Chromosomal imbalances in adult T-cell leukemia revealed by comparative genomic hybridization: gains at 14q32 and 2p16-22 in cell lines

被引:23
作者
Ariyama, Y
Mori, T
Shinomiya, T
Sakabe, T
Fukuda, Y
Kanamaru, A
Yamada, Y
Isobe, M
Seto, M
Nakamura, Y
Inazawa, J
机构
[1] Tokyo Med & Dent Univ, Med Res Inst, Dept Mol Cytogenet, Bunkyo Ku, Tokyo 1138519, Japan
[2] Kinki Univ, Sch Med, Dept Internal Med 3, Osaka 589, Japan
[3] Nagasaki Univ Hosp, Dept Clin Lab, Nagasaki, Japan
[4] Toyama Univ, Sch Technol, Dept Cell Technol, Toyama 930, Japan
[5] Aichi Canc Ctr Inst, Lab Chemotherapy, Nagoya, Aichi, Japan
[6] Univ Tokyo, Ctr Human Genome, Mol Med Lab, Tokyo, Japan
[7] Univ Tokyo, Inst Med Sci, Ctr Human Genome, Lab Genome Med, Tokyo, Japan
关键词
ATL; CGH; 14q32; TCL1; 2p; HTLF;
D O I
10.1007/s100380050178
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Comparative genomic hybridization was used to identify chromosomal imbalances in eight cell lines and 12 blood samples from patients with adult T-cell leukemia/lymphoma (ATL). The chromosomes most often over-represented in the cell lines were 2p (6 cases), 7q (4 cases), and 14q (4 cases), with minimal common regions at 2p16-22, 7q21-36, and 14q32, respectively. Distinct imbalances were detected in only 7 of the clinical samples. Chromosomes 14q32 and 2p16-22 harbor TCL1 and a transcription factor, HTLF (human T-cell leukemia virus enhancer factor), respectively. FISH analysis revealed that TCL1 did not juxtapose to TCRA, and we detected no expression of TCL1 in any of the ATL cell lines despite the 14q32 amplifications. Moreover, expression of HTLF was not elevated in the ATL cell lines bearing multiplication of 2p. These results suggest that chromosomal regions 2p16-22 and 14q32 harbor genes other than HTLF and TCL1 that are involved in cellular immortalization or in the pathogenesis of ATL.
引用
收藏
页码:357 / 363
页数:7
相关论文
共 26 条
[1]   Identification of amplified DNA sequences on double minute chromosomes in a leukemic cell line KY821 by means of spectral karyotyping and comparative genomic hybridization [J].
Ariyama, Y ;
Sakabe, T ;
Shinomiya, T ;
Mori, T ;
Fukuda, Y ;
Inazawa, J .
JOURNAL OF HUMAN GENETICS, 1998, 43 (03) :187-190
[2]  
Ariyama Y, 1998, GENE CHROMOSOME CANC, V23, P267, DOI 10.1002/(SICI)1098-2264(199811)23:3<267::AID-GCC10>3.3.CO
[3]  
2-0
[4]   MOLECULAR MECHANISMS OF HUMAN T-CELL LEUKEMIA/LYMPHOTROPIC VIRUS TYPE-I INFECTION [J].
FRANCHINI, G .
BLOOD, 1995, 86 (10) :3619-3639
[5]   FUNCTIONAL ACTIVATION OF THE LONG TERMINAL REPEAT OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE-I BY A TRANS-ACTING FACTOR [J].
FUJISAWA, J ;
SEIKI, M ;
KIYOKAWA, T ;
YOSHIDA, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1985, 82 (08) :2277-2281
[6]   ANTIBODIES TO ADULT T-CELL LEUKEMIA-VIRUS-ASSOCIATED ANTIGEN (ATLA) IN SERA FROM PATIENTS WITH ATL AND CONTROLS IN JAPAN - A NATION-WIDE SERO-EPIDEMIOLOGIC STUDY [J].
HINUMA, Y ;
KOMODA, H ;
CHOSA, T ;
KONDO, T ;
KOHAKURA, M ;
TAKENAKA, T ;
KIKUCHI, M ;
ICHIMARU, M ;
YUNOKI, K ;
SATO, I ;
MATSUO, R ;
TAKIUCHI, Y ;
UCHINO, H ;
HANAOKA, M .
INTERNATIONAL JOURNAL OF CANCER, 1982, 29 (06) :631-635
[7]   HIGH-RESOLUTION ORDERING OF DNA MARKERS BY MULTICOLOR FLUORESCENT IN-SITU HYBRIDIZATION OF PROPHASE CHROMOSOMES [J].
INAZAWA, J ;
ARIYAMA, T ;
TOKINO, T ;
TANIGAMI, A ;
NAKAMURA, Y ;
ABE, T .
CYTOGENETICS AND CELL GENETICS, 1994, 65 (1-2) :130-135
[8]   NOVEL INTERLEUKIN-2 DEPENDENT T-CELL LINE DERIVED FROM ADULT T-CELL LEUKEMIA NOT ASSOCIATED WITH HUMAN T-CELL LEUKEMIA-VIRUS TYPE-I [J].
KAGAMI, Y ;
TOBINAI, K ;
KINOSHITA, T ;
NAGAI, H ;
HOTTA, T ;
SETO, M ;
UEDA, R ;
SAITO, H .
JAPANESE JOURNAL OF CANCER RESEARCH, 1993, 84 (04) :371-378
[9]  
KALLIONIEMI OP, 1993, SEMIN CANCER BIOL, V4, P41
[10]  
KAMADA N, 1992, CANCER RES, V52, P1481