Malignant melanoma: modern black plague and genetic black box

Article Abstract:

Malignant melanoma has become the modern black plague and the black box of genetics. Cancer biologists are very clear that this skin cancer has strong links to genetics. The key genetic lesions associated with the development of melanoma include some involving the ras family oncogenes, receptor tyrosine kinases with ligands and the INK4a/ARF tumor suppressor locus. The pathogenetic roles of these pathways in melanoma have been verified on more than one experimental level. Mouse models likely will be helpful in the future.

Usage, Statistics, Genetic aspects, Observations, Autocrine mechanisms, Melanoma, Skin cancer, Genetically modified mice, Oncogenes

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Elevated telomere-telomere recombination in WRN-deficient, telomere dysfunctional cells promotes escape from senescence and engagement of the ALT pathway

Article Abstract:

Genetically defined mouse cells are utilized to understand the impact of WRN helicase deficiency on telomere maintenance, chromosomal stability, cellular mortality and tumorigenesis. It is indicated that the increased incidence of chromosomal instability and cancer in Werner Syndrome is found due to aberrant recombinations between sister chromatids specifically at telomeres, which promote the activation of the alternative lengthening of telomere (ALT) pathway and lead to chromosomal instability during tumorigenesis.

Cell death, Cancer, Cancer genetics

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Pot1 deficiency initiates DNA damage checkpoint activation and aberrant homologous recombination at telomeres

Article Abstract:

Study is presented to show that conditional deletion of POT1a elicits a DNA damage response at telomeres, resulting in p53-dependent replicative senescence. The results have shown that POT1a deletion results in chromosomal instability and POT1 are crucial for the maintenance of both telomere integrity and overall genomic stability.

DNA damage, Genetic research, Rats as laboratory animals, Laboratory rats

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