@article{845249e03ba645a89ca08e51768164ca,
title = "Chromosome 17 abnormalities and inactivation of the p53 gene in chronic myeloid leukemia and their prognostic significance",
abstract = "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 I7p (hemizygous I7p) 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 pS3 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-sup pressor gene on I7p might contribute to the diseasc progression. Both loss of a I7p and pS3 inactiation 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.",
keywords = "Blast crisis, Chronic myelogenous leukemia, P53 gene chromosome 17, Prognosis",
author = "Hiroyuki Nakai and Shinichi Misawa",
note = "Funding Information: In this review we describe recent advances regarding loss of a 17p andp53 inactivaticn in CML. It is now obvious that both of these abnormalitiesc ontribute to the disease progression in a significant subset of patients with CML: In about half these cases both may cooperate with each other while in the remaining half they may be associated with disease progression independently. Loss of a 17p andp53 inactivation may also serve as indicators of poor prognosis and contribute to the determination of optimal therapeutic regimens at the onset of the BC. Loss of a 17p and p53 inactivation could merely be only a visible peak of the iceberg and numerous parameters still remain to be clarified for the full understanding of the progression of CML. The next step in this respect will be to determine involvement of the MDM2 gene 57 or replication errors.58 Kashima for their constructive comments on this work and manuscript. This work was supported in part by Grants-in Aid from the Ministry of Education, Science, and Culture of Japan.",
year = "1995",
doi = "10.3109/10428199509107891",
language = "English (US)",
volume = "19",
pages = "213--221",
journal = "Leukemia and Lymphoma",
issn = "1042-8194",
publisher = "Informa Healthcare",
number = "3-4",
}