Urine has been in the center of attention among scientists of clinical proteomics in the past decade, because it is valuable source of proteins and peptides with a relative stable composition and easy to collect in large and repeated quantities with a noninvasive procedure. In this review, we discuss technical aspects of urinary proteomics in detail, including sample preparation, proteomic technologies, and their advantage and disadvantages. Several recent experiments are presented which applied urinary proteome for biomarker discovery in renal diseases including diabetic nephropathy, immunoglobulin A (IgA) nephropathy, focal segmental glomerulosclerosis, lupus nephritis, membranous nephropathy, and acute kidney injury. In addition, several available databases in urinary proteomics are also briefly introduced.

Background: It is well-described that the transcriptome of peripheral blood mononuclear cells (PBMCs) can be altered in the context of many malignancies to allow them avoid the effective immune response, which leads to cancer invasiveness. Here, we used an MS-based strategy to discover biomarkers in the PBMCs of breast cancer (BC) patients and validated them at different stages of BC. Methods: PBMCs were isolated from the breast cancer patients and were cultured alone or co-cultured with breast cancer cell lines. The role of PBMC in the invasion property of breast cancer cells was explored. NF-kB activity was also measured in the co-cultured breast cancer cells. Identification of protein profiles in the secretome and proteome of the co-cultured PBMCs was performed using SWATH mass spectrometry. Pathway enrichment and gene ontology analyses were carried out to look for the molecular pathways correlated with the protein expression profile of PBMCs in the breast cancer patients. Quantitative real-time polymerase chain reaction (qPCR) was performed to validate the candidate genes in the PBMC fraction of the breast cancer patients at the primary and metastatic stages. In silico survival analysis was performed to assess the potential clinical biomarkers in these PBMC subtypes. Results: PBMCs could significantly increase the invasion property of the BC cells concomitant with a decrease in E-cadherin and an increase in both Vimentin and N-cadherin expression. The NF-kB activity in the BC cells significantly increased following co-culturing implying the role of PBMCs in EMT induction. Enrichment analysis showed that the differentially expressed proteins in PBMCs are mainly associated with IL-17, PI3K-Akt, and HIF-1 signaling pathway, in which a set of seven proteins including TMSB4X, HSPA4, S100A9, SRSF6, THBS1, CUL4A, and CANX were frequently expressed. Finally, in silico analysis confirmed that a gene set consisting of S100A9, SRSF6, THBS1, CUL4A, and CANX were found to provide an insight for the identification of metastasis in breast cancer patients. Moradpoor et al. Stage-Associated PBMC Biomarkers, BCs Conclusion: In conclusion, our study revealed that the protein expression profile in PBMCs is a reflection of the proteins expressed in the BC tissue itself; however, the abundance level is different due to the stage of cancer.

Purpose: Chemotherapy-resistance of melanoma has led to poor prognosis and decreased survival in the patients. Therefore, the addition of adjuvant therapies to the conventional chemotherapy regimens has been taken into consideration to improve the clinical treatments efficiency. In this study, the effect of microwave (MW) Hyperthermia has been evaluated on the toxicity of cisplatin on the MM200 cell line in the presence and without gold nanoparticles (GNPs). Methods: Cells incubation was performed with and without cisplatin in the presence and absence of GNPs. To induce hyperthermia, the cells were immediately placed under MW irradiation for 25 and 30 minutes (41-43°C) following the addition of the drug and GNPs, then they were incubated for 24 hours. Finally, cell survival was determined by MTT assay.Results: GNPs (up to 6.6 µg/mL) showed no toxicity. GNPs at the concentration of 13.2 and 26.4 µg/mL caused 13% and 20.7% drop in cell survival rate, respectively. IC50 of cisplatin decreased from 4 to 2 µg/mL in the presence of GNPs. Hyperthermia (43°C) plus chemotherapy (2 µg/mL) resulted in no significant enhancement in cisplatin cytotoxicity relative to chemotherapy alone whereas by adding GNPs, an increase in cell mortality up to 15-fold in comparison to cisplatin alone was observed. Conclusions: There is a synergistic effect between cisplatin and GNPs, this could be due to the facilitated entrance of cisplatin in the presence of GNPs. MW exposure improves the efficacy of cisplatin therapy in the presence of GNPs on MM200 cells.