DNA ploidy in proliferative verrucous leukoplakia

Anatomic Site Based Ploidy Analysis of Oral Premalignant Lesions

“…Past studies have investigated convincingly, loss of heterozygosity, use of fluorescence and molecular markers such as telomerase, [12] epidermal growth factor receptor [13], survivin [14], hypermethylation of the promoters of specific genes [15], and p53 expression [16] to assess the probability of conversion of oral lesions to cancer. Over the years, analysis of DNA content (DNA ploidy) has been suggested to be an important predictor of malignant potential of leukoplakia or erythroplakia [17][18][19][20][21][22]. Normally, a non-dividing somatic cell has a diploid DNA content containing 23 pairs of chromosomes.…”

“…However, since many human cancers are aneuploid [23][24][25][26], it is reasonable to assume that aneuploidy of early nonmalignant lesions precedes the development of frank cancer. However, some oral cancers are diploid, so it is reasonable to assume that diploid cancers are preceded by diploid pre-malignant lesions [20]. As such, DNA analysis of at least some pre-malignant lesions would be expected to yield false negative results.…”

Salivary and serum interleukin-6 levels in proliferative verrucous leukoplakia

“…Others were not able to detect any definitive relationship with HPV [11,12]. Kresty et al [13] described some genetic changes in these patients, and Kkanrit et al [14] reported a ploidy anomaly. Tobacco does not play a significant role in PVL [2,5,15].…”

Pathological Aspects of Oral Precancer

“…The use of auxiliary methods such as DNA image cytometry, AgNOR analysis and cell cycle immunohistochemistry can increase accuracy even further [5,7]. A biopsy must be performed, however, whenever dysplasia is detected, not only because the architecture needs to be considered when grading lesions but also because invasion cannot be reliably assessed by exfoliative cytology alone.…”