Reseachers define the entire landscape of mutations (both point mutations as well as chromosome amplifications and deletions) that lead to mouse skin cancer formation and progression.
There striking similarity between mutated genes in carcinogen-induced mouse SCC and human SCCs, confirming the relevance of mouse models to understand human cancer.
By analyzing the genetic abnormalities that accompanied the progression from a benign tumor to fully malignant and invasive tumors, researchers found that tumor progression was not accompanied by additional point mutations but rather by larger chromosomal copy number alterations, leading to the amplification or deletion of important genes controlling tumor formation.
Finally, by reconstructing the lineage tree of primary cancers and their metastasis, the authors demonstrate that very few additional mutations were found in metastasis, suggesting that metastasis could be regulated by other additional non-genetic mechanisms
Edited
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