TEL AND KIP1 DEFINE THE SMALLEST REGION OF DELETIONS ON 12P13 IN HEMATOPOIETIC MALIGNANCIES

被引:101
作者
SATO, Y
SUTO, Y
PIETENPOL, J
GOLUB, TR
GILLILAND, DG
DAVIS, EM
LEBEAU, MM
ROBERTS, JM
VOGELSTEIN, B
ROWLEY, JD
BOHLANDER, SK
机构
[1] UNIV CHICAGO,DEPT MED,HEMATOL ONCOL SECT,CHICAGO,IL 60637
[2] JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD
[3] BRIGHAM & WOMENS HOSP,BOSTON,MA 02115
[4] FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104
关键词
D O I
10.1182/blood.V86.4.1525.bloodjournal8641525
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Unbalanced translocations as well as interstitial deletions of the short arm of chromosome 12 [del(12p)] are found as recurring chromosomal changes in a broad spectrum of hematopoietic malignancies. These changes result in the hemizygous deletion of genetic material from 12p. We mapped a yeast artificial chromosome containing the TEL gene, a cosmid contig containing part of TEL and a pi contig containing the KIP1 gene to 12p13. These probes were used for fluorescence in situ hybridization to analyze samples from 47 patients with various hematologic malignancies who had unbalanced translocations (25 patients) leading to loss of 12p or deletions (22 patients) involving 12p13. The patients had acute lymphoblastic leukemia (8 cases), myelodysplastic syndrome (MDS; 11 cases), acute myeloid leukemia (AML; 10 cases), myeloproliferative disorders (4 cases), therapy-related MDS or AML (7 cases), non-Hodgkin's lymphoma (2 cases), and other hematopoietic malignancies (5 cases). All three probes were hemizygously deleted in 26 cases and were completely retained in only 9 cases. In 12 cases probes for one of the two genes were deleted, allowing us to map the smallest region of overlap of these deletions to a small genomic region that is bordered on the telomeric side by the TEL gene and on the centromeric side by KIP1. The genomic distance between TEL and KIP1 is estimated to be about 1 to 2 Mbp. (C) 1995 by The American Society of Hematology.
引用
收藏
页码:1525 / 1533
页数:9
相关论文
共 36 条
[1]   SEQUENCE-INDEPENDENT AMPLIFICATION AND LABELING OF YEAST ARTIFICIAL CHROMOSOMES FOR FLUORESCENCE IN-SITU HYBRIDIZATION [J].
BOHLANDER, SK ;
ESPINOSA, R ;
FERNALD, AA ;
ROWLEY, JD ;
LEBEAU, MM ;
DIAZ, MO .
CYTOGENETICS AND CELL GENETICS, 1994, 65 (1-2) :108-110
[2]   A 1ST-GENERATION PHYSICAL MAP OF THE HUMAN GENOME [J].
COHEN, D ;
CHUMAKOV, I ;
WEISSENBACH, J .
NATURE, 1993, 366 (6456) :698-701
[3]  
DIAZ MO, 1990, NEW ENGL J MED, V322, P77, DOI 10.1056/NEJM199001113220202
[4]   INACTIVATION OF A CDK2 INHIBITOR DURING INTERLEUKIN 2-INDUCED PROLIFERATION OF HUMAN T-LYMPHOCYTES [J].
FIRPO, EJ ;
KOFF, A ;
SOLOMON, MJ ;
ROBERTS, JM .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (07) :4889-4901
[5]   FUSION OF PDGF RECEPTOR-BETA TO A NOVEL ETS-LIKE GENE, TEL, IN CHRONIC MYELOMONOCYTIC LEUKEMIA WITH T(512) CHROMOSOMAL TRANSLOCATION [J].
GOLUB, TR ;
BARKER, GF ;
LOVETT, M ;
GILLILAND, DG .
CELL, 1994, 77 (02) :307-316
[6]  
GOLUB TR, 1994, BLOOD, V84, pA229
[7]  
GOLUB TR, IN PRESS P NATL ACAD
[8]   P15(INK4B) IS A POTENTIAL EFFECTOR OF TGF-BETA-INDUCED CELL-CYCLE ARREST [J].
HANNON, GJ ;
BEACH, D .
NATURE, 1994, 371 (6494) :257-261
[9]   CYTOGENETIC DELETION MAPS OF HEMATOLOGIC NEOPLASMS - CIRCUMSTANTIAL EVIDENCE FOR TUMOR-SUPPRESSOR LOCI [J].
JOHANSSON, B ;
MERTENS, F ;
MITELMAN, F .
GENES CHROMOSOMES & CANCER, 1993, 8 (04) :205-218
[10]   A CELL-CYCLE REGULATOR POTENTIALLY INVOLVED IN GENESIS OF MANY TUMOR TYPES [J].
KAMB, A ;
GRUIS, NA ;
WEAVERFELDHAUS, J ;
LIU, QY ;
HARSHMAN, K ;
TAVTIGIAN, SV ;
STOCKERT, E ;
DAY, RS ;
JOHNSON, BE ;
SKOLNICK, MH .
SCIENCE, 1994, 264 (5157) :436-440