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As cell lines evolve from a normal to a cancerous state, mutations drive an increase in genetic diversity [7].
Given that among malignancies (brain or otherwise), non-GBM (as well as secondary GBM) are unique in exhibiting a high frequency (as high as 80%) of IDH mutations [ 15, 16, 29, 30], which appear to be early events in non-GBM development [ 16], one can speculate that these mutations drive an atypical path to malignancy.
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Therefore, initiating mutations drive senescence in a tissue-specific manner and shape the evolutionary landscape for the subsequent mutations that allow tumour progression.
Our GE profiling data suggest that the two main histone H3 mutations drive distinct oncogenic programmes, an observation further strengthened by the integration of histological and MR-imaging data.
Leukemia-associated mutations drive cell growth by creating a powerful transcriptional enhancer upstream of an oncogene.
Potassium channel mutations drive both cell growth and hormone production in an adrenal tumor that causes severe hypertension.
Our results demonstrate that the incidence of clonal hemopoiesis is much higher than suggested by exome-sequencing studies, that spliceosome gene mutations drive clonal outgrowth primarily in the context of an aging hemopoietic compartment, and that NPM1 mutations do not drive ARCH, indicating that their acquisition is closely associated with frank leukemia.
This may help explain how DNMT3A mutations drive tumor formation in hematopoietic malignancies, even in the absence of larger global methylation changes.
However, our in silico analysis provides supporting evidence that LATS1/2 mutations drive human tumor development based on the following observations: 1) Cancer mutations in hLATS1/2 do not appear to be random mutations.
The work suggests that the mutations drive lung cancer growth and that Iressa--which inhibits EGF receptor activity--checks that growth.
Since MSI tumors are prone to mutation throughout the genome, the question arises of whether the NKD1 mutations drive tumor progression or are merely "bystander" mutations.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com