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/ Health News / 2007 / November 2007 / November 9, 2007 Now, a new mathematical model to map cancer progression |
How cancer prevention drives aging
For the first time, researchers have found how cellular senescence, the well-known mechanism for preventing cancer, can trigger aging and age-related disease by changing the local tissue environment. ANI
Scientists unveil genes vital to vital to adult heart function
In a study on fruit fly Drosophila, scientists at the Burnham Institute for Medical Research (Burnham) have found that genes involved in embryonic heart development are vital to adult heart function in both fruit flies and humans. ANI
Psychiatric disorders common among college-aged
A new study has revealed that psychiatric disorders appear to be common among 18- to 24-year-olds, with overall rates similar among those attending or not attending college. ANI
Researchers at Harvard and Johns Hopkins Universities have developed a novel mathematical model to map cancer progression.
Washington, November 9 : Researchers at Harvard and Johns Hopkins Universities have developed a novel mathematical model to map cancer progression.
The researchers said that their study provides a new paradigm in calculating tumour development, showing that it appears to be driven by mutations in many genes.
Scientists' understanding of the progression of cancer has long been based on streamlined models where cancer is driven by mutations in only a few genes, according to the background information in an article published in PLoS Computational Biology.
The researchers have shown how tumour progression can be driven by hundreds of genes. They say that as many as 20 different mutated genes may be responsible for driving an individual tumour's development.
During the research, a case of colon cancer was studied. Cancer progression proceeds stochastically from a single genetically altered cell to billions of invasive cells through a series of clonal expansions.
According to the researchers' model, cancer progression is driven by mutations in many genes, each of which confers only a small selective advantage.
The researchers have found that the time that a benign tumour takes to transform into a malignant tumour is dominated by the selective advantage per mutation and the number of cancer genes, whereas tumour size and mutation rate have smaller impacts.
Niko Beerenwinkel, a member of the research team, says that the new mathematical model may help explain the large amount of variation between individual tumours that has long puzzled researchers and clinicians.
ANI
