#Holli ipa library driver
#Holli ipa library series

Similar to QTL analysis, differences in proteomic patterns across biological systems that exhibit quantitative differences in traits provide an unbiased perspective to identify molecular mechanism that underpin these differences in phenotype.

In contrast to genomic-based assays, proteomics provides an attractive platform to profile this regulatory layer of protein activity and differences in the level of protein expression. However, relating gene expression with the specific role that the corresponding protein plays in a signaling pathway is complicated by post-transcriptional control of protein expression and tight regulation of protein activity. Gene microarray platforms provide tremendous breadth in surveying the gene expression landscape within a cellular system. Collectively, these findings suggest a more global approach towards identifying the molecular alterations associated with oncogenic transformation. In addition, evolutionary theory suggests that cancer cells are alternative solutions to a multivariate optimization problem where the tumor microenvironment provides the selective landscape. These quantitative trait loci (QTL) manifest themselves by altering the flow of intracellular information among signaling pathways.

#Holli ipa library driver

These massive rearrangements suggest that there might not be single driver mutations, but that the quantitative alterations in cellular traits associated with malignant transformation is distributed among multiple genetic loci. Next generation sequencing efforts have revealed that, instead of a small number of genetic alteration associated with malignant transformation, genomic landscapes are extensively modified in solid tumors.

#Holli ipa library series

However, a series of recent developments challenge this oncogene paradigm. The focus on identifying specific oncogenes or tumor suppressors that drive malignant transformation embodies the genomic era in cancer research. Acquiring one of the hallmarks of cancer is associated with activating/deactivating particular genes, called oncogenes/tumor suppressors. Cancer cells exhibit a number of common traits that differentiate themselves from normal cells, including sustained proliferative signaling, resisting cell death, and evading growth suppressors.