Selected Topics in Cancer Modeling: Genesis, Evolution, by Natalia L. Komarova, Dominik Wodarz (auth.), Elena Angelis,

By Natalia L. Komarova, Dominik Wodarz (auth.), Elena Angelis, Mark A. J. Chaplain, Nicola Bellomo (eds.)

A significant problem within the modeling and simulation of tumor progress is the mathematical description of residing subject, that's way more advanced than a mathematical description of inert topic. One severe piece of this problem is growing multiscale types that consider subcellular, mobile, and macroscopic degrees of melanoma. The complexity of those diverse degrees calls for the advance of recent mathematical tools and ideas, that are tested during this work.

Written by means of best researchers within the box of mathematical biology, this selection of chosen chapters deals a finished assessment of cutting-edge mathematical tools and instruments for modeling and interpreting melanoma phenomena.

Topics coated include:

* Genetic and epigenetic pathways to colon cancer

* A video game theoretical point of view at the somatic evolution of cancer

* Nonlinear modeling and simulation of tumor growth

* Tumor cords and their reaction to anticancer agents

* Modeling diffusely invading mind tumors

* Multiphase types of tumor growth

* Mathematical modeling of breast carcinogenesis

* Predictive types in tumor immunology

* Multiscale modeling of strong tumor growth

Selected issues in melanoma Modeling is a superb reference for researchers, practitioners, and graduate scholars in utilized arithmetic, mathematical biology, and comparable fields. The ebook has an total goal of quantitative, predictive mathematical modeling of reliable tumor progress in any respect scales, from genetics throughout to therapy remedy for patients.

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Additional resources for Selected Topics in Cancer Modeling: Genesis, Evolution, Immune Competition, and Therapy

Sample text

Genetic instability in colorectal cancers. Nature 386(6625), 623–627 (1997) 59. : Genetic instabilities in human cancers. Nature 396(6712), 643–649 (1998) 60. : Chromatin modification and epigenetic reprogramming in mammalian development. Nat Rev Genet 3(9), 662–673 (2002) 61. : How does DNA methylation mark the fate of cells? Tumori 90(4), 367–372 (2004) 62. : Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability. Science 268(5215), 1336–1338 (1995).

8(a)). This should be compared with the observation that about 50% of FAP patients develop polyps (a more advanced stage of carcinogenesis compared with dysplastic crypts) by age 16. 6 20 40 60 80 100 0 20 40n 60 80 100 n c c Fig. 8. FAP: (a) the logarithm of the expected number of dysplastic crypts and (b) the fraction of CIN crypts, at 16 years of age, as functions of nc . Parameter values are as in Fig. 5. In (b), the fraction of MSI is nearly zero. The number of polyps in FAP patients does not grow linearly with time.

Morphological and molecular heterogeneity within nonmicrosatellite instability-high colorectal cancer. Cancer Res 62(21), 6011–6014 (2002) 106. : CDX2, a human homologue of Drosophila caudal, is mutated in both alleles in a replication error positive colorectal cancer. Oncogene 17(5), 657–659 (1998) 107. : Computational biology of cancer: lecture notes and mathematical modeling. World Scientific, New Jersey, London, Singapore (2005) 108. : Somatic frameshift mutations in DNA mismatch repair and proapoptosis genes in hereditary nonpolyposis colorectal cancer.

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