A hallmark of cancer cells is the possession of multiple gene mutations and aberrations in cell signaling pathways.
Until recently, multiple gene rearrangements and even genomic landscapes which reflect the structural aberrations throughout the genomes have been identified in multiple types of epithelial cancers, including prostate cancer [ 5, 6], breast cancer [ 7, 8], lung cancer [ 9, 10], colorectal cancer [ 11], gastric cancer [ 12], head and neck cancer [ 13], hepatocellular carcinoma [ 14] and so on.
Most BRCA1 or BRCA2 gene aberrations are small mutations involving a single or multiple changes in nucleotide sequence, but large genomic rearrangements (LGRs) have also been reported in patients who are negative for BRCA1 or BRCA2 sequence variations.
High-throughput sequencing often identifies multiple gene fusions in individual samples, presenting a challenge to distinguish oncogenic "driver" from unimportant "passenger" aberrations.
High-throughput sequencing of cancer samples frequently identifies multiple gene fusions in individual samples, often presenting a challenge for identifying potentially oncogenic driver fusions among irrelevant passenger aberrations.
Multiple gene alterations, including allelic deletion, insertion, polymorphism mutation, and methylation change, are marked in HCC, causing genetic and molecular aberrations.
Fusion gene aberrations are detected by karyotyping, FISH, or RT-PCR analysis.
Much attention is also paid to recurrent gene aberrations in STSs as the predictive biomarkers [11] [13].
However, despite numerous studies reporting chromosomal and gene aberrations in human osteosarcoma, no genetic aberrations of the VEGF pathway have been reported in this tumor type [27].
The dependencies between molecular aberrations and gene expressions may be modular, as multiple genes with coherent expression profiles are likely to be affected by common molecular aberrations.
