Differential proteomic alterations between localised and metastatic prostate cancer

Abstract

Molecular alterations in the prostate cancer proteome mediate the functional and phenotypic transformation from clinically localised to metastatic cancer, a transition that drives patient's mortality and challenges therapeutic intervention. A first approximation of differential proteomic alterations stratified by disease stage has yielded repertoires of potential diagnostic and prognostic markers, multiplex signatures of predictive value, and yield fundamental insight into molecular commonalities in cancer progression. Deciphering these causative proteomic alterations from the molecular noise will continue to mature our understanding of tumour biology and drive new computational and integrative approaches to model a system's view that accommodates the heterogeneity of prostate cancer progression.

Figure 1

Prostate cancer tissue staining for AMACR. High levels of the prostate cancer biomarker AMACR (green) stained mainly in clinically localised prostate cancer glands compared with internal adjacent benign glands. A higher magnification image is included on the right, and membrane E-cadherin expression is shown in red.

Figure 2

Overview of the conceptual flow in characterising proteomic alterations between prostate cancer stages. Starting from a diverse sample population, a vast array of sample preparation methods and high-throughput technologies can be leveraged to differentially profile tissue stratified by disease progression. A variety of resulting data types, formats, and dimensionality require significant integration and bioinformatic analyses to tease causal entities from the molecular noise and agglomerate the results into one of many desired outcome models motivated by study design.