Publications by authors named "V Rajendra"

Background: Depth of invasion (DOI) significantly influences prognosis and treatment strategies in oral squamous cell carcinoma (OSCC). Accurate preoperative imaging, such as contrast-enhanced computed tomography (CECT), alongside postoperative histopathological evaluations, aids in determining DOI. This study evaluates the correlation between radiological DOI (rDOI), macroscopic DOI (PDOI), and microscopic DOI (pDOI) in OSCC.

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Adenosine-to-inosine editing is catalyzed by adenosine deaminases acting on RNA (ADARs) in double-stranded RNA (dsRNA) regions. Although three ADARs exist in mammals, ADAR1 is responsible for the vast majority of the editing events and acts on thousands of sites in the human transcriptome. ADAR1 has been proposed to form a stable homodimer and dimerization is suggested to be important for editing activity.

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The high incidence of oral carcinomas is due to its multifactorial etiology and the presence of various risk factors. Human Papillomavirus (HPV) has a proven role in the pathogenesis of oral carcinomas, but in the recent times there has been an increasing incidence of oral cancers who are negative for HPV infection. Also, these patients are non-smokers and non-drinkers so it could be speculated that these oral cancers are due to some other etiological factor probably of other viral infections.

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Plasmablastic lymphoma (PBL) is a rare, aggressive lymphoma with no definite standard of care with a poor outcome. It occurs predominantly in HIV-infected individuals and is frequently seen in extranodal sites. The important differential diagnosis for this PBL is plasmablastic myeloma, where clinical and histopathological features are often ambiguous, rendering the correct diagnosis difficult without complete integration of clinical, morphological, phenotypic, and molecular features.

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Article Synopsis
  • ADAR1 promotes A-to-I RNA editing in double-stranded and structured RNAs, with two isoforms (ADAR1p150 and ADAR1p110) having distinct roles in cellular localization and expression.
  • Mutations in ADAR1 are linked to Aicardi-Goutières syndrome (AGS), with ADAR1p150 being crucial for preventing embryonic lethality caused by excessive interferon-stimulated gene expression.
  • Isoform-specific editing patterns were observed, showing that ADAR1p110 targets intronic regions while ADAR1p150 specializes in editing 3'UTRs, highlighting the importance of intracellular localization in their editing preferences.
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