Academic & Research Profile

This page provides a consolidated overview of my academic training, laboratory experience, translational research work, and scientific communication activities.

📄 Research Portfolio

A detailed academic portfolio describing my education, molecular biology training, clinical research experience, and bioinformatics skill development:

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💼 Professional Profile

Verified professional profile including education, research appointments, and institutional affiliations:

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💻 Bioinformatics & Computational Work

Reproducible bioinformatics workflows, analytical scripts, and method-focused repositories developed in R and Python:

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🎥 Science Communication & Educational Channels

StoryLens Depot — science narratives & documentaries
https://www.youtube.com/@storylensdepot

Mohin Sapara — molecular biology, cancer & research education
https://www.youtube.com/@mohinsapara

QuHub — interdisciplinary science, AI & future technologies
https://www.youtube.com/@quhub

This post serves as a centralized public entry point to my research, computational work, and scientific outreach activities.

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KRAS-Driven Oncogenic Signalling in Pancreatic Ductal Adenocarcinoma: Molecular Mechanisms, Regulatory Pathways, and Therapeutic Frontiers

Pancreatic ductal adenocarcinoma (PDAC) is a characteristically aggressive tumour resistant to chemotherapy, and at the centre of this malignant phenotype lies an almost universal dependency on activating mutations in the KRAS oncogene. More than 90 %of PDAC tumours present with alterations in the KRAS oncogene, most frequently at codon 12, and these mutations represent the primary cause of the tumour’s signalling complexity, metabolic heterogeneity and stromal orchestration. The predominance of KRAS in PDAC reflects the capacity of mutant KRAS to adversely affect cellular processes in the tumour microenvironment that sustain the tumour’s growth, plasticity, survival and resistance to therapy. The biochemical behaviour of KRAS is rooted in its role as a molecular switch cycling between inactive GDP-bound and active GTP-bound conformations. In physiologically normal cells, this transition is carefully modulated by guanine nucleotide exchange factors and GTPase-activat...

HMGN5-Mediated Chromatin Remodeling as a Driver of Breast Cancer Proliferation: Epigenetic Mechanisms, Transcriptional Accessibility, and Therapeutic Implications

Abstract High Mobility Group Nucleosome-binding protein 5 (HMGN5) has emerged as an important chromatin architectural regulator involved in the epigenetic control of transcription, chromatin accessibility, and oncogenic transformation. Recent evidence demonstrates that aberrant HMGN5 expression contributes significantly to breast cancer progression through modulation of chromatin dynamics and activation of proliferation-associated transcriptional programs. HMGN5 belongs to the HMGN family of non-histone chromosomal proteins that interact directly with nucleosomes and regulate higher-order chromatin structure. Unlike sequence-specific transcription factors, HMGN proteins exert genome-wide regulatory effects by altering nucleosomal stability, histone modification accessibility, and transcriptional competency. In breast carcinoma, elevated HMGN5 expression correlates with aggressive clinical phenotypes, enhanced proliferative capacity, increased DNA replication activity, and poor prognosi...

KMT2D-Mediated Chromatin Remodeling in Developmental Disorders and Cancer

Introduction Epigenetic regulation is one of the most fundamental mechanisms controlling gene expression in human cells. Although every somatic cell contains nearly identical DNA sequences, different cell types exhibit highly specialized functions because distinct transcriptional programs are activated or suppressed through chromatin remodeling. Histone modifications represent a major component of this epigenetic control system, regulating chromatin accessibility and transcription factor recruitment. Among the most important histone-modifying enzymes involved in enhancer activation is KMT2D, also known as Lysine Methyltransferase 2D or MLL2. KMT2D encodes a large nuclear histone methyltransferase located on chromosome 12q13.12. The protein belongs to the COMPASS-like family of chromatin regulators and primarily catalyzes mono- and di-methylation of histone H3 lysine 4 (H3K4me1 and H3K4me2). These histone modifications are characteristic epigenetic signatures of active enhancers, which ...

Mohin Sapara

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