Kobayashi Y, Hayashi Y, Ozawa K, Asano S
Department of Hematology/Oncology, University of Tokyo, Japan.
Leuk Lymphoma. 1995 May;17(5-6):391-9. doi: 10.3109/10428199509056849.
The human tri-thorax gene (HRX) also called ALL-1 (Acute Lymphocytic Leukemia-1) as well as MLL (Myeloid-lymphoid or Mixed-lineage Leukemia) gene, is disrupted in the majority of leukemias with chromosomal abnormalities involving 11q23. The alteration of the gene is related to leukemogenesis of various types such as acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), and acute mixed lineage leukemia. The gene is also rearranged in cases of secondary AML developing after exposure to chemotherapeutic agents, especially topoisomerase II inhibitors. In at least one report, genomic analysis of this recombination site showed the breakpoint to be a topoisomerase II binding site and that exposure to the inhibitor could induce the rearrangement. If exposure induces the rearrangement of the gene, secondary ALL as well as secondary AML could occur after exposure to these agents, because the type of leukemias with rearranged HRX gene is not limited to AML. We present here such a case of secondary ALL with this gene rearrangement which occurred during adjuvant chemotherapy for breast cancer. Although less cases of secondary ALL are reported in comparison with those of secondary AML, such case reports have been accumulating. The incidence of this type of leukemia should be clarified in the future.
人类三胸基因（HRX），也被称为急性淋巴细胞白血病1（ALL-1）以及髓系-淋巴系或混合谱系白血病（MLL）基因，在大多数伴有涉及11q23染色体异常的白血病中会发生破坏。该基因的改变与多种类型白血病的发生有关，如急性髓系白血病（AML）、急性淋巴细胞白血病（ALL）和急性混合谱系白血病。在接触化疗药物尤其是拓扑异构酶II抑制剂后发生的继发性AML病例中，该基因也会发生重排。至少有一份报告显示，对该重组位点的基因组分析表明断点是一个拓扑异构酶II结合位点，并且接触抑制剂可诱导重排。如果接触诱导了该基因的重排，那么在接触这些药物后可能会发生继发性ALL以及继发性AML，因为具有重排HRX基因的白血病类型并不局限于AML。我们在此呈现这样一例在乳腺癌辅助化疗期间发生该基因重排的继发性ALL病例。尽管与继发性AML相比，继发性ALL的报告病例较少，但此类病例报告一直在增加。这种类型白血病的发病率未来应予以明确。
