DNA derived from different sites in nine cases had the same pattern of p53 mutation, even in cases manifesting heterogeneous histology within a single tumor.
Except for a single report, tumor loss of heterozygosity (LOH) mapping of the putative MEN1 suppressor gene on chromosome 11q13 in the past has been restricted by analysis of a single tumor from individual patients and somatic cellular contamination.
Our observations suggest that the abnormalities of p53 and HER-2 may be involved in the pathogenesis of RCC and that other mechanisms leading to protein expression of p53 and HER-2 may coexist within a single tumor in addition to the genetic aberrations.
Our observations suggest that the abnormalities of p53 and HER-2 may be involved in the pathogenesis of RCC and that other mechanisms leading to protein expression of p53 and HER-2 may coexist within a single tumor in addition to the genetic aberrations.
At entry into the study, 45% of the patients had a positive albumin mRNA test, 53% a single tumor, 16% a portal or venous hepatic thrombosis, and 16% had proven metastasis.
To further assess the potential impact of IRF-2 mutations in tumorigenesis, we screened fresh pancreatic tumor explants and identified 2 IRF-2 point mutations in the 2 alleles of IRF-2 from a single tumor specimen.
In most of these tumors, cells that exhibited EGFR overexpression and gene amplification were distributed heterogeneously, even within a single tumor nodule.
The polymorphisms of genes involved in carcinogen metabolic activation (CYP1A1, CYP2E1), detoxication (GSTM1, GSTT1, GSTM3, NAT2,) and DNA repair (XPD /A35931C-exon 23 and C22541A-exon 6/, XRCC1 /G28152A-exon 10 and C26304T-exon 6/, XRCC3/C18067T/) were studied by PCR-based techniques to analyze genotypes and allele distribution in 84 patients with MPT correlated with 182 subjects with a single tumor of head and neck and 143 cancer-free male volunteers recruited from healthy smokers.
The polymorphisms of genes involved in carcinogen metabolic activation (CYP1A1, CYP2E1), detoxication (GSTM1, GSTT1, GSTM3, NAT2,) and DNA repair (XPD /A35931C-exon 23 and C22541A-exon 6/, XRCC1 /G28152A-exon 10 and C26304T-exon 6/, XRCC3/C18067T/) were studied by PCR-based techniques to analyze genotypes and allele distribution in 84 patients with MPT correlated with 182 subjects with a single tumor of head and neck and 143 cancer-free male volunteers recruited from healthy smokers.
The polymorphisms of genes involved in carcinogen metabolic activation (CYP1A1, CYP2E1), detoxication (GSTM1, GSTT1, GSTM3, NAT2,) and DNA repair (XPD /A35931C-exon 23 and C22541A-exon 6/, XRCC1 /G28152A-exon 10 and C26304T-exon 6/, XRCC3/C18067T/) were studied by PCR-based techniques to analyze genotypes and allele distribution in 84 patients with MPT correlated with 182 subjects with a single tumor of head and neck and 143 cancer-free male volunteers recruited from healthy smokers.
The polymorphisms of genes involved in carcinogen metabolic activation (CYP1A1, CYP2E1), detoxication (GSTM1, GSTT1, GSTM3, NAT2,) and DNA repair (XPD /A35931C-exon 23 and C22541A-exon 6/, XRCC1 /G28152A-exon 10 and C26304T-exon 6/, XRCC3/C18067T/) were studied by PCR-based techniques to analyze genotypes and allele distribution in 84 patients with MPT correlated with 182 subjects with a single tumor of head and neck and 143 cancer-free male volunteers recruited from healthy smokers.