Secondary cytogenetic abnormalities in core-binding factor AML harboring inv(16) vs t(8;21).
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Han Se Young, Mrózek Krzysztof, Voutsinas Jenna, Wu Qian, Morgan Elizabeth A, Vestergaard Hanne, Ohgami Robert, Kluin Philip M, Kristensen Thomas Kielsgaard, Pullarkat Sheeja, Møller Michael Boe, Schiefer Ana-Iris, Baughn Linda B, Kim Young, Czuchlewski David, Hilberink Jacobien R, Horny Hans-Peter, George Tracy I, Dolan Michelle, Ku Nam K, Arana Yi Cecilia, Pullarkat Vinod, Kohlschmidt Jessica, Salhotra Amandeep, Soma Lori, Bloomfield Clara D, Chen Dong, Sperr Wolfgang R, Marcucci Guido, Cho Christina, Akin Cem, Gotlib Jason, Broesby-Olsen Sigurd, Larson Melissa, Linden Michael A, Deeg H Joachim, Hoermann Gregor, Perales Miguel-Angel, Hornick Jason L, Litzow Mark R, Nakamura Ryotaro, Weisdorf Daniel, Borthakur Gautam, Huls Gerwin, Valent Peter, Ustun Celalettin, Yeung Cecilia C S
Аннотация
Patients with core-binding factor (CBF) acute myeloid leukemia (AML), caused by either t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), have higher complete remission rates and longer survival than patients with other subtypes of AML. However, ∼40% of patients relapse, and the literature suggests that patients with inv(16) fare differently from those with t(8;21). We retrospectively analyzed 537 patients with CBF-AML, focusing on additional cytogenetic aberrations to examine their impact on clinical outcomes. Trisomies of chromosomes 8, 21, or 22 were significantly more common in patients with inv(16)/t(16;16): 16% vs 7%, 6% vs 0%, and 17% vs 0%, respectively. In contrast, del(9q) and loss of a sex chromosome were more frequent in patients with t(8;21): 15% vs 0.4% for del(9q), 37% vs 0% for loss of X in females, and 44% vs 5% for loss of Y in males. Hyperdiploidy was more frequent in patients with inv(16) (25% vs 9%, whereas hypodiploidy was more frequent in patients with t(8;21) (37% vs 3%. In multivariable analyses (adjusted for age, white blood counts at diagnosis, and KIT mutation status), trisomy 8 was associated with improved overall survival (OS) in inv(16), whereas the presence of other chromosomal abnormalities (not trisomy 8) was associated with decreased OS. In patients with t(8;21), hypodiploidy was associated with improved disease-free survival; hyperdiploidy and del(9q) were associated with improved OS. KIT mutation (either positive or not tested, compared with negative) conferred poor prognoses in univariate analysis only in patients with t(8;21).