P. K. Maini

This paper develops a DNA-structured mathematical model to predict how cyclic hypoxia affects cell-cycle progression, showing that prolonged re-oxygenation slows proliferation while short cycles inhibit it.

This study shows how spatial structure affects adaptive therapy by influencing intra-tumoral competition between drug-sensitive and resistant cells.

The paper investigates how abnormal vascular morphology affects haematocrit distribution and tissue oxygenation in tumours, introducing a metric λ to monitor anti-angiogenic treatment efficacy.

The paper uses a phenotype-structured model to show how fluctuating oxygen levels affect cell population dynamics and competitive advantage through phenotypic variation rates.

This study uses a mathematical model to show that stable coexistence of different cancer cell phenotypes enhances tumour invasion by allowing complementary traits to work synergistically.

The paper unifies the cancer stem cell and stochastic models using a continuum model of microenvironmental forces, supported by clonogenic assay results.

This paper introduces a non-linear age-structured population model to explain the two-phase proliferation observed in scratch assays, showing that resource concentration regulates the transition between phases.

This study uses computational modeling to infer tumour proliferative hierarchy by analyzing phylogenetic tree measures under cancer stem cell and neutral evolution assumptions.

This paper develops a 3D mathematical model of corneal angiogenesis to assess how geometry affects vascular patterning and compares results to planar models.

This study models how tumour oxygen levels change during radiotherapy and shows how oxygen heterogeneity affects radiation response and treatment outcomes.

This study shows that logistic growth models misrepresent cell proliferation in scratch assays due to a disturbance phase, and that distinguishing between phases improves parameter estimates.