХ) представляет собой уникальное злокачественное новообразование лимфатической системы, характеризующееся наличием опухолевых клеток (Ходжкина и Рид—Штернберга) в воспалительном и иммуносупрессивном микроокружении. Микроокружение ЛХ — комплексная динамичная среда, включающая иммунные клетки, стромальные элементы и компоненты внеклеточного матрикса, которые взаимодействуют друг с другом и с опухолевыми клетками. От характера этих взаимодействий во многом зависит как прогрессирование заболевания, так и ответ на терапию. В настоящее время возрастает интерес к изучению структуры и функции микроокружения ЛХ, его прогностического значения, потенциала его компонентов в качестве новых мишеней для лекарственной терапии. В последнее десятилетие значительно улучшились результаты лечения рефрактерных форм ЛХ, в частности, за счет применения ингибиторов PD-1 ниволумаба и пембролизумаба. Высокая чувствительность ЛХ к анти-PD-1-терапии обусловлена формированием PD-1/PD-L1-ассоциированной ниши в ткани опухоли. Основой ниши является интенсивная экспрессия PD-L1 опухолевыми клетками, макрофагами и экспрессия его рецептора PD-1 Т-клетками и М2-макрофагами. Накапливается все больше сведений о возможных механизмах противоопухолевого ответа у пациентов с ЛХ при анти-PD-1-терапии, противоречащих концепции классического CD8-опосредованного ответа при солидных опухолях. Вероятно, цитотоксические эффекты анти-PD-1-терапии в ткани ЛХ достигаются путем взаимодействия между опухолевыми клетками, макрофагами и CD4-позитивными Т-лимфоцитами. В обзоре представлены сведения о структурных и регуляторных взаимоотношениях опухолевых клеток и элементов микроокружения, описываются новые терапевтические подходы, основанные на использовании в качестве мишеней различных компонентов опухолевого микроокружения, суммированы имеющиеся к настоящему времени данные о возможности прогнозирования на основе изучения характеристик микроокружения ЛХ.

Ключевые слова: классическая лимфома Ходжкина, микроокружение, иммунные контрольные точки, поляризация макрофагов, иммуносупрессивная ниша.

Получено: 12 апреля 2023 г.

Принято в печать: 25 июня 2023 г.

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Статистика Plumx русский

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Перспективы применения иммуномодулирующих препаратов и модуляторов цереблон Е3-лигазы в лечении множественной миеломы

ОБЗОРЫ , , , , ,

С.В. Семочкин1,2

1 МНИОИ им. П.А. Герцена — филиал ФГБУ «НМИЦ радиологии» Минздрава России, 2-й Боткинский пр-д, д. 3, Москва, Российская Федерация, 125284

2 ФГАОУ ВО «РНИМУ им. Н.И. Пирогова» Минздрава России, ул. Островитянова, д. 1, Москва, Российская Федерация, 117997

Для переписки: Сергей Вячеславович Семочкин, д-р мед. наук, профессор, 2-й Боткинский пр-д, д. 3, Москва, Российская Федерация, 125284; e-mail: semochkin_sv@rsmu.ru

Для цитирования: Семочкин С.В. Перспективы применения иммуномодулирующих препаратов и модуляторов цереблон Е3-лигазы в лечении множественной миеломы. Клиническая онкогематология. 2023;16(3):229–41.

DOI: 10.21320/2500-2139-2023-16-3-229-241

РЕФЕРАТ

За последние десятилетия прогресс в лечении множественной миеломы (ММ) связан с лучшим пониманием биологии этого заболевания и внедрением в практику новых классов лекарственных средств, таких как иммуномодулирующие препараты (IMiD), ингибиторы протеасом (ИП) и моноклональные антитела (МАТ). Современные IMiD (леналидомид, помалидомид) являются производными талидомида, которые, несмотря на сходство химической структуры, проявляют лишь относительную перекрестную резистентность. Леналидомид — иммуномодулятор 2-го поколения с высокой противоопухолевой активностью и благоприятным профилем безопасности. В 2006 г. применение леналидомида в комбинации с дексаметазоном (схема Rd) было одобрено FDA (США) для лечения рецидивов/рефрактерной MM, а через 9 лет, в 2015 г., — для впервые диагностированной ММ. В 2015–2019 гг. для лечения рецидивов MM были разработаны схемы, построенные на комбинации Rd с бортезомибом (VRd), карфилзомибом (KRd), иксазомибом (IRd), элотузумабом (ERd) и даратумумабом (DRd), — так называемые триплеты. Помалидомид — препарат 3-го поколения, используемый у пациентов с рефрактерностью к леналидомиду. Для лечения пациентов с рецидивами/рефрактерной ММ, которые получили не менее двух линий терапии, включавших леналидомид и бортезомиб, в практику внедрены схемы из трех препаратов на основе помалидомида и дексаметазона в комбинации с элотузумабом (EPd), изатуксимабом (Isa-Pd) и даратумумабом (DPd). В 2010 г. была открыта молекулярная мишень действия IMiD — белок цереблон (CRBN), входящий в ферментный комплекс CRBN E3-лигазы. Понимание данного механизма позволило создать новое семейство производных талидомида, получившее название модуляторов CRBN E3-лигазы (CELMoD). Два препарата этой группы (ибердомид, мезигдомид) в исследованиях I–II фазы продемонстрировали обнадеживающую активность при ММ с рефрактерностью к трем классам противоопухолевых препаратов (IMiD, ИП и анти-CD38 МАТ). Фокус представленного обзора направлен на проспективные исследования IMiD и CELMoD на разных этапах лечения ММ.

Ключевые слова: множественная миелома, иммуномодулирующие препараты, модуляторы цереблон Е3-лигазы, леналидомид, помалидомид, ибердомиб, мезигдомид.

Получено: 25 января 2023 г.

Принято в печать: 28 мая 2023 г.

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Статистика Plumx русский

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KIR-генетические факторы и ответ на терапию ингибиторами тирозинкиназ при хроническом миелоидном лейкозе

ОБЗОРЫ , , ,

Е.В. Кузьмич1, И.Е. Павлова1, Л.Н. Бубнова1,2, С.С. Бессмельцев1

1 ФГБУ «Российский НИИ гематологии и трансфузиологии ФМБА России», ул. 2-я Советская, д. 16, Санкт-Петербург, Российская Федерация, 191024

2 ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет им. акад. И.П. Павлова» Минздрава России, ул. Льва Толстого, д. 6/8, Санкт-Петербург, Российская Федерация, 197022

Для переписки: Елена Витальевна Кузьмич, канд. биол. наук, ул. 2-я Советская, д. 16, Санкт-Петербург, Российская Федерация, 191024; тел.: +7(921)912-52-07; e-mail: yelenakuzmich@gmail.com

Для цитирования: Кузьмич Е.В., Павлова И.Е., Бубнова Л.Н., Бессмельцев С.С. KIR-генетические факторы и ответ на терапию ингибиторами тирозинкиназ при хроническом миелоидном лейкозе. Клиническая онкогематология. 2023;16(2):119–27.

DOI: 10.21320/2500-2139-2023-16-2-119-127

РЕФЕРАТ

Разработка и внедрение в клиническую практику ингибиторов тирозинкиназ (ИТК) значительно улучшили прогноз у пациентов с хроническим миелоидным лейкозом (ХМЛ). Примерно 50 % пациентов, достигающих глубокого молекулярного ответа, могут быть кандидатами на безопасное прекращение приема ИТК. Несмотря на достигнутые результаты, до настоящего времени не существует надежных биомаркеров для прогнозирования ответа и сохранения ремиссии без лечения после прекращения приема ИТК. Поскольку ИТК не уничтожают лейкозные стволовые клетки, остающиеся потенциальным источником рецидива, важную роль при ХМЛ играют естественные киллеры (NK-клетки), обладающие противоопухолевой активностью. Функциональная активность NK-клеток определяется уровнем экспрессии и репертуаром иммуноглобулиноподобных рецепторов киллерных клеток (KIR). Современные исследования свидетельствуют о том, что KIR-генотип пациента оказывает влияние на возможность достижения раннего и глубокого молекулярных ответов на ИТК первого и второго поколений, выживаемость без прогрессирования и общую выживаемость больных, а также сохранение ремиссии без лечения. На этом основании KIR-генетические факторы могут рассматриваться в качестве перспективных предикторов ответа на терапию ИТК у пациентов с ХМЛ. Ранние клинические исследования моноклональных антител, блокирующих ингибирующие KIR с целью повысить активность NK-клеток, показали приемлемые профиль безопасности и эффективность при некоторых гематологических заболеваниях (таких, как острый миелоидный лейкоз, множественная миелома, Т-клеточная лимфома) при использовании в комбинации с цитостатическими препаратами или противоопухолевыми моноклональными антителами. Определение KIR-генотипа при ХМЛ может способствовать разработке эффективных средств иммунотерапии этой злокачественной опухоли системы крови.

Ключевые слова: гены иммуноглобулиноподобных рецепторов киллерных клеток, ингибиторы тирозинкиназ, ремиссия без лечения, хронический миелоидный лейкоз.

Получено: 8 ноября 2022 г.

Принято в печать: 1 марта 2023 г.

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Статистика Plumx русский

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Морфо-иммуногистохимические особенности различных стадий грибовидного микоза: обзор литературы

ОБЗОРЫ , ,

А.А. Шерстнев, А.М. Ковригина

ФГБУ «НМИЦ гематологии» Минздрава России, Новый Зыковский пр-д, д. 4, Москва, Российская Федерация, 125167

Для переписки: Андрей Алексеевич Шерстнев, Новый Зыковский пр-д, д. 4, Москва, Российская Федерация, 125167; e-mail: sherstnevandrejj@mail.ru

Для цитирования: Шерстнев А.А., Ковригина А.М. Морфо-иммуногистохимические особенности различных стадий грибовидного микоза: обзор литературы. Клиническая онкогематология. 2023;16(2):109–18.

DOI: 10.21320/2500-2139-2023-16-2-109-118

РЕФЕРАТ

Грибовидный микоз (ГМ) — наиболее распространенный вариант Т-клеточной лимфомы кожи. Патогенез ГМ до настоящего времени полностью не изучен. Дифференциальная диагностика заболевания, в особенности на ранних стадиях, сложна и представляет серьезную задачу. В настоящем обзоре литературы освещаются современные представления о патогенезе ГМ и методах диагностики данного заболевания.

Ключевые слова: грибовидный микоз, наивные Т-клетки, Т-хелперы, реактивное микроокружение.

Получено: 21 сентября 2022 г.

Принято в печать: 3 марта 2023 г.

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Статистика Plumx русский

ЛИТЕРАТУРА

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Хронический гепатит С и онкогематологические заболевания

ОБЗОРЫ , , , ,

Т.В. Антонова1, М.С. Ножкин1, Д.А. Лиознов1,2

1 ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет им. акад. И.П. Павлова» Минздрава России, ул. Льва Толстого, д. 6/8, Санкт-Петербург, Российская Федерация, 197022

2 ФГБУ «НИИ гриппа им. А.А. Смородинцева» Минздрава России, ул. Профессора Попова, д. 15/17, Санкт-Петербург, Российская Федерация, 197376

Для переписки: Тамара Васильевна Антонова, д-р мед. наук, профессор, ул. Льва Толстого, д. 6/8, Санкт-Петербург, Российская Федерация, 197022; e-mail: antonovatv28@yandex.ru

Для цитирования: Антонова Т.В., Ножкин М.С., Лиознов Д.А. Хронический гепатит С и онкогематологические заболевания. Клиническая онкогематология. 2023;16(1):46–53.

DOI: 10.21320/2500-2139-2023-16-1-46-53

РЕФЕРАТ

В обзоре обсуждается HCV-инфекция у онкогематологических больных. Высокий риск инфицирования вирусом гепатита С (HCV) при онкогематологических заболеваниях доказан значимо большей частотой HCV-инфекции (в 2–2,5 раза) у пациентов с неходжкинскими лимфомами в сравнении с популяционными данными. Кроме того, установлено значение HCV в развитии и прогрессировании В-клеточных неходжкинских лимфом, что подтверждает его онкогенный потенциал. Рассмотрен вариант серонегативного (оккультного) гепатита С, при котором РНК HCV определяется в ткани печени и в мононуклеарах периферической крови высокочувствительным методом ПЦР с обратной транскрипцией при отсутствии антител к HCV и РНК HCV в сыворотке. При этом пациенты могут быть источниками инфекции. Серонегативный гепатит С выявляется у доноров крови в 2,2–3,4 % случаев. Этот вариант инфекции встречается у 20–85 % онкогематологических пациентов, что требует дальнейшего изучения. Сопутствующая HCV-инфекция является потенциальным фактором, влияющим на прогноз онкогематологических заболеваний. У онкогематологических пациентов с сопутствующим хроническим гепатитом С (ХГС) доказана значимо худшая выживаемость в сравнении с больными без него. Установлена связь HCV-инфекции с увеличением частоты осложнений как противоопухолевой терапии, так и трансплантации гемопоэтических стволовых клеток (ТГСК). Иммунохимиотерапия, в свою очередь, влияет на обострение и прогрессирование ХГС. Высокая эффективность и удовлетворительная переносимость препаратов прямого противовирусного действия (ППД) для лечения ХГС открыли перспективы для широкого их использования при наличии сопутствующих заболеваний. Остается сложным вопрос о лечении инфекции у пациентов после ТГСК. Рекомендации по лечению ХГС преимущественно ориентированы на проведение противовирусного лечения до ТГСК. В реальной клинической практике это не всегда возможно. Имеются примеры эффективного применения препаратов ППД до или после ТГСК, описано клиническое наблюдение противовирусного лечения одновременно с ТГСК.

Ключевые слова: вирус гепатита С, HCV-инфекция, онкогематология, трансплантация гемопоэтических стволовых клеток, иммунохимиотерапия, препараты прямого противовирусного действия.

Получено: 17 июня 2022 г.

Принято в печать: 10 декабря 2022 г.

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Комбинация ибрутиниба и венетоклакса в терапии хронического лимфолейкоза: обзор последних данных клинических исследований

ОБЗОРЫ , , , , ,

А.А. Петренко1,2, М.И. Кислова1, Е.А. Дмитриева1, Е.А. Никитин1,2, В.В. Птушкин1,2,3

1 ГБУЗ «Городская клиническая больница им. С.П. Боткина ДЗМ», 2-й Боткинский пр-д, д. 5, Москва, Российская Федерация, 125284

2 ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России, ул. Баррикадная, д. 2/1, Москва, Российская Федерация, 125993

3 ФГАОУ ВО «РНИМУ им. Н.И. Пирогова» Минздрава России, ул. Островитянова, д. 1, Москва, Российская Федерация, 117997

Для переписки: Мария Игоревна Кислова, 2-й Боткинский пр-д, д. 5, Москва, Российская Федерация, 125284; e-mail: xkislovamariax@gmail.com

Для цитирования: Петренко А.А., Кислова М.И., Дмитриева Е.А. и др. Комбинация ибрутиниба и венетоклакса в терапии хронического лимфолейкоза: обзор последних данных клинических исследований. Клиническая онкогематология. 2023;16(1):37–45.

DOI: 10.21320/2500-2139-2023-16-1-37-45

РЕФЕРАТ

Появление ингибиторов тирозинкиназы Брутона (BTK) изменило лечение пациентов с хроническим лимфолейкозом (ХЛЛ). Ибрутиниб, первый в своем классе ингибитор BTK, продемонстрировал высокую эффективность в многочисленных клинических исследованиях. Однако использование ингибиторов BTK в качестве монотерапии требует непрерывного лечения. Резистентность к ингибиторам BTK и тяжелые побочные эффекты неизбежно возникают при монотерапии ибрутинибом, что часто приводит к неэффективности лечения. Комбинация ингибитора BCL-2 венетоклакса с ингибитором BTK может улучшить эффективность терапии за счет синергизма действия препаратов на разные субпопуляции клеток ХЛЛ. Комбинированная терапия может привести к более глубоким ответам, обеспечивая потенциально фиксированную продолжительность лечения. В настоящем обзоре, сосредоточив внимание на комбинации ибрутиниба и венетоклакса, мы обобщаем последние данные клинических исследований, а также отвечаем на вопрос, касающийся обоснованности комбинированной терапии с точки зрения ее эффективности и профиля безопасности.

Ключевые слова: ибрутиниб, ингибиторы BTK, венетоклакс, ингибиторы BCL-2, таргетные препараты, хронический лимфолейкоз.

Получено: 17 октября 2022 г.

Принято в печать: 10 ноября 2022 г.

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Статистика Plumx русский

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Прогностические модели в медицине

ОБЗОРЫ ,

А.С. Лучинин

ФГБУН «Кировский НИИ гематологии и переливания крови ФМБА», ул. Красноармейская, д. 72, Киров, Российская Федерация, 610027

Для переписки: Александр Сергеевич Лучинин, канд. мед. наук, ул. Красноармейская, д. 72, Киров, Российская Федерация, 610027; тел.: +7(919)506-87-86; e-mail: glivec@mail.ru

Для цитирования: Лучинин А.С. Прогностические модели в медицине. Клиническая онкогематология. 2023;16(1):27–36.

DOI: 10.21320/2500-2139-2023-16-1-27-36

РЕФЕРАТ

Медицинские прогностические (предиктивные) модели (МПМ) имеют важное значение в современном здравоохранении. Они определяют риски для здоровья и возникновения заболеваний. Целью их создания является улучшение результатов диагностики и лечения. Все МПМ можно разделить на две категории. Диагностические медицинские модели (ДММ) помогают рассчитать индивидуальный риск присутствия заболевания, в то время как прогностические медицинские модели (ПММ) — риск возникновения болезни или его осложнения в будущем. В обзоре обсуждаются характеристики ДММ и ПММ, условия их разработки, критерии применения в медицине, в частности в гематологии, а также проблемы, возникающие на этапе их создания и проверки качества.

Ключевые слова: прогностическая модель, искусственный интеллект.

Получено: 13 сентября 2022 г.

Принято в печать: 7 декабря 2022 г.

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Острые миелоидные лейкозы после лечения классической лимфомы Ходжкина: обзор литературы

ОБЗОРЫ

А.А. Даниленко, С.В. Шахтарина, Н.А. Фалалеева

Медицинский радиологический научный центр им. А.Ф. Цыба — филиал ФГБУ «НМИЦ радиологии» Минздрава России, ул. Королева, д. 4, Обнинск, Калужская область, Российская Федерация, 249036

Для переписки: Анатолий Александрович Даниленко, д-р мед. наук, ул. Королева, д. 4, Обнинск, Калужская область, Российская Федерация, 249036; тел.: +7(909)250-18-10; e-mail: danilenkoanatol@mail.ru

Для цитирования: Даниленко А.А., Шахтарина С.В., Фалалеева Н.А. Острые миелоидные лейкозы после лечения классической лимфомы Ходжкина: обзор литературы. Клиническая онкогематология. 2022;15(4):414–23.

DOI: 10.21320/2500-2139-2022-15-4-414-423

РЕФЕРАТ

Вторые злокачественные опухоли, развивающиеся у больных классической лимфомой Ходжкина (кЛХ) после лечения, представлены преимущественно солидными новообразованиями и в значительно меньшей степени острыми миелоидными лейкозами (ОМЛ). Вместе с тем относительный риск развития вторичного ОМЛ существенно превышает риск развития вторых (солидных) опухолей, а эффективность лечения больных вторичным ОМЛ значительно уступает результатам лечения первичного ОМЛ, что делает проблему значимой и актуальной. Настоящий обзор литературы посвящен эпидемиологии развития вторичных ОМЛ у больных, получавших лечение по поводу кЛХ. Кроме того, уделяется внимание современным лекарственным препаратам и технологиям, эффективным в отношении вторичных ОМЛ.

Ключевые слова: классическая лимфома Ходжкина, вторичные острые миелоидные лейкозы.

Получено: 15 апреля 2022 г.

Принято в печать: 28 августа 2022 г.

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ЛИТЕРАТУРА

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