Premium
Deletions in the 13q14 locus in adult lymphoblastic leukemia
Author(s) -
Chung ChingYang,
Kantarjian Hagop,
Haidar Mohammed,
Starostik Petr,
Manshouri Taghi,
Gidel Cristi,
Freireich Emil,
Keating Michael,
Albitar Maher
Publication year - 2000
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/(sici)1097-0142(20000315)88:6<1359::aid-cncr12>3.0.co;2-q
Subject(s) - loss of heterozygosity , locus (genetics) , retinoblastoma , tumor suppressor gene , chronic lymphocytic leukemia , microsatellite , leukemia , clinical significance , biology , cancer research , gene , genetics , medicine , allele , carcinogenesis
BACKGROUND A putative tumor suppressor gene involved in chronic lymphocytic leukemia (CLL) has been localized to the 13q14 locus. Microsatellite analysis was used to test whether this locus also is involved in acute lymphoblastic leukemia (ALL) and its prognostic relevance determined. METHODS The authors analyzed 49 patients with adult ALL for deletions at the 13q14 locus using a battery of 6 microsatellite markers corresponding to this region (D13S260, STR257, D13S263, D13S153, D13S319, and AFMa301wb5). RESULTS Five of the 49 adult ALL patients analyzed (10%) showed loss of heterozygosity (LOH) or deletions at 13q14. Similar to CLL, the significant minimal deletions appeared to be localized between D13S260 and AFMa301wb5 and did not involve the retinoblastoma or BRCA2 genes. Among newly diagnosed patients, LOH was associated with shorter survival ( P = 0.007). CONCLUSIONS These data suggest that the 13q14 gene, commonly deleted in CLL patients, also is deleted in some patients with adult ALL. Although the number of the cases in the current study is small, 13q deletions in ALL patients may play a role in the clinical behavior of this disease. Cancer 2000;88:1359–64. © 2000 American Cancer Society.