A better understanding of the most frequent driving mutations in lung cancer will aid in the progression towards more personalized therapy.
Moreover, identifying the cooperating molecular events that occur alongside FGFR3 mutation to drive UCC will aid the development of genetic models of UCC to test combinatorial therapies.
Proponents of continued research in this area suggest that knowing the mutations involved in mammalian airborne transmission will aid surveillance, allowing us to see whether there is evolution in the direction of a pandemic virus.
This will aid the interpretation of mutations through assessment of their function at the RNA level.
Additionally, we investigated the accuracy of the publicly available mutation detection algorithms to detect cancer specific SNVs which will aid researchers and clinicians in study design and implementation of WGS for the identification of somatic mutations in other cancers.
It is observed that the pathological genetic mutations and their structural and functional significance of OCA genes will aid in development of personalized medicine for albinism patients.
As such, other structural and complex mutations that disrupt MMR gene function through similar mechanisms are likely to exist and it is possible that the progression from Sanger sequencing and MLPA-based testing to targeted resequencing of the MMR genes will aid in the routine detection of such structural mutations.
Deciphering how these mutations alter M-band structure, contractile activity, signaling networks, posttranslational modifications, and energy production will aid in improving clinical diagnosis and developing individualized therapeutic approaches for affected individuals.
However, the use of established and emerging tissue biomarkers will aid in the interpretation of difficult melanocytic lesions, provide prognostic information, identify mutation status, and allow the selection of patients who may benefit from targeted therapy.
Such studies will aid the rational design of therapeutics for treatment of skeletal disorders in humans with inherited SHP-2 mutations.
