Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-6-4
pubmed:abstractText
Invasive squamous carcinoma of the uterine cervix (CC) arises from sequential progression of low-grade (L) and high-grade (H) squamous intraepithelial lesions (SILs). In clinical observations, these lesions are frequently found as synchronous multiple foci. The nature and evolutionary mechanism of these lesions are largely unknown. We have performed allelotyping of three 3p markers (at 3p14, 3p22-24, and 3p25) on 22 LSILs and 15 HSILs microdissected from patients with multiple (n = 21) or uniform (n = 6) cervical lesions. The results were analyzed together with our previous allelotyping of 57 deeply invasive CCs. Loss of heterozygosity at one of the three markers was observed in 23%, 27%, and 31 % of LSILs, HSILs, and CCs, respectively. Frequent and early allelic loss was noted (in 30% of LSILs and 50% of HSILs) at 3p14, which may harbor tumor suppressor genes involved in early stages of cervical carcinogenesis. A high frequency of microsatellite alteration (MA) was found in LSIL (41%) and HSIL (67%) but not in CC (5.3%). In particular, MA was more frequently found in low-grade lesions in association with invasive cancers (75%, 6/8) than in those associated with SILs (29%, 4/14) (P < 0.05). Together with the finding of a monoclonal origin of premalignant and malignant cervical lesions, the present results allow us to propose a model of local field effect of genomic instability that progressively affects the clonal evolution of SIL of uterine cervix.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1045-2257
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-34
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9885979-Carcinoma, Squamous Cell, pubmed-meshheading:9885979-Carcinoma in Situ, pubmed-meshheading:9885979-Cervical Intraepithelial Neoplasia, pubmed-meshheading:9885979-Chromosome Mapping, pubmed-meshheading:9885979-Chromosomes, Human, Pair 3, pubmed-meshheading:9885979-Clone Cells, pubmed-meshheading:9885979-DNA, Neoplasm, pubmed-meshheading:9885979-DNA, Viral, pubmed-meshheading:9885979-Female, pubmed-meshheading:9885979-Genetic Markers, pubmed-meshheading:9885979-Genotype, pubmed-meshheading:9885979-Humans, pubmed-meshheading:9885979-Loss of Heterozygosity, pubmed-meshheading:9885979-Microsatellite Repeats, pubmed-meshheading:9885979-Neoplasm Invasiveness, pubmed-meshheading:9885979-Papillomaviridae, pubmed-meshheading:9885979-Papillomavirus Infections, pubmed-meshheading:9885979-Precancerous Conditions, pubmed-meshheading:9885979-Trinucleotide Repeat Expansion, pubmed-meshheading:9885979-Tumor Virus Infections, pubmed-meshheading:9885979-Uterine Cervical Neoplasms, pubmed-meshheading:9885979-Uterine Neoplasms
pubmed:year
1999
pubmed:articleTitle
Monoclonality and surface lesion-specific microsatellite alterations in premalignant and malignant neoplasia of uterine cervix: a local field effect of genomic instability and clonal evolution.
pubmed:affiliation
Department of Obstetrics and Gynecology, Tri-Service General Hospital, Taiwan, Republic of China. tychu@email.gen.net.tw
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't