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Genetic basis for aggressive tumours discovered

A checkpoint mutation in mice might provide clues to the progression towards aggressive, treatment-resistant cancers, according to a study published in 18 January Nature. Researchers from the Memorial Sloan-Kettering Cancer Center in New York genetically engineered a mutation in the MAD2 gene that eliminates a checkpoint in mitotic division essential for ensuring the equal distribution of chromosomes to the two daughter cells. The mutation caused the tumour cells to become very genetically unsta

By | January 18, 2001

A checkpoint mutation in mice might provide clues to the progression towards aggressive, treatment-resistant cancers, according to a study published in 18 January Nature. Researchers from the Memorial Sloan-Kettering Cancer Center in New York genetically engineered a mutation in the MAD2 gene that eliminates a checkpoint in mitotic division essential for ensuring the equal distribution of chromosomes to the two daughter cells. The mutation caused the tumour cells to become very genetically unstable and resistant to taxanes. "Although the loss of one copy of MAD2 caused only subtle decreases in the amount of MAD2 protein levels, it had a great impact on the cell's genetic behaviour," said Loren Michel, one of the authors. "Our results suggest that developing a similar test to detect the changes in this genetic pathway in human cancer could be used to predict disease progression."

Michel et al also found that the same mutation could initiate malignant tumours in mice. When both copies of MAD2 were inactive, the mice died; when just one copy was inactivated, cancer resulted. Vasco Liberal, another of the study's authors, said: "Uniquely, this mutation resulted in a high frequency of lung carcinomas despite the fact that these genes are found in every cell of the body and the disease is extremely rare in most mice. Interestingly, in humans, low levels of MAD2 have been observed in breast tumour cell lines."

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