Area of research
Pulmonary and Respiratory Medicine · Oncology
Research interest
Research interests include Prostate Cancer Treatment and Research, PARP inhibition in cancer therapy, Epigenetics and DNA Methylation, and Cancer-related molecular mechanisms research.
DKC1 promotes colorectal cancer progression and therapy resistance by dysregulating sphingolipid biosynthesis.
An integrative proteomics approach identifies tyrosine kinase KIT as a therapeutic target for SPINK1-positive prostate cancer.
The future of precision cancer medicine in India.
2024cited by 0position: contributor
Targeting MALAT1 Augments Sensitivity to PARP Inhibition by Impairing Homologous Recombination in Prostate Cancer.
Transcription networks rewire gene repertoire to coordinate cellular reprograming in prostate cancer.
Canonical WNT signaling-driven DKC1 dysregulates sphingolipid biosynthesis and drives colorectal cancer.
Targeting MALAT1 Augments Sensitivity to PARP Inhibition by Impairing Homologous Recombination in Prostate Cancer
An integrative proteomics approach identifies tyrosine kinase KIT as a novel therapeutic target for SPINK1-positive prostate cancer
Transcriptional regulation of Dyskerin <i>via</i> canonical WNT signaling modulates sphingolipid biosynthesis and drives colorectal cancer
Human ERG oncoprotein represses <i>a Drosophila</i> LIM domain binding protein-coding gene <i>Chip</i>.
Epigenetic reprogramming during prostate cancer progression: A perspective from development.
The Histone H3K27me3 Demethylases KDM6A/B Resist Anoikis and Transcriptionally Regulate Stemness-Related Genes.
Untargeted Metabolomics Showed Accumulation of One-Carbon Metabolites to Facilitate DNA Methylation during Extracellular Matrix Detachment of Cancer Cells.
Nuclear magnetic resonance spectroscopy reveals dysregulation of monounsaturated fatty acid metabolism upon SPINK1 attenuation in colorectal cancer.
Red-emitting polyaniline-based nanoparticle probe for pH-sensitive fluorescence imaging.
Targeting MALAT1 Augments Sensitivity to PARP Inhibition by Impairing Homologous Recombination in Prostate Cancer.
Corrigendum to "Pharmacological inhibition of DNA methylation induces proinvasive and prometastatic genes in vitro and in vivo" [Neoplasia 10/3 (2008) 266-278].
Human ERG Oncoprotein Represses <i>Chip/LDB1</i> LIM-Domain Binding Gene in <i>Drosophila</i>
Nutritive vitamins as epidrugs.
Transcriptional network involving ERG and AR orchestrates Distal-less homeobox-1 mediated prostate cancer progression.
Correction: SPINK1 promotes colorectal cancer progression by downregulating Metallothioneins expression.
Molecular profiling of ETS and non-ETS aberrations in prostate cancer patients from northern India.
Histone H3K27me3 Demethylase act as Key Regulator of Stem Cell Markers in Matrix Detached Cancer Cells
Nuclear biocondensate-forming lncRNA and cellular stress surveillance shape host cancer susceptibility
Androgen deprivation upregulates SPINK1 expression and potentiates cellular plasticity in prostate cancer
Androgen deprivation upregulates SPINK1 expression and potentiates cellular plasticity in prostate cancer.
Dynamics of Cellular Plasticity in Prostate Cancer Progression.
Targeting AGTR1/NF-κB/CXCR4 axis by miR-155 attenuates oncogenesis in glioblastoma.
A <i>Drosophila</i> model of oral peptide therapeutics for adult intestinal stem cell tumors
Computational Design of BH3-Mimetic Peptide Inhibitors That Can Bind Specifically to Mcl-1 or Bcl-X<sub>L</sub>: Role of Non-Hot Spot Residues.