Browsing by Author "Riquelme, E"

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    Microsatellite instability and loss of heterozygosity have distinct prognostic value for testicular germ cell tumor recurrence
    (TAYLOR & FRANCIS INC, 2004) Velasco, A; Riquelme, E; Schultz, M; Wistuba, II; Villarroel, L; Koh, MS; Leach, FS
    Germ cell tumor (GCT) is the most common genitourinary malignancy of men between the ages of 18 and 35 years. Therapy is ultimately successful in over 90% of patients, however significant morbidity and mortality can be associated with adjuvant treatment and relapse. Molecular markers that predict treatment response and/or poor outcome would have immediate clinical benefit since adjuvant treatment could be selectively reserved for patients at higher risk for relapse and those patients most likely to respond to treatment. In order to identify potential prognostic molecular markers, we evaluated 118 GCT for microsatellite instability (MSI), loss of heterozygosity (LOH) and MSH2 immunostaining to identify tumors associated with relapse and/or poor outcome following initial surgical, medical and/or radiation therapy.
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    Mismatch repair gene expression and genetic instability in testicular germ cell tumor
    (2004) Velasco, A; Riquelme, E; Schultz, M; Wistuba, II; Villarroel, L; Pizarro, J; Berlin, A; Ittmann, M; Koh, MS; Leach, FS
    Human mismatch repair (MMR) genes encode highly conserved interacting proteins that correct replication errors predisposing to hereditary gastrointestinal and genitourinary malignancies. A subset of sporadic genitourinary tumors also exhibits MMR deficiency and can be identified by measuring the frequency of microsatellite instability (MSI) in cancer cell DNA. We investigated expression of the two most commonly mutated MMR genes, MSH2 and MLH1, in sporadic testicular germ cell tumor (GCT) in order to: (1) determine the expression pattern of MSH2 and MLH1 proteins in normal seminiferous tubules and histologically distinct GCT subtypes, (2) correlate MMR gene expression with genetic instability in GCT and (3) develop a panel of molecular markers that can identify genetically distinct subsets of GCT for prognostic assessment.