tugHall (tumor gene-Hallmark) is a cancer-cell evolution model simulator, wherein gene mutations are linked to the hallmarks of cancer, which influence tumor cell behaviors.
This is an R-based script to simulate the cancer cell evolution in the framework of the model proposed by Prof. Mamoru Kato, Head of Bioinformatics Department, Research Institute, National Cancer Center, Tokyo, JAPAN.
Iurii Nagornov
Jo Nishino
Mamoru Kato
Division of Bioinformatics, Research Institute, National Cancer Center Japan, Tokyo, Japan
All questions and requests can be sent to inagonov@ncc.go.jp
https://github.com/tugHall/ - the developing resource
The wide availability of recent cancer genomic data requires a coherent model that can sort out the relevant findings to systematically explain the clonal evolution and resultant intra-tumor heterogeneity (ITH). Here, we present a new mathematical model designed to computationally simulate the evolution of cancer cells. The model connects well-known cancer hallmarks with the specific mutational states of tumor-related genes. The cell behavior phenotypes are stochastically determined and the hallmarks interfere probabilistically with the phenotypic probabilities. In turn, the hallmark variables depend on the mutational states of tumor-related genes. Thus, it is expected our software can be used to deepen our understanding of cancer-cell evolution and generation of ITH.
How to use tugHall and how to analyze data, kindly see user-guides in Documentation folder in prefered format Rmd, pdf, html.
This version is based on the clone consideration instead cell-based version 1.1. Each clone has one or more cells, that allows to accelerate the calculations when number of clones is much less than number of cells. Definition of clone: the clone is set of cell with same set of genes, which have same mutated / not mutated sites in genes.
This version can calculate the copy number alterations (CNA) caused by deletions and duplications in comparison with version 2.1. CNAs may malfunction genes and change variant allel frequences if the point mutations are located on CNAs.