The mutation rate in PIG-A is normal in patients with paroxysmal nocturnal hemoglobinuria (PNH)

被引:35
作者
Araten, David J.
Luzzatto, Lucio
机构
[1] NYU, Inst Canc, Sch Med, Div Hematol, New York, NY 10016 USA
[2] New York Vet Adm Med Ctr, New York, NY USA
[3] Ist Tuscano Tumori, Florence, Italy
关键词
D O I
10.1182/blood-2006-01-0256
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by the presence in the patient's hematopoietic system of a large cell population with a mutation in the X-linked PIG-A gene. Although this abnormal cell population is often found to be monoclonal, it is not unusual that 2 or even several PIG-A mutant clones coexist in the same patient. Therefore, it has been suggested that the PIG-A gene may be hypermutable in PNH. By a method we have recently developed for measuring the intrinsic rate of somatic mutations (mu) in humans, in which PIG-A itself is used as a sentinel gene, we have found that in 5 patients with PNH, mu ranged from 1.24 x 10(-7) to 11.2 x 10(-7), against a normal range of 2.4 x 10(-7) to 29.6 x 10(-7) mutations per cell division. We conclude that genetic instability of the PIG-A gene is not a factor in the pathogenesis of PNH.
引用
收藏
页码:734 / 736
页数:3
相关论文
共 28 条
[1]   T-CELLS RESPONSIVE TO MYELIN BASIC-PROTEIN IN PATIENTS WITH MULTIPLE-SCLEROSIS [J].
ALLEGRETTA, M ;
NICKLAS, JA ;
SRIRAM, S ;
ALBERTINI, RJ .
SCIENCE, 1990, 247 (4943) :718-721
[2]   A quantitative measurement of the human somatic mutation rate [J].
Araten, DJ ;
Golde, DW ;
Zhang, RH ;
Thaler, HT ;
Gargiulo, L ;
Notaro, R ;
Luzzatto, L .
CANCER RESEARCH, 2005, 65 (18) :8111-8117
[3]   Dynamics of hematopoiesis in paroxysmal nocturnal hemoglobinuria (PNH): no evidence for intrinsic growth advantage of PNH clones [J].
Araten, DJ ;
Bessler, M ;
McKenzie, S ;
Castro-Malaspina, H ;
Childs, BH ;
Boulad, F ;
Karadimitris, A ;
Notaro, R ;
Luzzatto, L .
LEUKEMIA, 2002, 16 (11) :2243-2248
[4]   Clonal populations of hematopoietic cells with paroxysmal nocturnal hemoglobinuria genotype and phenotype are present in normal individuals [J].
Araten, DJ ;
Nafa, K ;
Pakdeesuwan, K ;
Luzzatto, L .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (09) :5209-5214
[5]   SOMATIC MUTATIONS AND CELLULAR-SELECTION IN PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA [J].
BESSLER, M ;
MASON, P ;
HILLMEN, P ;
LUZZATTO, L .
LANCET, 1994, 343 (8903) :951-953
[6]   Frequent HPRT mutations in paroxysmal nocturnal haemoglobinuria reflect T cell clonal expansion, not genomic instability [J].
Chen, GB ;
Zeng, WH ;
Green, S ;
Young, NS .
BRITISH JOURNAL OF HAEMATOLOGY, 2004, 125 (03) :383-391
[7]   Evaluation of the haemopoietic reservoir in de novo haemolytic paroxysmal nocturnal haemoglobinuria [J].
Elebute, MO ;
Rizzo, S ;
Tooze, JA ;
Marsh, JCW ;
Gordon-Smith, EC ;
Gibson, FM .
BRITISH JOURNAL OF HAEMATOLOGY, 2003, 123 (03) :552-560
[8]   Molecular basis of the heterogeneity of expression of glycosyl phosphatidylinositol anchored proteins in paroxysmal nocturnal hemoglobinuria [J].
Endo, M ;
Ware, RE ;
Vreeke, TM ;
Singh, SP ;
Howard, TA ;
Tomita, A ;
Holguin, MH ;
Parker, CJ .
BLOOD, 1996, 87 (06) :2546-2557
[9]   The use of monoclonal antibodies and flow cytometry in the diagnosis of paroxysmal nocturnal hemoglobinuria [J].
Hall, SE ;
Rosse, WF .
BLOOD, 1996, 87 (12) :5332-5340
[10]   Increased frequency of somatic mutations at glycophorin A loci in patients with aplastic anaemia, myelodysplastic syndrome and paroxysmal nocturnal haemoglobinuria [J].
Hattori, H ;
Machii, T ;
Ueda, E ;
Shibano, M ;
Kageyama, T ;
Kitani, T .
BRITISH JOURNAL OF HAEMATOLOGY, 1997, 98 (02) :384-391