Chemical carcinogens are supposedly considered to be the key etiological factor of malignancy. The covalent or non-covalent bonds between these chemical and the DNA, RNA, and proteins of human tissue help in the initiation of carcinogenesis wherein, genetic mutation and alteration in the genome transcription supervenes. These carcinogens behave as initiators or promoters of cancer cell growth. Alkylation of DNA, RNA, or proteins and the formation of covalent bonds with them begins initially followed by the promoting effect. Numerous molecular and cellular events causing the transformation of normal cells into neoplastic cells occur in the process. It is assumed though that endogenous molecular pathways could instigate mutations in respective genes with the support of reactive oxygen species thus leading to DNA damage. Thus, this review deals with the basic mechanism and metabolism of chemical carcinogenesis.
Background: Odontogenic lesions can bring about diagnostic challenges due to overlapping histology among pathologists. Thus, there are few tumor markers that provide accurate diagnosis. Syndecan-1 (CD-138) and podoplanin (PDPN) are proteoglycans that have been described as substantial diagnostic and prognostic markers in various odontogenic lesions. Aim: This study aims to evaluate and compare the immunohistochemical expression of syndecan-1 (CD-138) and podoplanin in keratocystic odontogenic tumor, orthokeratinized odontogenic cyst (OOC), and dentigerous cyst (DC). Materials and Methods: The formalin-fixed paraffin-embedded tissue blocks of KCOT, OOC, and DCs were retrieved form the archives of department. Three sections each of 3 μm thickness were made using a rotary microtome and they were stained with syndecan-1 (CD-138) and podoplanin (PDPN) using immunohistochemical methods and standard hematoxylin and eosin stain. Results: Immunohistochemical expression of syndecan-1in KCOT was found to be weakly to moderately positive in 6 cases with 2 cases exhibiting positive expression. In OOC, 3 cases displayed negative expression-1 whereas 7 cases were weakly to moderately positive. Immunohistochemical expression of podoplanin in KCOT was observed to be weakly to moderately positive in 4 cases with 5 cases exhibiting strongly positive expression. In OOC, 3 cases displayed negative immunohistochemical expression for podoplanin and 4 cases were strongly positive. Immunoreactivity for podoplanin in DC was negative in 3 cases whereas 5 cases were weakly to moderately positive. Conclusion: The absence of significant correlation between expression of syndecan-1 and podoplanin reinforces the exact role of these proteins in the differentiation of odontogenic lesions which need to be elucidated further.
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