Ishikura H, Yufu Y, Yamashita S, Abe Y, Okamura T, Motomura S, Nishimura J, Nawata H
Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Leuk Lymphoma. 1997 May;25(5-6):573-8. doi: 10.3109/10428199709039046.
The molecular mechanisms responsible for progression of chronic myelogenous leukemia (CML) to blast crisis have not been well defined. Blast crisis may be partially related to inactivation of tumor suppressor genes/such as p53 or retinoblastoma (Rb) gene. There is evidence for an association of blast cell phenotypes in CML with alterations of these genes: a strong association of myeloid phenotypes with abnormalities of the p53 gene and a weaker association of lymphoid phenotypes with abnormalities of the Rb system. We found a marked decrease in Rb gene product and rearrangements of the p53 gene simultaneously in two cases of biphenotypic blast crisis of CML (myeloid and B-lymphoid). These results support the association of blast cell phenotypes with alterations in tumor suppressor genes in CML blast crisis.
慢性粒细胞白血病（CML）进展为急变期的分子机制尚未完全明确。急变期可能部分与肿瘤抑制基因（如p53或视网膜母细胞瘤（Rb）基因）的失活有关。有证据表明CML中的原始细胞表型与这些基因的改变有关：髓系表型与p53基因异常有很强的相关性，而淋巴系表型与Rb系统异常的相关性较弱。我们在两例CML双表型急变期（髓系和B淋巴细胞系）病例中同时发现Rb基因产物显著减少和p53基因重排。这些结果支持了CML急变期原始细胞表型与肿瘤抑制基因改变之间的关联。
