DELETION OF IRF-1, MAPPING TO CHROMOSOME 5Q31.1 IN HUMAN LEUKEMIA AND PRELEUKEMIC MYELODYSPLASIA

被引：364

作者：

WILLMAN, CL

SEVER, CE

PALLAVICINI, MG

HARADA, H

TANAKA, N

SLOVAK, ML

YAMAMOTO, H

HARADA, K

MEEKER, TC

LIST, AF

TANIGUCHI, T

机构：

[1] OSAKA UNIV,INST MOLEC & CELLULAR BIOL,SUITA,OSAKA 565,JAPAN

[2] CITY HOPE NATL MED CTR,DEPT PATHOL,DUARTE,CA 91010

[3] UNIV NEW MEXICO,SCH MED,DEPT CELL BIOL,ALBUQUERQUE,NM 87131

[4] UNIV CALIF SAN FRANCISCO,DEPT LAB MED,DIV MOLEC CYTOMETRY,SAN FRANCISCO,CA 94143

[5] UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143

[6] UNIV ARIZONA,CTR CANC,TUCSON,AZ 85724

来源：

SCIENCE | 1993年 / 259卷 / 5097期

关键词：

D O I：

10.1126/science.8438156

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

One of the most frequent cytogenetic abnormalities in human leukemia and myelodysplasia is an interstitial deletion within chromosome 5q. A tumor suppressor gene has been hypothesized to lie in 5q31, the smallest commonly deleted region. IRF-1, a gene whose product manifests anti-oncogenic activity, was mapped to 5q31.1. IRF-1 lies between IL-5 and CDC25C and is centromeric to IL-3 and GM-CSF. Among these genes, only IRF-1 was consistently deleted at one or both alleles in 13 cases of leukemia or myelodysplasia with aberrations of 5q31. Inactivating rearrangements of one IRF-1 allele, accompanied by deletion of the second allele, were also identified in one case of acute leukemia. Thus, IRF-1 may be a critically deleted gene in human leukemia and myelodysplasia.

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页码：968 / 971

页数：4

相关论文

共 40 条

[1] THE GENE FOR HUMAN-COMPLEMENT COMPONENT C9 MAPPED TO CHROMOSOME-5 BY POLYMERASE CHAIN-REACTION [J].

ABBOTT, C ;

WEST, L ;

POVEY, S ;

JEREMIAH, S ;

MURAD, Z ;

DISCIPIO, R ;

FEY, G .

GENOMICS, 1989, 4 (04) :606-609

[2]

ABDOLLAHI A, 1991, CELL GROWTH DIFFER, V2, P401

[3]

DEWALD GW, 1985, BLOOD, V66, P189

[4] NUCLEOTIDE-SEQUENCE OF CDNA AND DERIVED AMINO-ACID-SEQUENCE OF HUMAN-COMPLEMENT COMPONENT-C9 [J].

DISCIPIO, RG ;

GEHRING, MR ;

PODACK, ER ;

KAN, CC ;

HUGLI, TE ;

FEY, GH .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1984, 81 (23) :7298-7302

[5] INDUCTION OF THE TRANSCRIPTION FACTOR IRF-1 AND INTERFERON-BETA MESSENGER-RNAS BY CYTOKINES AND ACTIVATORS OF 2ND-MESSENGER PATHWAYS [J].

FUJITA, T ;

REIS, LFL ;

WATANABE, N ;

KIMURA, Y ;

TANIGUCHI, T ;

VILCEK, J .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (24) :9936-9940

[6] INDUCTION OF ENDOGENOUS IFN-ALPHA AND IFN-BETA GENES BY A REGULATORY TRANSCRIPTION FACTOR, IRF-1 [J].

FUJITA, T ;

KIMURA, Y ;

MIYAMOTO, M ;

BARSOUMIAN, EL ;

TANIGUCHI, T .

NATURE, 1989, 337 (6204) :270-272

[7] IDENTIFICATION AND CHARACTERIZATION OF THE FAMILIAL ADENOMATOUS POLYPOSIS-COLI GENE [J].

GRODEN, J ;

THLIVERIS, A ;

SAMOWITZ, W ;

CARLSON, M ;

GELBERT, L ;

ALBERTSEN, H ;

JOSLYN, G ;

STEVENS, J ;

SPIRIO, L ;

ROBERTSON, M ;

SARGEANT, L ;

KRAPCHO, K ;

WOLFF, E ;

BURT, R ;

HUGHES, JP ;

WARRINGTON, J ;

MCPHERSON, J ;

WASMUTH, J ;

LEPASLIER, D ;

ABDERRAHIM, H ;

COHEN, D ;

LEPPERT, M ;

WHITE, R .

CELL, 1991, 66 (03) :589-600

[8] AN INTERNAL DELETION WITHIN AN 11P13 ZINC FINGER GENE CONTRIBUTES TO THE DEVELOPMENT OF WILMS-TUMOR [J].

HABER, DA ;

BUCKLER, AJ ;

GLASER, T ;

CALL, KM ;

PELLETIER, J ;

SOHN, RL ;

DOUGLASS, EC ;

HOUSMAN, DE .

CELL, 1990, 61 (07) :1257-1269

[9] ANTI-ONCOGENIC AND ONCOGENIC POTENTIALS OF INTERFERON REGULATORY FACTOR-I AND FACTOR-II [J].

HARADA, H ;

KITAGAWA, M ;

TANAKA, N ;

YAMAMOTO, H ;

HARADA, K ;

ISHIHARA, M ;

TANIGUCHI, T .

SCIENCE, 1993, 259 (5097) :971-974

[10] STRUCTURALLY SIMILAR BUT FUNCTIONALLY DISTINCT FACTORS, IRF-1 AND IRF-2, BIND TO THE SAME REGULATORY ELEMENTS OF IFN AND IFN-INDUCIBLE GENES [J].

HARADA, H ;

FUJITA, T ;

MIYAMOTO, M ;

KIMURA, Y ;

MARUYAMA, M ;

FURIA, A ;

MIYATA, T ;

TANIGUCHI, T .

CELL, 1989, 58 (04) :729-739

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