Linked Life Data

8683987

Source:http://linkedlifedata.com/resource/pubmed/id/8683987

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1996-8-20
pubmed:abstractText
We analyzed 60 B precursor acute lymphoblastic leukemia (ALL) primary samples and 15 cell lines for homozygous deletions of p16 and p15 genes and mutations of p16 gene. These included five cell lines and 13 primary samples with the t(1;19)(q23;pl3), and eight primary samples with the t(9;22)(q34;qll). Of 10 cell lines without t(1;19), homozygous deletion of both p16 and p15 genes was found in eight cell lines (80%), and a rearrangement of p16 in one cell line (10%). In contrast, only one (20%) of the five cell lines with t(1;19) showed homozygous deletion or rearrangement of p16/p15 gene. Thirteen of 60 (22%) primary samples demonstrated p16 gene homozygous deletion. No case with t(1;19) showed homozygous deletion of p16 gene (0/13, 0%), while cases without t(1;19) showed considerable incidence of p16 gene homozygous deletion (13/47, 28%). These results suggest that the incidence of deletions of p16 gene differs according to the subtypes of B precursor ALL. We also compared the frequency of p16 gene homozygous deletion between the patients at diagnosis and at relapse. Nine of 45 (20%) samples at diagnosis and four of 22 (18%) samples at relapse showed p16 homozygous deletions. The similarity of the rate in these two groups raises the question of the role of p16 gene in progression of B precursor ALL. Mutations were found in three of the primary cases (5%); the mutations included two nonsense mutations at codon 72 and one missense mutation at codon 98. All the mutations found in this study were heterozygous, and the clinical relevance of p16 gene mutation is yet to be determined in these case
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0887-6924
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1104-10
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:8683987-Base Sequence, pubmed-meshheading:8683987-Blotting, Southern, pubmed-meshheading:8683987-Carrier Proteins, pubmed-meshheading:8683987-Cell Cycle Proteins, pubmed-meshheading:8683987-Child, pubmed-meshheading:8683987-Chromosomes, Human, Pair 1, pubmed-meshheading:8683987-Chromosomes, Human, Pair 19, pubmed-meshheading:8683987-Cyclin-Dependent Kinase Inhibitor p15, pubmed-meshheading:8683987-Cyclin-Dependent Kinase Inhibitor p16, pubmed-meshheading:8683987-Gene Deletion, pubmed-meshheading:8683987-Genes, Tumor Suppressor, pubmed-meshheading:8683987-Homozygote, pubmed-meshheading:8683987-Humans, pubmed-meshheading:8683987-Molecular Sequence Data, pubmed-meshheading:8683987-Mutation, pubmed-meshheading:8683987-Polymerase Chain Reaction, pubmed-meshheading:8683987-Polymorphism, Single-Stranded Conformational, pubmed-meshheading:8683987-Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, pubmed-meshheading:8683987-Precursor Cell Lymphoblastic Leukemia-Lymphoma, pubmed-meshheading:8683987-Translocation, Genetic, pubmed-meshheading:8683987-Tumor Suppressor Proteins
pubmed:year
1996
pubmed:articleTitle
Homozygous deletions of p16/MTS1 and p15/MTS2 genes are frequent in t(1;19)-negative but not in t(1;19)-positive B precursor acute lymphoblastic leukemia in childhood.
pubmed:affiliation
Department of Pediatrics, Faculty of Medicine, University of Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't