Publications by authors named "Neerja Sethi"

Introduction: Oral squamous cell carcinoma (OSCC) comprises one of the largest subsets of cancers with a tendency for regional metastasis. Nodal status is a key prognostic indicator in patients with OSCC, particularly with N0 neck. Occult metastasis in the form of micrometastasis (MM) and isolated tumor cells (ITCs), often goes undetected by routine hematoxylin and eosin (H&E) examination using 1-2 sections for analysis.

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Burkitt's lymphoma is an undifferentiated non-Hodgkin's B-cell lymphoma. Three clinical subtypes are recognized: African (endemic), American and other areas (sporadic) and human immunodeficiency virus (HIV) associated. Sporadic Burkitt's lymphoma is a rare malignancy among Asian population.

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Background: WHO has recently renamed odontogenic keratocyst as keratocystic odontogenic tumour (KCOT) depending on its tumour like behaviour.

Aim: To quantitate and qualitate different types of collagen fibers in KCOT using picrosirius red stain under polarising microscopy and to correlate with different radiographic patterns of KCOT to elucidate its biological behaviour in order to determine whether all KCOTs behave like a tumour.

Materials And Methods: Sixty histopathologically confirmed cases of KCOT were selected and stained histochemically using picrosirius red and examined under polarising microscope to evaluate colour of collagen fibers in the wall.

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In the K14-HPV16 transgenic mouse model of human papillomavirus (HPV)-associated squamous cell cancers, HPV16 E6 and E7 oncogenes and E1 and E2 regulatory genes are driven by the K14 keratinocyte-specific promoter. HPV transcription varies within the different layers of the epithelium. The correlation between HPV transcription patterns and disease pathogenesis is not well understood.

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Human papillomavirus type 16 (HPV-16) is associated with development of anogenital squamous cell cancers (SCCs) and their precursor, intraepithelial neoplasia (IN). Few approaches to the treatment of IN to prevent SCC are targeted specifically to HPV. We have designed an HPV-specific therapy using the herpes simplex virus type 1 thymidine kinase (HSV-1 TK) gene driven by an HPV-specific promoter in the HPV-16 long control region (LCR) (nucleotide 7450-nucleotide 104), which is regulated by the HPV E2 protein.

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