Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-1-11
pubmed:abstractText
We analyzed a group of gastric carcinomas treated with a cisplatin-based neoadjuvant chemotherapy regimen for microsatellite instability (MSI) and loss of heterozygosity (LOH) to determine whether there is any relation between microsatellite alterations and therapy response. Pretherapeutic endoscopic biopsies of 37 patients were studied at 11 microsatellite loci. Thirteen (35%) had a complete or partial clinical response (responders), and 24 (65%) had only a minor or no response (nonresponders). High-grade MSI was found in two tumors, both nonresponders, whereas low-grade MSI was found in five biopsies, including three non-responders and two responders. Regarding LOH, the most obvious differences between the groups were observed on chromosome 17p13, the location of the p53 gene, with 7 of 12 (58%) and 3 of 20 (15%) of the informative tumors exhibiting LOH in responders and nonresponders, respectively (P = 0.018). A statistically significant difference was also observed in the fractional allelic loss (FAL) ratio of the groups. Among the 13 responding patients, 7 (54%) tumors exhibited high FAL (>0.5-0.75), 2 (15%) showed medium FAL (>0.25-0.5), and 4 (31%) demonstrated low FAL values (0-0.25), whereas among the 22 nonresponding patients, 2 (9%) tumors showed high FAL, 5 (23%) showed medium FAL, and 15 (68%) showed low FAL (P = 0.020). These data suggest that LOH at chromosome 17p13 is associated with a good clinical response to cisplatin-based chemotherapy, suggesting that altered p53 function might render cells more sensitive to therapy. Furthermore, the association of FAL with therapy response indicates that gastric carcinomas with a high level of chromosomal alteration may be more sensitive to this type of chemotherapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1078-0432
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4782-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11156235-Adult, pubmed-meshheading:11156235-Aged, pubmed-meshheading:11156235-Alleles, pubmed-meshheading:11156235-Antineoplastic Agents, pubmed-meshheading:11156235-Carcinoma, pubmed-meshheading:11156235-Chemotherapy, Adjuvant, pubmed-meshheading:11156235-Chromosomes, Human, Pair 17, pubmed-meshheading:11156235-Female, pubmed-meshheading:11156235-Genes, p53, pubmed-meshheading:11156235-Humans, pubmed-meshheading:11156235-Immunohistochemistry, pubmed-meshheading:11156235-Loss of Heterozygosity, pubmed-meshheading:11156235-Male, pubmed-meshheading:11156235-Microsatellite Repeats, pubmed-meshheading:11156235-Middle Aged, pubmed-meshheading:11156235-Polymerase Chain Reaction, pubmed-meshheading:11156235-Retrospective Studies, pubmed-meshheading:11156235-Stomach Neoplasms, pubmed-meshheading:11156235-Treatment Outcome
pubmed:year
2000
pubmed:articleTitle
Loss of heterozygosity and microsatellite instability as predictive markers for neoadjuvant treatment in gastric carcinoma.
pubmed:affiliation
Department of Surgery, Klinikum rechts der Isar, Technische Universität München, Munich, Germany. grundei@nt1.chir.med.tu-muechen.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't