Analysis of genetic alterations in uterine leiomyomas and leiomyosarcomas by comparative genomic hybridization. 1997

J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.

Uterine leiomyomas are the most prevalent tumor type in women of reproductive age and are the most common reason for hysterectomies. Although uterine leiomyomas are considered to be benign, they are a major public health concern for women. In contrast, leiomyosarcomas are rare but highly malignant uterine tumors. They may arise in uteri with preexisting leiomyomas and histologically sometimes resemble leiomyomas, thus causing controversy about whether leiomyosarcomas arise within leiomyomas. In this study, we used comparative genomic hybridization (CGH) to identify genetic alterations unique to each tumor type and alterations that are common between the two tumors. We analyzed 14 cases of uterine leiomyomas and eight cases of uterine leiomyosarcomas. Only two of the 14 leiomyomas exhibited genetic alterations, and those were restricted to gains on chromosomes 14 and 19 and losses on chromosomes 1 and 4. In addition, 68 leiomyomas were examined for loss of heterozygosity on chromosomes 1 and 4, and only three tumors exhibited any losses. In contrast, all eight leiomyosarcomas showed gains and losses of DNA by CGH, and in many cases multiple changes were observed. The most commonly observed genetic aberration, occurring in five tumors, was gains on both arms of chromosome 1, suggesting that this chromosome contains loci involved in the development of leiomyosarcoma. Our results do not provide evidence for the progression from benign leiomyoma to malignant leiomyosarcoma. Moreover, the large number of random chromosomal alterations in the leiomyosarcomas suggests that increased genetic instability plays a role in the formation of these tumors.

UI MeSH Term Description Entries
D007889 Leiomyoma A benign tumor derived from smooth muscle tissue, also known as a fibroid tumor. They rarely occur outside of the UTERUS and the GASTROINTESTINAL TRACT but can occur in the SKIN and SUBCUTANEOUS TISSUE, probably arising from the smooth muscle of small blood vessels in these tissues. Fibroid,Fibroid Tumor,Fibroid Uterus,Fibroids, Uterine,Fibroma, Uterine,Fibromyoma,Leiomyoma, Uterine,Fibroid Tumors,Fibroid, Uterine,Fibroids,Fibromas, Uterine,Fibromyomas,Leiomyomas,Tumor, Fibroid,Tumors, Fibroid,Uterine Fibroid,Uterine Fibroids,Uterine Fibroma,Uterine Fibromas,Uterus, Fibroid
D007890 Leiomyosarcoma A sarcoma containing large spindle cells of smooth muscle. Although it rarely occurs in soft tissue, it is common in the viscera. It is the most common soft tissue sarcoma of the gastrointestinal tract and uterus. The median age of patients is 60 years. (From Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p1865) Leiomyosarcoma, Epithelioid,Leiomyosarcoma, Myxoid,Epithelioid Leiomyosarcoma,Epithelioid Leiomyosarcomas,Leiomyosarcomas,Leiomyosarcomas, Epithelioid,Leiomyosarcomas, Myxoid,Myxoid Leiomyosarcoma,Myxoid Leiomyosarcomas
D009693 Nucleic Acid Hybridization Widely used technique which exploits the ability of complementary sequences in single-stranded DNAs or RNAs to pair with each other to form a double helix. Hybridization can take place between two complimentary DNA sequences, between a single-stranded DNA and a complementary RNA, or between two RNA sequences. The technique is used to detect and isolate specific sequences, measure homology, or define other characteristics of one or both strands. (Kendrew, Encyclopedia of Molecular Biology, 1994, p503) Genomic Hybridization,Acid Hybridization, Nucleic,Acid Hybridizations, Nucleic,Genomic Hybridizations,Hybridization, Genomic,Hybridization, Nucleic Acid,Hybridizations, Genomic,Hybridizations, Nucleic Acid,Nucleic Acid Hybridizations
D002869 Chromosome Aberrations Abnormal number or structure of chromosomes. Chromosome aberrations may result in CHROMOSOME DISORDERS. Autosome Abnormalities,Cytogenetic Aberrations,Abnormalities, Autosome,Abnormalities, Chromosomal,Abnormalities, Chromosome,Chromosomal Aberrations,Chromosome Abnormalities,Cytogenetic Abnormalities,Aberration, Chromosomal,Aberration, Chromosome,Aberration, Cytogenetic,Aberrations, Chromosomal,Aberrations, Chromosome,Aberrations, Cytogenetic,Abnormalities, Cytogenetic,Abnormality, Autosome,Abnormality, Chromosomal,Abnormality, Chromosome,Abnormality, Cytogenetic,Autosome Abnormality,Chromosomal Aberration,Chromosomal Abnormalities,Chromosomal Abnormality,Chromosome Aberration,Chromosome Abnormality,Cytogenetic Aberration,Cytogenetic Abnormality
D002878 Chromosomes, Human, Pair 1 A specific pair of human chromosomes in group A (CHROMOSOMES, HUMAN, 1-3) of the human chromosome classification. Chromosome 1
D002894 Chromosomes, Human, Pair 4 A specific pair of GROUP B CHROMOSOMES of the human chromosome classification. Chromosome 4
D004273 DNA, Neoplasm DNA present in neoplastic tissue. Neoplasm DNA
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D014594 Uterine Neoplasms Tumors or cancer of the UTERUS. Cancer of Uterus,Uterine Cancer,Cancer of the Uterus,Neoplasms, Uterine,Neoplasms, Uterus,Uterus Cancer,Uterus Neoplasms,Cancer, Uterine,Cancer, Uterus,Cancers, Uterine,Cancers, Uterus,Neoplasm, Uterine,Neoplasm, Uterus,Uterine Cancers,Uterine Neoplasm,Uterus Cancers,Uterus Neoplasm

Related Publications

J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
August 1994, Gynecologic oncology,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
March 2001, Genes, chromosomes & cancer,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
May 2001, Cancer genetics and cytogenetics,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
July 2012, Journal of cancer research and clinical oncology,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
February 2002, Analytical and quantitative cytology and histology,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
April 1999, Cancer genetics and cytogenetics,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
October 1997, International journal of cancer,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
January 2002, Journal of pediatric hematology/oncology,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
July 1999, Pediatric neurosurgery,
J P Packenham, and S du Manoir, and E Schrock, and J I Risinger, and D Dixon, and D N Denz, and J A Evans, and A Berchuck, and J C Barrett, and T R Devereux, and T Ried
June 2002, Human pathology,
Copied contents to your clipboard!