Mohit Kumar Jolly

This study combines live-cell imaging and mathematical modeling to show how cancer cells adapt to stress in spatially confined environments, revealing cooperative and competitive strategies influenced by spatial organization and microenvironment dynamics.

The paper shows that in mixed E-qM breast tumors, qM cancer cells create immunosuppressive niches leading to MHC-I downregulation and immune evasion.

This study shows cyclic hypoxia promotes breast cancer growth through WNT5A-ROR1 signaling between stromal and tumor cells in a co-culture model.

The paper identifies malignant and stromal partial EMT programs in head and neck cancer and shows that malignant measures correlate with better cetuximab outcomes.

This study shows that rapid oxygen fluctuations alter tumor growth dynamics in a go-or-grow model, with the full model outperforming a reduced version under these conditions.

This study maps 5mC and H3K9me3 co-localization on individual chromosomes using AFM, revealing mechanical stiffness differences between cancer and non-tumorigenic cells.

This paper models endosomal pH dysregulation in Alzheimer's disease, showing how NHE6 loss leads to hyperacidification, maladaptive plasticity, and Aβ oligomerization.

The paper shows how regulatory noise affects cell-fate decisions by altering phenotype occupancy in gene regulatory networks.

This study identifies network structures that support multi-fate cellular decisions by analyzing gene regulatory networks using monotone Boolean models.

This paper introduces WENDy, a method for parameter estimation in systems biology models using weak-form regression, demonstrating its application on real experimental data for glycolytic oscillators and cell-state transitions.

The paper analyzes a go-or-grow invasion model with ECM-regulated phenotypic switching, showing that the reduced model captures the dynamics and deriving the minimum traveling wave speed.

The paper identifies distinct geometrical landscapes for two gene regulatory motifs that exhibit tristability and shows how these landscapes can model cell fate transitions in cancer.

This study identifies hepatobiliary progenitor-like reprogramming in liver metastases, driven by TGF-β and hypoxia, and shows its association with poor survival.

The paper identifies IRF6 as an inhibitor of epithelial-mesenchymal transition (EMT) through integrated computational and experimental analysis.

The paper identifies a feedback loop between AMPK, ERK, and TFEB in matrix-detached cancer cells that generates non-genetic heterogeneity, affecting autophagy and cell survival.

This study identifies drug-specific resistance mechanisms in ER+ breast cancer by analyzing multi-omic data, revealing distinct transcriptional and chromatin states associated with SERM, SERD, and ESR1 mutant resistance.

The paper models tumor-immune interactions as a two-team ecosystem using a generalized Lotka-Volterra framework to predict ecological outcomes in the tumor microenvironment.

This study shows that targeting CD73 in quasi-mesenchymal breast tumors enhances their response to anti-CTLA4 therapy through CD4+ T-cell dependence.

The paper shows hypoxic memory in cancer cells affects tumor invasion dynamics through time-dependent changes in cell state and spatial oxygen dynamics.

This paper analyzes gene regulatory networks to show how cell fate transitions and spatial pattern formation arise from temporal multistability and network topology.

The paper develops a mathematical model showing that Androgen Receptor stabilizes a hybrid epithelial/mesenchymal phenotype in prostate cancer cells with Notch-Jagged signaling, correlating with worse patient outcomes.

This study models regulatory networks and spatial dynamics in ER+ breast cancer to show how resistance and immune escape co-occur and how combination therapies can counteract these mechanisms.

The paper introduces a coherence matrix to analyze directional regulatory coordination in gene regulatory networks, showing how hierarchical structures mitigate scaling penalties in sparse networks.

This study identifies sudden transitions in Notch signaling using early warning signals and analyzes how system parameters influence these transitions in one- and two-cell models.

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

This paper develops a PDE framework to model hypoxic memory's impact on tumor invasion under cyclic hypoxia, showing enhanced invasion without reduced tumor volume.

The paper investigates how cancer cells adapt to soft extracellular matrix by analyzing multi-omics data to identify molecular mechanisms underlying fitness differences.

This study evaluates lovastatin's efficacy in combination with chemotherapy to ablate chemoresistant metastatic breast cancer cells by targeting Macc1 overexpression.

ONCOchannelome identifies altered ion channels in tumors using transcriptomic data, revealing their correlation with metastasis and biological changes.