In real life, whenever we say driver, our mind will shift to the word passenger too because we know the driver is the one who drives the car for some passenger. Similarly, drivers are less in number as compared to passengers so the fraction of driver mutation is less as compared to passenger mutation to be in part. For example, in a tissue where the tumor is forming and the no. of gene alterations are 40â€“100, 5â€“15 would be driver mutations, which may be playing role in the initiation of the defect called as tumor; an example includes colon cancer; some other may play a role in the growth of the tumor or metastasis (a term used to define as the malignancy of cancer cells that can move or spread from one tissue to other via any route of lymph or bloodstream itself). It is also seen that the driver mutations and driver genes differ with each other in terms that the former only cause driver gene mutation but the latter contribute both in the driver as well as passenger gene mutations.
The diagram shown above represents that the APC driver gene is a large driver gene, but the mutation that occurs for 1600 amino acids is by driver mutations and the rest of the 1200 amino acids by the help of passenger mutation.
Cancer sequencing is much important because the driver events play a great or important role in the progress of cancer, and its goal is to discover a whole genome. Therefore, due to this, many researchers focus on isolating and analyzing the driver mutations, although there is a little problem that the early stages of tumor formation are not properly clear or understood.
Talking about passenger mutation, it clearly states that it does not involve the advantage of clonal growth unlike driver mutations; therefore, due to this, it does not contribute much to cancer development. One important thing that research clears that the driver mutation does not imply resistance to cell cancer therapy.
Identifying Driver Mutations:
The very first step of identifying the driver mutation involves genome sequencing; for example, if we want to identify mutations in the genome beforehand in a cancerous situation, we will first sequence the whole genome and then further the mutations will be identified, specifically the driver mutations because they lead to the actual mutation. The basic outflow is shown by the below figure that states that after whole-genome sequencing, any somatic mutation identification is performed followed by recurrent mutations and functional mutations; these all mutations are validated via in-vitro and in-vivo experimental methodologies. One of the drawbacks is that these experimental methods cannot distinguish between passenger and driver mutations merely by the functional or structural changes.
Overview of strategies for cancer-genome sequencing: A cancer-genome sequencing project begins with whole-genome or whole-exome sequencing. Various methods are used to detect somatic mutations in the resulting sequence, yielding a long list of somatic mutations. Several strategies can then be employed to prioritize these mutations for experimental or functional validation. These strategies include testing for recurrent mutations, predicting functional impact, and assessing combinations of mutations. None of these approaches are perfect, and each returns a subset of driver mutations as well as passenger mutations. The mutations returned by these approaches can then be validated using a variety of experimental techniques.
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