M. K. Jolly

This study shows CDK8/19 inhibition can reverse anoikis resistance and metastasis in ovarian cancer by altering transcriptional programs.

This paper reveals a density-dependent collective metabolic heterogeneity in epithelial cells during contact inhibition of proliferation, showing distinct metabolic patterns in different stages.

The paper identifies mutually exclusive gene regulation patterns between noradrenergic and mesenchymal states in neuroblastoma, linking them to phenotypic plasticity and therapy resistance.

The paper analyzes CRC subtypes to show how EMT and metabolic axes vary across CMS subtypes, revealing subtype-specific metabolic and mesenchymal correlations.

The paper shows p53 amyloid load correlates with cancer grades and shows both mutant and wild-type p53 form amyloids in cancer tissues.

The paper identifies a proliferating DTP state in TNBC subtypes that is vulnerable to autophagy and glutathione inhibition, linking GPX4-VIM expression to survival outcomes.

The paper identifies distinct melanocyte states and shows stochastic gene expression and epigenetic modification enable their co-existence and response to environmental cues.

The paper identifies JAK/STAT signaling as a therapeutic target for Snail-induced enzalutamide-resistant prostate cancer through synthetic lethal screens and validation in a resistant cell model.

This study investigates the role of BMP signaling in maintaining EMT and migration in ovarian cancer cells, showing that inhibiting BMP reduces EMT and migration.

This study identifies FLASH as a regulator of EMT plasticity, showing it influences hybrid E/M states through its effects on EMT-TFs and cell junction proteins.

The paper develops an AR-driven gene score to identify tumors with EMT features in triple-negative breast cancer, finding AR high tumors have better clinical outcomes and higher EMT marker expression.

This paper develops a computational framework to infer and predict EMT-related trajectories from single-cell RNA sequencing data, revealing population dynamics and timing of phenotypic intra-tumoral heterogeneity.

This study uses dynamical modeling to uncover how IFN-gamma signaling and proliferative-invasive transitions shape PD-L1 expression heterogeneity in melanoma, with experimental validation in cell lines and datasets.

The paper models a regulatory network linking EMT and AR resistance in prostate cancer, identifying four phenotypes and showing stochastic switching between states.

This study develops a mathematical model to show how miRNA-mediated negative feedback affects gene expression noise and creates bimodal mRNA distributions near an expression threshold.

The paper investigates spatio-temporal pattern formation in a cellular array with non-cooperative positive feedback, analyzing stability and spatial distribution under varying diffusion conditions.

The paper identifies a link between PD-L1 activity, partial EMT, and metabolic reprogramming in carcinomas using transcriptomic data and single-cell RNA-seq.

This study shows that low miR-18a levels in ER-negative breast cancer drive hybrid E/M cell traits linked to migration, drug resistance, and stemness.

The paper shows that long-term EMT induction in MCF10A cells can be reversible with longer timescales, and epigenetic memory via miR-200 silencing by ZEB slows recovery to the epithelial state.

The paper analyzes transcriptomics data to identify common gene regulatory features in oncovirus-positive samples, revealing partial EMT and metabolic changes linked to immune checkpoint molecules.

The paper identifies ELF3 as an epithelial-associated transcription factor that inhibits EMT and stabilizes hybrid E/M phenotypes, with potential prognostic implications in solid tumors.

The paper investigates how spatiotemporal patterns emerge from synthetic gene regulatory networks with diffusion in 1D and 2D space, analyzing stability and diffusion effects.

This study maps phenotypic heterogeneity in melanoma onto the epithelial-hybrid-mesenchymal axis, showing a biphasic mesenchymal response during de-differentiation and metabolic shifts.

This study identifies P4HA2 as a central regulator linking tumor-intrinsic hypoxia, partial EMT, and collective migration using microtumor models and differential gene expression analysis.

The paper develops an analytical pipeline to identify and characterize functional migratory subsets from 2D time-lapse migration data, revealing previously unappreciated heterogeneity in non-migratory cells.

The paper analyzes metabolic pathway associations with EMT status across cancer datasets, revealing both general trends and heterogeneity in metabolic plasticity.

This paper develops a continuum model to explain how planar cell polarity (PCP) proteins localize asymmetrically on cell membranes and how tissue-level expression gradients stabilize PCP.

The paper develops a lattice-based agent model driven by microenvironmental uncertainty to study multicellular phenotypic decision-making, comparing it with Notch-Delta-Jagged signaling.

The paper analyzes SCLC subtypes using gene expression data to determine their similarities and differences, identifying co-expressed modules and classifying cell lines into clusters.

This study shows KLF4 suppresses EMT-inducing transcription factors and promotes MET, acting as a potential MET-TF with implications for cancer survival.