Pancreatic ductal adenocarcinoma (PDAC) is one of the most prevalent and aggressive forms of pancreatic cancer with low survival rates and limited treatment options. Aberrant expression of the MYC oncogene promotes PDAC progression. Recent reports have established a role for enhancer RNAs (eRNAs), originating from active enhancers, in controlling gene transcription.
View Article and Find Full Text PDFBackground And Objective: Accurate identification and prioritization of driver-mutations in cancer is critical for effective patient management. Despite the presence of numerous bioinformatic algorithms for estimating mutation pathogenicity, there is significant variation in their assessments. This inconsistency is evident even for well-established cancer driver mutations.
View Article and Find Full Text PDFThe signaling pathways behind severe astrocytic lysis with Aquaporin4 auto-antibody (AQP4-IgG) seropositivity, and reactive astrocytosis with myelin oligodendrocyte glycoprotein auto-antibody (MOG-IgG) seropositivity, remain largely unexplored in Neuromyelitis optica spectrum disorder (NMOSD), while almost no molecular details being known about double-seronegative (DN) patients. Recent discovery of glial fibrillary acidic protein (GFAP) in DN NMOSD patients' cerebrospinal fluid, akin to AQP4-IgG + ve cases, suggests astrocytopathy. Here, we aim to study small non coding RNA (sncRNA) signature alterations in astrocytes exposed to AQP4-IgG + ve and MOG-IgG + ve patient sera, and their potential resemblance with DN-NMOSD.
View Article and Find Full Text PDFThe aggressiveness of pancreatic ductal adenocarcinoma is primarily due to lack of effective early detection biomarkers. Circulating non-coding RNAs serve as diagnostic or prognostic biomarkers in multiple types of cancer. Comparison of their expression between diseased tissue and relevant body fluids such as saliva, urine, bile, pancreatic juice, blood etc.
View Article and Find Full Text PDFBackground: Precancerous and malignant tumours arise within the oral cavity from a predisposed "field" of epithelial cells upon exposure to carcinogenic stimulus. This phenomenon is known as "Field Cancerization". The molecular genomic and transcriptomic alterations that lead to field cancerization and tumour progression is unknown in Indian Oral squamous cell carcinoma (OSCC) patients.
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