Genomic alterations in uterine leiomyosarcomas: Potential markers for clinical diagnosis and prognosis

Genomic alterations were analyzed in 21 uterine leiomyosarcomas (ULMSs) by comparative genomic hybridization. DNA copy number changes were detected in all 21 tumors. The most frequent losses were 13q (16/21 = 76%), 10q (13/21 = 62%), 16q (8/21 = 38%), 12p (7/21 = 33%), and 2p (9/21 = 43%). The most...

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Bibliographic Details
Published in:Genes chromosomes & cancer 2001-06, Vol.31 (2), p.117-124
Main Authors: Hu, Jie, Khanna, Vineesh, Jones, Mirka, Surti, Urvashi
Format: Article
Language:English
Subjects:
chromosome 1
chromosome 10
chromosome 12
chromosome 13
chromosome 16
chromosome 17
chromosome 2
Chromosome Aberrations - genetics
Chromosome Deletion
Chromosome Disorders
Female
Gene Dosage
Genetic Markers - genetics
Humans
leiomyosarcoma
Leiomyosarcoma - diagnosis
Leiomyosarcoma - genetics
Metaphase - genetics
Nucleic Acid Hybridization - methods
Prognosis
Survival Rate
Uterine Neoplasms - diagnosis
Uterine Neoplasms - genetics
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Summary:Genomic alterations were analyzed in 21 uterine leiomyosarcomas (ULMSs) by comparative genomic hybridization. DNA copy number changes were detected in all 21 tumors. The most frequent losses were 13q (16/21 = 76%), 10q (13/21 = 62%), 16q (8/21 = 38%), 12p (7/21 = 33%), and 2p (9/21 = 43%). The most common gains were 17p (8/21 = 38%), Xp (7/21 = 33%), and 1q (7/21 = 33%). High‐copy‐number gains (ratio > 1.5) were identified in Xp, 1q, and 17p. Loss of 13q was identified in both low‐grade and high‐grade tumors. Inactivation of a tumor suppressor gene in 13q may be an early event in the development of leiomyosarcomas. Loss of 10q, 2p, and 12p and gains of 1q as well as 17p were frequently found in high‐grade tumors and recurrent tumors. Inactivation of tumor suppressor genes and activation of oncogenes in these regions may be associated with a more aggressive behavior of ULMS. Patients with only loss of 13q and without the other alterations listed above had longer survival times. Gains of Xp, 17p, and 1q and losses of 13q, 10q, 16q, 12p, and 2p have been reported in extra‐uterine leiomyosarcomas. Our findings indicate that the pathogenesis of uterine leiomyosarcomas and extra‐uterine leiomyosarcomas follows the same genetic pathways. © 2001 Wiley‐Liss, Inc.
ISSN:1045-2257
1098-2264
DOI:10.1002/gcc.1125