I. Bozic

Accumulation of Oncogenic Mutations During Progression from Healthy Tissue to Cancer

The paper models mutation accumulation during cancer progression, analyzing premalignant population sizes and waiting times to malignancy in colorectal cancer and chronic myeloid leukemia.

Early-stage cancer results in a multiplicative increase in cell-free DNA originating from healthy tissue

The paper quantifies how early-stage cancer increases cell-free DNA levels from healthy tissue, not tumors, and explains this through a saturation model of clearance.

Stochastic model for cell population dynamics quantifies homeostasis in colonic crypts and its disruption in early tumorigenesis

The paper develops a stochastic model of colonic crypt cell dynamics to quantify homeostasis and predict early tumorigenesis by analyzing the effects of APC and KRAS mutations.

Waiting times in a branching process model of colorectal cancer initiation

The paper analyzes a branching process model of colorectal cancer initiation to estimate waiting times for novel driver mutations.

A mechanistic model of malignant transformation in vestibular schwannoma

The paper develops a mechanistic model of malignant transformation in vestibular schwannoma, estimating mutation and LOH rates and assessing radiation-induced malignancy risk.

Modelling CAR T-cell Therapy with Patient Preconditioning

This paper models CAR T-cell therapy with patient preconditioning using differential equations to assess how different chemotherapy schedules affect treatment success and minimum required dose.

Estimating the rate of plasmid transfer with an adapted Luria-Delbrück fluctuation analysis

This paper introduces a new method to estimate plasmid transfer rates between bacterial cells, showing it is more accurate than existing methods.

Inferring parameters of cancer evolution from sequencing and clinical data

This study infers cancer evolution parameters from sequencing and clinical data, showing accurate estimation of mutation rates and event timing in chronic lymphocytic leukemia.

Mathematical Model of Colorectal Cancer Initiation

The paper develops a mathematical model of colorectal cancer initiation, showing that mutation rates and fitness effects determine the order of driver events and that immune suppression may not significantly affect colorectal lesions.

On measuring selection in cancer from subclonal mutation frequencies

The paper develops a stochastic model to analyze subclonal mutation frequencies in cancer, showing that driver mutations are biased towards extreme frequencies and that the 1/f power law may overestimate neutral evolution.