TRANSLOCATION OF BCL-2 GENE IN NON-HODGKINS-LYMPHOMAS IN HONG-KONG CHINESE

被引:27
作者
LOKE, SL
PITTALUGA, S
SRIVASTAVA, G
RAFFELD, M
HO, FCS
机构
[1] UNIV HONG KONG,QUEEN MARY HOSP,DEPT PATHOL,HONG KONG,HONG KONG
[2] NCI,PATHOL LAB,BETHESDA,MD 20892
关键词
D O I
10.1111/j.1365-2141.1990.tb07837.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Summary. The close association between translocation of the proto‐oncogene bcl‐2 and follicular lymphomas has been well established in Caucasian patients and the de‐regulation of bcl‐2 has been implicated in follicular lymphomagenesis. Similar molecular structural alterations have also been detected in diffuse lymphomas with a previous history of a follicular pattern as well as in a smaller proportion of de novo diffuse lymphomas. There is a lower incidence of follicular lymphomas in Chinese. In order to investigate further this phenomenon, we used bcl‐2 translocation as a genetic marker of follicular lymphomas, to study 31 cases of B cell non‐Hodgkin's lymphomas in Chinese patients by Southern blot analysis. Eight out of 16 cases of follicular lymphomas showed bcl‐2 translocation with involvement of the major breakpoint region (MBR). Six of these cases utilized breakpoints within the 4.3 kb HindIII fragment, while in two cases the breakpoints were more dispersed, but still within the BamHI fragment. An additional case of follicular lymphoma showed translocation of bcl‐2 gene with involvement of the minor cluster region (mcr), making a total of nine out of 16. None of the 15 cases of diffuse lymphomas showed similar molecular structural alterations. These data show that bcl‐2 translocation is present in 57% of follicular lymphomas in Chinese patients, and support the notion that bcl‐2 translocation is a consistent marker for follicular lymphomas irrespective of ethnic differences. As the translocation is not detected in the diffuse lymphomas, there is no evidence to suggest that the low incidence of follicular lymphomas in Chinese patients is due to a greater tendency for follicular tumours to progress rapidly and present as diffuse lymphomas. Copyright © 1990, Wiley Blackwell. All rights reserved
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页码:65 / 69
页数:5
相关论文
共 28 条
[1]  
AISENBERG AC, 1988, BLOOD, V71, P969
[2]  
AMAKAWA R, 1989, BLOOD, V73, P787
[3]  
[Anonymous], 1982, CANCER, V49, P2112
[4]   MECHANISM OF THE T(14-18) CHROMOSOMAL TRANSLOCATION - STRUCTURAL-ANALYSIS OF BOTH DERIVATIVE-14 AND DERIVATIVE-18 RECIPROCAL PARTNERS [J].
BAKHSHI, A ;
WRIGHT, JJ ;
GRANINGER, W ;
SETO, M ;
OWENS, J ;
COSSMAN, J ;
JENSEN, JP ;
GOLDMAN, P ;
KORSMEYER, SJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (08) :2396-2400
[5]   CLONING THE CHROMOSOMAL BREAKPOINT OF T(14-18) HUMAN LYMPHOMAS - CLUSTERING AROUND JH ON CHROMOSOME-14 AND NEAR A TRANSCRIPTIONAL UNIT ON 18 [J].
BAKHSHI, A ;
JENSEN, JP ;
GOLDMAN, P ;
WRIGHT, JJ ;
MCBRIDE, OW ;
EPSTEIN, AL ;
KORSMEYER, SJ .
CELL, 1985, 41 (03) :899-906
[6]   CLONING AND STRUCTURAL-ANALYSIS OF CDNAS FOR BCL-2 AND A HYBRID BCL-2/IMMUNOGLOBULIN TRANSCRIPT RESULTING FROM THE T(14-18) TRANSLOCATION [J].
CLEARY, ML ;
SMITH, SD ;
SKLAR, J .
CELL, 1986, 47 (01) :19-28
[7]   DETECTION OF A 2ND T(14-18) BREAKPOINT CLUSTER REGION IN HUMAN FOLLICULAR LYMPHOMAS [J].
CLEARY, ML ;
GALILI, N ;
SKLAR, J .
JOURNAL OF EXPERIMENTAL MEDICINE, 1986, 164 (01) :315-320
[9]   TRANSLOCATION T(14-18) IN B-CELL LYMPHOMAS AS A CAUSE FOR DEFECTIVE IMMUNOGLOBULIN PRODUCTION [J].
DEJONG, D ;
VOETDIJK, BMH ;
VANOMMEN, GJB ;
KLUINNELEMANS, JC ;
BEVERSTOCK, GC ;
KLUIN, PM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 169 (03) :613-624
[10]   CLINICOPATHOLOGICAL FEATURES OF MALIGNANT-LYMPHOMAS IN 294 HONG-KONG CHINESE PATIENTS, RETROSPECTIVE STUDY COVERING AN 8-YEAR PERIOD [J].
HO, FCS ;
TODD, D ;
LOKE, SL ;
NG, RP ;
KHOO, RKK .
INTERNATIONAL JOURNAL OF CANCER, 1984, 34 (02) :143-148