The difference between p53 mutation frequency in haematological and non haematological malignancies: possible explanations

被引:4
作者
Calin, G
Ivan, M
Stefanescu, D
机构
[1] Victor Babes Inst, Dept Med Genet, R-76201 Bucharest, Romania
[2] Univ Wales, Coll Med, Dept Pathol, Cardiff, S Glam, Wales
[3] Univ Ferrara, Dept Diagnost & Expt Med, I-44100 Ferrara, Italy
关键词
D O I
10.1054/mehy.1999.0764
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
p53 gene mutations are the most frequent alterations in human cancers. In the published literature, a highly significant statistical difference between the prevalence of p53 mutations in haematological (H) and nonhaematological (NH) malignancies can be found. However, no consistent reasons have been suggested to explain it. We propose two non-exclusive possibilities: (i) in H tumours p53 is altered with the same frequency as in NH tumours, but mechanisms other than mutations are involved and (ii) in H malignancies the prevalence of p53 mutations is much lower than in NH cancers because other genetic disturbances are involved. We hypothesized that retention of wildtype p53 in H cancers may be a consequence of: (a) the presence of telomerase activity in haematological cells and/or (b) the absence of hypoxia in the majority of H tumours. (C) 1999 Harcourt Publishers Ltd.
引用
收藏
页码:326 / 328
页数:3
相关论文
共 20 条
[1]  
ASHLEY DJB, 1990, EVANS HISTOLOGICAL A, P191
[2]   Multiple tumor-suppressor gene 1 inactivation is the most frequent genetic alteration in T-cell acute lymphoblastic leukemia [J].
Cayuela, JM ;
Madani, A ;
Sanhes, L ;
Stern, MH ;
Sigaux, F .
BLOOD, 1996, 87 (06) :2180-2186
[3]   ABNORMAL EXPRESSION OF THE P53-BINDING PROTEIN MDM2 IN HODGKINS-DISEASE [J].
CHILOSI, M ;
DOGLIONI, C ;
MENESTRINA, F ;
MONTAGNA, L ;
RIGO, A ;
LESTANI, M ;
BARBARESCHI, M ;
SCARPA, A ;
MARIUZZI, GM ;
PIZZOLO, G .
BLOOD, 1994, 84 (12) :4295-4300
[4]   ALTERATIONS IN DNA METHYLATION MAY PLAY A VARIETY OF ROLES IN CARCINOGENESIS [J].
COUNTS, JL ;
GOODMAN, JI .
CELL, 1995, 83 (01) :13-15
[5]   Mismatch repair defects in human carcinogenesis [J].
Eshleman, JR ;
Markowitz, SD .
HUMAN MOLECULAR GENETICS, 1996, 5 :1489-1494
[6]   Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours [J].
Graeber, TG ;
Osmanian, C ;
Jacks, T ;
Housman, DE ;
Koch, CJ ;
Lowe, SW ;
Giaccia, AJ .
NATURE, 1996, 379 (6560) :88-91
[7]  
GREENBLATT MS, 1994, CANCER RES, V54, P4855
[8]   Telomerase activity, cell proliferation, and cancer [J].
Greider, CW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (01) :90-92
[9]   Inactivation of multiple tumor-suppressor genes involved in negative regulation of the cell cycle, MTS1/p16(INK4A)/CDKN2, MTS2/p15(INK4B), p53, and Rb genes in primary lymphoid malignancies [J].
Hangaishi, A ;
Ogawa, S ;
Imamura, N ;
Miyawaki, S ;
Miura, Y ;
Uike, N ;
Shimazaki, C ;
Emi, N ;
Takeyama, K ;
Hirosawa, S ;
Kamada, N ;
Kobayashi, Y ;
Takemoto, Y ;
Kitani, T ;
Toyama, K ;
Ohtake, S ;
Yazaki, Y ;
Ueda, R ;
Hirai, H .
BLOOD, 1996, 87 (12) :4949-4958
[10]   SPONTANEOUS AND CARCINOGEN-INDUCED TUMORIGENESIS IN P53-DEFICIENT MICE [J].
HARVEY, M ;
MCARTHUR, MJ ;
MONTGOMERY, CA ;
BUTEL, JS ;
BRADLEY, A ;
DONEHOWER, LA .
NATURE GENETICS, 1993, 5 (03) :225-229