In cancer research, cancer there are key mutations to each different type of cancer, tumors, aberration, translocations, fusions, indels, or mutations that have popped up somewhere in the human body. Since many of these alterations might never have been observed before and might not necessarily reside in coding regions of the genome, whole-genome sequencing is increasingly seen as the only rigorous approach that can find all the variants in a cancer genome. Among all these alterations are a select few that drive the progression of the disease. Genetic alterations have the potential to impact all cellular processes, including chromatin structure, DNA methylation, RNA splice variants, RNA editing, and microRNA (miRNA) to name but a few. Now, we all hear about tumors. Every individual carries a unique set of inherited germline mutations. As cancer progresses, additional somatic mutations and genomic rearrangements accumulate. These changes can trigger drug resistance and metastasis. Increasing evidence suggests that these …show more content…
The combination of a strong promoter with a functional gene (proto-oncogene) downstream is common in some cancers. It is estimated that half of prostate cancers harbor gene fusions between TMPRSS2 and members of the ETS transcription factor family. Gene fusions are formed by the joining of two previously separate genes or loci and may lead to a gene product with a new or different function from the two fusion partners. It may also result in an oncogenic activation, as in the case of Philadelphia chromosome positive-acute lymphoblastic leukemia. This gene fusion results in expression of the BCR-ABL tyrosine kinase, which activates cellular proliferation. Gene fusions can be generated by several mechanisms, which can be characteristic for some cancer types. Pancreatic cancer is characterized by frequent breakage–fusion– bridge cycles of chromosomal