Deletion of chromosome arm 3p in hematologic malignancies

被引:48
作者
Johansson, B
Billstrom, R
Kristoffersson, U
Akerman, M
Garwicz, S
Ahlgren, T
Malm, C
Mitelman, F
机构
[1] UNIV LUND HOSP,DEPT INTERNAL MED,DIV HEMATOL,S-22185 LUND,SWEDEN
[2] UNIV LUND HOSP,DEPT PATHOL & CYTOL,S-22185 LUND,SWEDEN
[3] UNIV LUND HOSP,DEPT PEDIAT,S-22185 LUND,SWEDEN
[4] MALMO UNIV HOSP,DEPT MED,MALMO,SWEDEN
[5] LINKOPING UNIV HOSP,DEPT INTERNAL MED,S-58185 LINKOPING,SWEDEN
关键词
deletion; chromosome arm 3p; hematologic malignancy; therapy-associated AML;
D O I
10.1038/sj.leu.2400718
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cytogenetic aberrations resulting in deletion of 3p are common in solid tumors, indicating the presence of tumor suppressor genes (TSG) on this chromosome arm. The present study was undertaken to investigate 3p loss in hematologic disorders. Ten acute myeloid leukemias (AML), two myelodysplastic syndromes (MDS), one Philadelphia chromosome-positive chronic myeloid leukemia (CML), three acute lymphoblastic leukemias (ALL), one chronic lymphoproliferative disorder (CLD), and three non-Hodgkin's lymphomas (NHL) with abnormalities leading to 3p deletions were identified, constituting 2.9% of AML, 0.7% of MDS, 1.0% of CML with changes in addition to t(9;22), 1.5% of ALL, 4.2% of CLD, and 1.1% of NHL with cytogenetic abnormalities analyzed at our Department. Among 19042 karyotypically aberrant published cases, 1.2% of 6260 AML, 1.3% of 2285 MDS, 0.8% of 840 chronic myeloproliferative disorders (CMD), 0.7% of 1894 CML with additional aberrations to t(9;22), 0.6% of 3589 ALL 2.4% of 1602 CLD, 4.5% of 178 Hodgkin disease (HD), and 3.1% of 2394 NHL displayed partial loss of 3p (0.6-4.5%; P < 0.001); the majority occurring together with other abnormalities. The frequencies of 3p loss did not differ significantly among the MDS, ALL, and CLD morphologic subgroups, between B and T cell ALL, CLD, and NHL, among low-, intermediate-, and high-grade NHL, or between therapy-related MDS and de novo MDS, whereas the incidence of 3p deletions was higher in treatment-associated AML (P < 0.001) than in de novo AML and varied among the AML FAB groups (P < 0.001). The most frequently deleted chromosome bands were 3p25 in AML, 3p26 in MDS, 3p14 in CMD, 3p25, 3p23, and 3p21 in CML, 3p26 and 3p25 in ALL, 3p26 and 3p25 in CLD, 3p26 in HD, and 3p26 in NHL. These deletion hot spots are more distal than those reported in most solid tumor types, suggesting that different TSG are involved in hematologic malignancies and solid neoplasms.
引用
收藏
页码:1207 / 1213
页数:7
相关论文
共 43 条
  • [1] PROPOSALS FOR THE CLASSIFICATION OF THE MYELODYSPLASTIC SYNDROMES
    BENNETT, JM
    CATOVSKY, D
    DANIEL, MT
    FLANDRIN, G
    GALTON, DAG
    GRALNICK, HR
    SULTAN, C
    [J]. BRITISH JOURNAL OF HAEMATOLOGY, 1982, 51 (02) : 189 - 199
  • [2] BENNETT JM, 1985, ANN INTERN MED, V103, P626
  • [3] BILLSTROM R, 1995, EUR J HAEMATOL, V55, P42
  • [4] BOULTWOOD J, 1993, BLOOD, V82, P2611
  • [5] DREXLER HG, 1995, LEUKEMIA, V9, P480
  • [6] Translocations and deletions of 5q13.1 in myelodysplasia and acute myelogenous leukemia: Evidence for a novel critical locus
    Fairman, J
    Wang, RY
    Liang, H
    Zhao, L
    Saltman, D
    Liang, JC
    Nagarajan, L
    [J]. BLOOD, 1996, 88 (06) : 2259 - 2266
  • [7] A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS
    FEARON, ER
    VOGELSTEIN, B
    [J]. CELL, 1990, 61 (05) : 759 - 767
  • [8] SOMATIC MUTATIONS OF THE VON HIPPEL-LINDAU DISEASE TUMOR-SUPPRESSOR GENE IN NONFAMILIAL CLEAR-CELL RENAL-CARCINOMA
    FOSTER, K
    PROWSE, A
    VANDENBERG, A
    FLEMING, S
    HULSBEEK, MMF
    CROSSEY, PA
    RICHARDS, FM
    CAIRNS, P
    AFFARA, NA
    FERGUSONSMITH, MA
    BUYS, CHCM
    MAHER, ER
    [J]. HUMAN MOLECULAR GENETICS, 1994, 3 (12) : 2169 - 2173
  • [9] GREENBLATT MS, 1994, CANCER RES, V54, P4855
  • [10] P15(INK4B) IS A POTENTIAL EFFECTOR OF TGF-BETA-INDUCED CELL-CYCLE ARREST
    HANNON, GJ
    BEACH, D
    [J]. NATURE, 1994, 371 (6494) : 257 - 261