Satake N, Ishida Y, Otoh Y, Hinohara S, Kobayashi H, Sakashita A, Maseki N, Kaneko Y
Third Clinical Department, Saitama Cancer Center Hospital, Japan.
Genes Chromosomes Cancer. 1997 Sep;20(1):60-3.
CBP, which is located on 16p13 and encodes a transcriptional adaptor/coactivator protein, has been shown to fuse by the t(8;16)(p11;p13) translocation to MOZ on 8p11 in acute myeloid leukemia. We found a t(11;16)(q23;p13) in a child with therapy-related chronic myelomonocytic leukemia. Subsequent reverse transcriptase-polymerase chain reaction and direct sequencing analyses revealed the MLL-CBP fusion transcript in CMML cells. Because 11q23 translocations involving MLL and t(8;16) involving MOZ and CBP have been reported in therapy-related leukemias, both the MLL and CBP genes may be targets for topoisomerase II inhibitors. Accordingly, we believe that most t(11;16)-associated leukemias may develop in patients who have been treated with cytotoxic chemotherapy for primary malignant diseases.
CBP位于16p13，编码一种转录衔接子/共激活蛋白，在急性髓系白血病中，它已被证明通过t(8;16)(p11;p13)易位与8p11上的MOZ融合。我们在一名患有治疗相关慢性粒单核细胞白血病的儿童中发现了t(11;16)(q23;p13)。随后的逆转录酶-聚合酶链反应和直接测序分析揭示了慢性粒单核细胞白血病细胞中的MLL-CBP融合转录本。由于在治疗相关白血病中已报道了涉及MLL的11q23易位以及涉及MOZ和CBP的t(8;16)，MLL和CBP基因可能都是拓扑异构酶II抑制剂的作用靶点。因此，我们认为大多数与t(11;16)相关的白血病可能发生在因原发性恶性疾病接受过细胞毒性化疗的患者中。
