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PMID: 11264177 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Nucleotide sequence, transcription map, and mutation analysis of the 13q14 chromosomal region deleted in B-cell chronic lymphocytic leukemia.

Blood ·Vol. 97 ·No. 7 ·2001-04-01 ·Pages 2098-104

Migliazza A, Bosch F, Komatsu H, Cayanis E, Martinotti S, Toniato E, Guccione E, Qu X, Chien M, Murty VV, Gaidano G, Inghirami G, Zhang P, Fischer S, Kalachikov SM, Russo J, Edelman I, Efstratiadis A, Dalla-Favera R

Abstract

Deletions of the 13q14 chromosome region are associated with B-cell chronic lymphocytic leukemia (B-CLL) and several other types of cancer, suggesting the presence of a tumor suppressor gene. In previous studies the minimal region of deletion (MDR) was mapped to a less than 300-kilobase (kb) interval bordered by the markers 173a12-82 and 138G4/1.3R. For the identification of the putative tumor suppressor gene, the entire MDR (approximately 347 kb) has been sequenced, and transcribed regions have been identified by exon trapping, EST-based full-length complementary DNA cloning, database homology searches, and computer-assisted gene prediction analyses. The MDR contains 2 pseudogenes and 3 transcribed genes: CAR, encoding a putative RING-finger containing protein; 1B4/Leu2, generating noncoding transcripts; and EST70/Leu1, probably representing another noncoding gene (longest open reading frame of 78 codons). These genes have been sequenced in 20 B-CLL cases with 13q14 hemizygous deletion, and no mutations were found. Moreover, no somatic variants were found in the entire MDR analyzed for nucleotide substitutions by a combination of direct sequencing and fluorescence-assisted mismatch analysis in 5 B-CLL cases displaying 13q14-monoallelic deletion. The nondeleted allele of the CAR and EST70/Leu1 genes was expressed in B-CLL specimens, including those with monoallelic loss, whereas no expression of 1B4/Leu2 was detectable in B-CLL, regardless of the 13q14 status. These results indicate that allelic loss and mutation of a gene within the MDR is an unlikely pathogenetic mechanism for B-CLL. However, haplo-insufficiency of one of the identified genes may contribute to tumorigenesis. (Blood. 2001;97:2098-2104)

MeSH Terms
Animals Base Sequence Cell Transformation, Neoplastic/genetics Chromosome Mapping Chromosomes, Human, Pair 13/genetics,ultrastructure DNA Mutational Analysis DNA, Complementary/genetics DNA, Neoplasm/genetics Expressed Sequence Tags Gene Expression Regulation, Leukemic Genes, Tumor Suppressor Humans Leukemia, Lymphocytic, Chronic, B-Cell/genetics Mice Molecular Sequence Data Proteins/genetics Pseudogenes RNA, Long Noncoding RNA, Messenger/biosynthesis,genetics RNA, Neoplasm/biosynthesis,genetics Sequence Deletion Transcription, Genetic Transferases Tumor Suppressor Proteins
Chemicals
DLEU1 lncRNA, human DLEU2 lncRNA, human DNA, Complementary DNA, Neoplasm Proteins RNA, Long Noncoding RNA, Messenger RNA, Neoplasm Tumor Suppressor Proteins Dleu2 protein, mouse Transferases
Authors & Affiliations
19 authors, click to expand affiliations / ORCID
Migliazza A
Institute of Cancer Genetics, Columbia University, New York, New York 10032, USA.
Bosch F
Komatsu H
Cayanis E
Martinotti S
Toniato E
Guccione E
Qu X
Chien M
Murty V V
Gaidano G
Inghirami G
Zhang P
Fischer S
Kalachikov S M
Russo J
Edelman I
Efstratiadis A
Dalla-Favera R
Article Info
Journal
Blood
Abbr.
Blood
ISSN
0006-4971
Published
2001-04-01
Pages
2098-104
Language
English
Region
United States
NLM ID
7603509
Subset
IM
Databases
GENBANK
AF272953, AF279658, AF279659, AF279660
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