Abstract:Generalized genomic instability, detected as somatic changes in allele sizes at microsatellite loci in tumors compared to peripheral lymphocyte DNA, is a recently recognized mechanism of mutation in cancer. Such instability results from the somatic loss of DNA mismatch repair capability. Germ-line mutations at DNA mismatch repair loci confer susceptibility to colon cancer in hereditary non-polyposis colorectal cancer. Somatic loss of DNA mismatch repair has been reported in a large variety of other tumor types… Show more
“…25 Another study reported only 7% SCCHN with MIN; all of them exhibited instability at 40% or more loci. 35 In a French study only 1 tumor exhibited high MIN type, and 6 tumors were classified as low MIN type out of 56 tumors analyzed. 27 Thus SCCHN tumors from Indian patients show much higher MIN frequency than patients from other populations.…”
Section: Comparison Of Min In Different Clinicopathological Stages Ofmentioning
Genomic instability in simple repeated sequences has been observed in several human cancers. We have analyzed 50 squamous cell carcinomas of the head and neck (SCCHN) and 5 pre-malignant severe dysplastic tissues from Indian patient populations for microsatellite instability in 18 different loci spread over eight different chromosomes. Among the tumors analyzed, 45% exhibited instability at two or more loci, and 15% exhibited instability at 40% of the markers tested. Similar analysis of SCCHN tumors from other populations (British, American and French) showed much less frequency of instability. SCCHN tumors in the present study did not show any instability in the mononucleotide repeat sequences. There is also a clear distinction in the nature of the instability in these tumors in comparison with colorectal tumors. These results suggest that the underlying mechanism generating this type of instability is different from those reported for colorectal tumors.
“…25 Another study reported only 7% SCCHN with MIN; all of them exhibited instability at 40% or more loci. 35 In a French study only 1 tumor exhibited high MIN type, and 6 tumors were classified as low MIN type out of 56 tumors analyzed. 27 Thus SCCHN tumors from Indian patients show much higher MIN frequency than patients from other populations.…”
Section: Comparison Of Min In Different Clinicopathological Stages Ofmentioning
Genomic instability in simple repeated sequences has been observed in several human cancers. We have analyzed 50 squamous cell carcinomas of the head and neck (SCCHN) and 5 pre-malignant severe dysplastic tissues from Indian patient populations for microsatellite instability in 18 different loci spread over eight different chromosomes. Among the tumors analyzed, 45% exhibited instability at two or more loci, and 15% exhibited instability at 40% of the markers tested. Similar analysis of SCCHN tumors from other populations (British, American and French) showed much less frequency of instability. SCCHN tumors in the present study did not show any instability in the mononucleotide repeat sequences. There is also a clear distinction in the nature of the instability in these tumors in comparison with colorectal tumors. These results suggest that the underlying mechanism generating this type of instability is different from those reported for colorectal tumors.
“…However, none of these markers universally identifies OSCC. Microsatellite markers are the most promising amongst these, where at least one of a panel of 23 markers can detect the presence of an oral cancer cell in the saliva of 79% of oral cancer patients [16][17][18][19]. However, microsatellite instability analysis is not particularly sensitive and requires large amounts of cancer cell DNA, approximately one cancer cell among 200 normal cells.…”
Section: Current Oral Cancer Diagnostic and Screening Approachesmentioning
“…Ă kervall et al (1995) Chromosomen 3p, 5q, 9p, 9q, 11p, 13q, 17q und 18q festgestellt (Ah-See et al, 1994;BockmĂŒhl et al, 1996a;Field et al, 1995a;Ishwad et al, 1995;Scully & Field 1997). Li et al (1994) Reed et al, 1996).…”
Section: Molekulargenetische Basis Der Karzinogenesementioning
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