Stochastic Modelling of Multiple Random Genetic Mutations Under the Cancer Stem Cell Hypothesis
DOI10.1080/08898480.2012.725379zbMATH Open1409.92215OpenAlexW2071097316MaRDI QIDQ4628522FDOQ4628522
Authors: Cristian Tomasetti 
Publication date: 14 March 2019
Published in: Mathematical Population Studies (Search for Journal in Brave)
Full work available at URL: https://doi.org/10.1080/08898480.2012.725379
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Genetics and epigenetics (92D10) Applications of branching processes (60J85) Population dynamics (general) (92D25) Developmental biology, pattern formation (92C15)
Cites Work
- Population-size-dependent, age-structured branching processes linger around
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- Evolution of resistance and progression to disease during clonal expansion of cancer
- A stochastic model for the origin and treatment of tumors containing drug-resistant cells
- Waiting time models of cancer progression
- Biomechanical and Nutrient Controls in the Growth of Mammalian Cell Populations
- Viability of Small Populations Experiencing Recurring Catastrophes
Cited In (14)
- On the probability of random genetic mutations for various types of tumor growth
- Probabilistic methods in cancer biology
- Probability distribution of the number of initiated cells of carcinogenesis under prevention
- Evolutionary dynamics of tumor progression with random fitness values
- STOCHASTIC MODELING OF LOSS- AND GAIN-OF-FUNCTION MUTATIONS IN CANCER
- A stochastic model of chromosome segregation errors with reference to cancer cells
- Somatic mosaicism and cancer: inference based on a conditional Luria-Delbrück distribution
- Erratum to ``A stochastic carcinogenesis model incorporating multiple types of genomic instability fitted to colon cancer data
- A stochastic model of mutant growth due to mutation in tumors, based on stem cell considerations
- A sticky multinomial mixture model of strand-coordinated mutational processes in cancer
- Loss- and gain-of-function mutations in cancer: mass-action, spatial and hierarchical models
- A stochastic model of mutant growth
- A Statistical Test of the Hypothesis that Polyclonal Intestinal Tumors Arise by Random Collision of Initiated Clones
- Spatial measures of genetic heterogeneity during carcinogenesis
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