Related papers: Clonal Diversity at Cancer Recurrence
Motivation: Driver (epi)genomic alterations underlie the positive selection of cancer subpopulations, which promotes drug resistance and relapse. Even though substantial heterogeneity is witnessed in most cancer types, mutation accumulation…
Although the survival rate of cancer patients has significantly increased due to advances in anti-cancer therapeutics, one of the major side effects of these therapies, particularly radiotherapy, is the potential manifestation of…
The emergence and development of cancer is a consequence of the accumulation over time of genomic mutations involving a specific set of genes, which provides the cancer clones with a functional selective advantage. In this work, we model…
We present TreeClone, a latent feature allocation model to reconstruct tumor subclones subject to phylogenetic evolution that mimics tumor evolution. Similar to most current methods, we consider data from next-generation sequencing of tumor…
Heterogeneity is a hallmark of all cancers. Tumor heterogeneity is found at different levels -- interpatient, intrapatient, and intratumor heterogeneity. All of them pose challenges for clinical treatments. The latter two scenarios can also…
Cancers evolve from mutation of a single cell with sequential clonal and subclonal expansion of somatic mutation acquisition. Inferring clonal and subclonal structures from bulk or single cell tumor genomic sequencing data has a huge impact…
Extracting associations that recur across multiple studies while controlling the false discovery rate is a fundamental challenge. Here, we consider an extension of Efron's single-study two-groups model to allow joint analysis of multiple…
We propose a one mutation model for cancer with a mutation rate that increases with time. Under rather general hypotheses the number of mutations is necessarily a (non homogeneous) Poisson process with the prescribed mutation rate. We show…
We investigate a new dynamical system that describes tumor-host interaction. The equation that describes the untreated tumor growth is based on non-extensive statistical mechanics. Recently, this model has been shown to fit successfully…
In this paper we propose a systematic approach to construct mathematical models describing populations of cancer-cells at different stages of disease development. The methodology we propose is based on stochastic Concurrent Constraint…
Most neoplastic tumors originate from a single cell, and their evolution can be genetically traced through lineages characterized by common alterations such as small somatic mutations (SSMs), copy number alterations (CNAs), structural…
The long-term efficacy of targeted therapeutics for cancer treatment can be significantly limited by the type of therapy and development of drug resistance, inter alia. Experimental studies indicate that the factors enhancing acquisition of…
Self-renewal is a constitutive property of stem cells. Testing the cancer stem cell hypothesis requires investigation of the impact of self-renewal on cancer expansion. To understand better this impact, we propose a mathematical model…
Multitype branching processes are ideal for studying the population dynamics of stem cell populations undergoing mutation accumulation over the years following transplant. In such stochastic models, several quantities are of clinical…
Cancer is a genetic disorder whose clonal evolution can be monitored by tracking noisy genome-wide copy number variants. We introduce the Copy Number Stochastic Block Model (CN-SBM), a probabilistic framework that jointly clusters samples…
Cancer progression and monotonic accumulation models were developed to discover dependencies in the irreversible acquisition of binary traits from cross-sectional data. They have been used in computational oncology and virology but also in…
We consider two minimal mathematical models for cancer dynamics and self-adaptation. We aim to capture the interplay between the rapid progression of cancer growth and the possibility to leverage and enhance self-adaptive defense mechanisms…
Cancer cell lines have frequently been used to link drug sensitivity and resistance with genomic profiles. To capture genomic complexity in cancer, the Cancer Genome Project (CGP) (Garnett et al., 2012) screened 639 human tumor cell lines…
In this work, we propose two novel methodologies to study temporal and morphological phenotypic effects caused by different experimental conditions using imaging data. As a proof of concept, we apply them to analyze drug effects in 2D…
Melanoma is an aggressive form of skin cancer. Survival rates are excellent if it is detected early but fall markedly if it metastasises. A key step in early tumour progression is the formation of cell clusters, which can promote…