2001
DOI: 10.1002/1097-0142(20011101)92:9<2349::aid-cncr1582>3.0.co;2-i
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Accumulative increase of loss of heterozygosity from leukoplakia to foci of early cancerization in leukoplakia of the oral cavity

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Cited by 47 publications
(38 citation statements)
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“…OSCC begins as a focal clonal overgrowth of altered stem cells near the basement membrane, expands upward and laterally, replacing the normal epithelium [44]. With advanced techniques, short DNA sequences repeated throughout the genome (microsatellite markers) can be used to detect imbalance or loss of heterozygosity (LOH) or allelic loss, in the genetic sequence of specific chromosomes [2, 42,43,[45][46][47]. LOH is defined as the loss of normal function of one allele of a gene in which the other allele becomes inactivated by mutation and results in a loss of tumor suppressor genes promoting carcinogenesis.…”
Section: Oral Cancerogenesismentioning
confidence: 99%
“…OSCC begins as a focal clonal overgrowth of altered stem cells near the basement membrane, expands upward and laterally, replacing the normal epithelium [44]. With advanced techniques, short DNA sequences repeated throughout the genome (microsatellite markers) can be used to detect imbalance or loss of heterozygosity (LOH) or allelic loss, in the genetic sequence of specific chromosomes [2, 42,43,[45][46][47]. LOH is defined as the loss of normal function of one allele of a gene in which the other allele becomes inactivated by mutation and results in a loss of tumor suppressor genes promoting carcinogenesis.…”
Section: Oral Cancerogenesismentioning
confidence: 99%
“…However, telomerase activity is normally found in lymphocytes; and considering that leukoplakias are often associated with chronic inflammation in the submucosa, interpretations of telomerase activity may be confounded. 40,41 Jiang et al 33 analyzed oral leukoplakias with respect to loss of heterozygosity (LOH) and found a high prevalence of LOH in oral leukoplakias and an increase in LOH from leukoplakias to foci of early cancerization. These results notwithstanding, their prognostic impact was not documented.…”
Section: Molecular Markers Of Malignant Transition In Oral Premalignamentioning
confidence: 99%
“…32 This theory hypothesizes that the entire epithelial surface of the upper aerodigestive tract has an increased risk for the development of premalignant lesions because of multiple genetic abnormalities in the entire mucosal lining. However, a common clonal origin of multiple head-and-neck cancers is also possible and has been suggested by Jiang et al 33 Irrespective of whether multiple lesions have a common clonal origin, the multifocality of the lesions has important therapeutic implications as it significantly reduces the effectiveness of local therapeutic measures such as surgical excision. Again, this favors a chemopreventive approach using systemic agents.…”
mentioning
confidence: 99%
“…Recognized markers include DNA ploidy, loss of heterozygosity (LOH), tumour suppressor genes (p53), and proto-oncogenes (cyclin D1, c-Myc, ras, epidermal growth factor receptor). [35][36][37][38][39][40][41][42][43] In the meantime however, there are many clinical diagnostic investigations that can be undertaken to help detect oral cancer, each with its inherent strengths and weaknesses. It should be noted from the outset that these aids do not replace the need for referral or biopsy of any suspicious lesion, but they can be used to help identify and monitor tissue alterations of the oral cavity by suitably trained practitioners.…”
Section: Diagnostic Aidsmentioning
confidence: 99%