Nakai H, Misawa S
Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
Leuk Lymphoma. 1995 Oct;19(3-4):213-21. doi: 10.3109/10428199509107891.
We have reviewed all the relevant studies on the loss of the short arm of chromosome 17 (17p) and inactivation of the p53 gene in chronic myelogenous leukemia (CML) in an attempt to clarify their roles in the progression of CML. Loss of a 17p (hemizygous 17p) and p53 inactivation emerged as the disease progressed and were closely associated with each other. About half of the cases with loss of a 17p, however, did not show p53 inactivation. In these cases loss of a 17p preceded p53 inactivation, which suggested that either reduction of the p53 gene dosage or inactivation of another tumor-suppressor gene on 17p might contribute to the disease progression. Both loss of a 17p and p53 inactivation may serve as poor prognostic factors but the prognostic significance of the former only emerged when metaphase cells with loss of a 17p were dominant amongst the total cell population analyzed.
我们回顾了所有关于慢性粒细胞白血病（CML）中17号染色体短臂（17p）缺失和p53基因失活的相关研究，试图阐明它们在CML进展中的作用。随着疾病进展出现了17p缺失（半合子17p）和p53失活，且二者密切相关。然而，约一半17p缺失的病例并未表现出p53失活。在这些病例中，17p缺失先于p53失活，这表明要么是p53基因剂量减少，要么是17p上另一个肿瘤抑制基因失活，可能促成了疾病进展。17p缺失和p53失活均可能作为不良预后因素，但只有当分析的全部细胞群体中17p缺失的中期细胞占主导时，前者的预后意义才显现出来。
