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The more mutated anticancer genes there are in a cell, the more it will reproduce.
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The mutations will accumulate as time passes, so the older ones must contain more mutated sites; however the methylation status will not always become increasingly intensive.
In this case we grew the cells for three weeks to obtain more DNA and generate more mutated clones.
In addition to tumor development, more mutated genes contribute to malignant phenotypes.
This greatly improved our specificity while maintaining sensitivity to older, more mutated elements.
It arises from the underlying functional involvement of one or more mutated genes [ 1, 2].
Mechanistically, BRCA2-mutated but not the BRCA1-mutated cases exhibited a "mutator phenotype," containing significantly more mutations than wild-type BRCA cases across the whole exome.
Together, the compound 2 holds promise for a more effective anticancer treatment approach in humans.
A more effective anticancer therapy is required.
Moreover, along with novel therapeutic targets, more potent anticancer molecules have been discovered recently.
Thus, there is immense social and economic pressure to develop new and more efficacious anticancer therapies.
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