The phrase "alterations driver" is not a standard expression in written English and may not be widely understood.
It could potentially be used in a specific context related to software or systems that manage changes or modifications, but clarity would depend on the surrounding text.
Example: "The alterations driver is essential for ensuring that all updates are applied correctly to the system."
Alternatives: "modification tool" or "change manager".
Several known copy number alteration drivers in cancers include receptor tyrosine kinases such as EGFR, FGFR, and ERBB2, which are targets for drugs therapy [ 11].
In fact, the metachronous lesions in these cases are seemingly independent from the corresponding primary tumor, due to both the different genetic alterations involving driver genes and the different histological features.
Communities of mutations, or alterations to driver genes, can lead to increases in proliferation, a higher frequency of errors in transcription and replication, and/or the enabling of apoptotic evasion [6, 7].
Mutual exclusivity of alterations of driver TF circuits.
In cancer, it is not clear whether KLKs alterations are driver mutations or deleterious passenger mutations.
This may exert effects by accumulating alterations in driver genes and promoting cancer cell growth and proliferation.
Recently, integrated large-scale analyses have identified alterations in driver genes including CTNNB1, TP53, CDKN2A, RB1, ZNRF3, and MEN1 (Barzon et al. 2001, Tissier et al. 2005, Assie et al. 2014, Juhlin et al. 2015).
It is reasonable to expect that tumors bearing alterations in driver genes connected in a circuit will follow similar evolution patterns, resulting in similar outcomes and exhibit similar response to a given therapeutic strategy.
Note that because the targets obtained from the four aforementioned sources have been detected irrespective of the tissue type and normally in healthy tissues, the differential expression analysis acts as a filter to detect those targets most likely misregulated upon alterations of driver TFs.
Is the alteration a driver of an oncogenic phenotype?
