NONRANDOM CHROMOSOMAL-ABNORMALITIES IN BOVINE LYMPHOMA

Citation
Mw. Schnurr et al., NONRANDOM CHROMOSOMAL-ABNORMALITIES IN BOVINE LYMPHOMA, Leukemia research, 18(2), 1994, pp. 91-99
Citations number
47
Categorie Soggetti
Oncology,Hematology
Journal title
ISSN journal
01452126
Volume
18
Issue
2
Year of publication
1994
Pages
91 - 99
Database
ISI
SICI code
0145-2126(1994)18:2<91:NCIBL>2.0.ZU;2-Z
Abstract
Despite detailed knowledge of the genetic map of the bovine leukemia v irus (BLV), the mechanism whereby BLV infection results in transformat ion and B-lineage restriction of tumors is poorly understood. The aim of this study was to gain new insight into pathogenetic mechanisms of BLV-induced tumorigenesis by determining the karyotypes of BLV-associa ted lymphomas in cattle. Metaphases in cells from lymphoid tumors from 20 mature dairy cows were banded and analyzed after short-term, unsti mulated culture. Nineteen out of twenty cases exhibited clonal abnorma lities, 17 cases were hyperdiploid, and 16 cases had extremely complex chromosomal changes. Recurrent chromosomal anomalies were identified and there was clear evidence for the evolution of increasing chromosom al instability in 12 cases. The most common abnormalities were the acq uisition of additional small chromosomes (23-29); trisomy of chromosom es 5 and 7, and Robertsonian translocations and isochromosome rearrang ements involving chromosomes 10, 12, 23, and 26. Monosomy X, trisomy X , and translocations involving the X chromosome were also detected. Ch romosomes 2, 3, 4, 6, 8, 9, 11, 13, 14, 19, and 21 were infrequently i nvolved in either structural or numerical changes. Structural rearrang ements of chromosomes 10, 12, 23, and 26 may reflect primary abnormali ties occurring relatively early in transformation, whereas trisomy 5 m ay be an extremely common secondary abnormality. While comparison of t hese findings with the current bovine gene map raises intriguing possi bilities for pathogenetic mechanisms, further studies are needed befor e hypothetical mechanisms linking chromosomal abnormalities with BLV-i nduced transformation can be made.