Oligonucleotide microarrays demonstrate the highest frequency of ATM mutations in the mantle cell subtype of lymphoma

被引:75
作者
Fang, NY
Greiner, TC
Weisenburger, DD
Chan, WC
Vose, JM
Smith, LM
Armitage, JO
Mayer, RA
Pike, BL
Collins, FS
Hacia, JG
机构
[1] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA
[2] Univ Nebraska, Med Ctr, Dept Prevent & Societal Med, Omaha, NE 68198 USA
[3] Univ Nebraska, Med Ctr, Dept Internal Med, Omaha, NE 68198 USA
[4] NHGRI, Genome Technol Branch, Bethesda, MD 20892 USA
[5] Univ So Calif, Inst Med Genet, Los Angeles, CA 90089 USA
关键词
D O I
10.1073/pnas.0831102100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Mutations have been described in the ataxia telangiectasia mutated (ATM) gene in small numbers of cases of lymphoid neoplasia. However, surveys of the ATM mutation status in lymphoma have been limited due to the large size (62 exons) and complex mutational spectrum of this gene. We have used microarray-based assays with 250,000 oligonucleotides to screen lymphomas from 120 patients for all possible ATM coding and splice junction mutations. The subtypes included were diffuse large B cell, mantle cell, immunoblastic large B cell, follicular, posttransplant lymphoproliferative disorder, and peripheral T cell lymphoma. We found the highest percentage of ATM mutations within the mantle cell (MCL) subtype (43%, 12 of 28 cases), followed by a lower level (10% of cases) in the other subtypes. A frame-shift ATM mutation was found in one peripheral T cell lymphoma patient. In six MCL cases examined, four ATM variants were due to somatic mutation in the tumor cells whereas two others seemed to be germ-line in origin. There was no difference in p53 mutation status in the ATM mutant and wild-type groups of MCL. There was no statistically significant difference in the median overall survival of patients with wild-type vs. mutated ATM in MCL. Additional mutational and functional analyses are needed to determine whether ATM mutations contribute to the development and progression of MCL or are just the consequence of genomic instability in MCL.
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页码:5372 / 5377
页数:6
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