Quantitative Proteomic Approach Targeted to Fibrinogen β Chain in Tissue Gastric Carcinoma

Abstract

Elevated plasma fibrinogen levels and tumor progression in patients with gastric cancer (GC) have been largely reported. However, distinct fibrinogen chains and domains have different effects on coagulation, inflammation, and angiogenesis. The aim of this study was to characterize fibrinogen β chain (FGB) in GC tissues. Retrospectively we analyzed the data of matched pairs of normal (N) and malignant tissues (T) of 28 consecutive patients with GC at diagnosis by combining one- and two-dimensional electrophoresis (1DE and 2DE) with immunoblotting and mass spectrometry together with two-dimensional difference in gel electrophoresis (2D-DIGE). 1DE showed bands of the intact FGB at 50 kDa and the cleaved forms containing the fragment D at ~37–40 kDa, which corresponded to 19 spots in 2DE. In particular, spot 402 at ~50 kDa and spots 526 and 548 at ~37 kDa were of interest by showing an increased expression in tumor tissues. A higher content of spot 402 was associated with stomach antrum, while spots 526 and 548 amounts correlated with corpus and high platelet count (>208 × 109/L). The quantification of FGB and cleaved products may help to further characterize the interconnections between GC and platelet/coagulation pathways.

Proteomic Identification of Plasma Biomarkers in Children and Adolescents with Recurrent Hodgkin Lymphoma

“…Furthermore, our study like others highlighted that single fibrinogen subunits are more informative than the entire proteins to distinguish patients with cancer (e.g. fibrinogen β chain for gastric and bladder cancers 36-37; fibrinogen α and γ chains for central nervous system lymphomas 38 as well as response to treatment (e.g. fragment D of fibrinogen β chain in rectal cancer patients receiving neoadjuvant chemo-radiotherapy 39).…”

Hub Genes and Key Pathway Identification in Wilms Tumor Based on Bioinformatics Analysis

“…In pathway enrichment analysis for up regulated genes were carried out.. High expression of enriched genes such as SERPINA1 [61], FGB ( brinogen beta chain) [62], SCG3 [63], ITIH3 [64], FST (follistatin) [65], AMBP (alpha-1-microglobulin/bikunin precursor) [66], IGFBP1 [67], IGFBP6 [68] and PLOD3 [69] were responsible for advancement of various cancers types, but over expression of these genes may linked with pathogenesis of WT. Enriched genes such as CLU (clusterin) [70], VTN (vitronectin) [71], SERPINE1 [72], SERPINE2 [73], FN1 [74], SLC3A2 [75], ITGA2 [76], ITGA3 [77], ITGA5 [78], DOCK2 [79], L1CAM [80], CAV1 [81], TSPAN7 [82], CRLF1 [83], SRPX (sushi-repeat-containing protein, X-linked) [84], FGL1 [85], CCL20 [86], COL1A2 [87], SEMA3C [88], GDF15 [89], ANXA11 [90], SPP1 [91], LAMA1 [92], TDGF1 [93], CXCL3 [94], LGALS3 [95], SERPINB1 [96] and LUM (lumican) [97] were associated with invasion of various cancer cells types, but these genes may be liable for invasion of WT cells.…”

Classical Hodgkin’s Lymphoma in the Era of Immune Checkpoint Inhibition

“…A link between cancer and thrombosis was established several years ago [71,72,73]; thrombosis is the second-leading cause of death in hematologic malignancies [74]. Coagulation homeostasis is often altered in patients with cancer [73], including patients with HL [75].…”

“…A link between cancer and thrombosis was established several years ago [71,72,73]; thrombosis is the second-leading cause of death in hematologic malignancies [74]. Coagulation homeostasis is often altered in patients with cancer [73], including patients with HL [75]. Proteomic analysis of plasma from patients with relapsed HL showed an up-regulation of important proteins involved in the coagulation process, like fibrinogen and complement C3; a reduction of coagulation inhibitors like antithrombin and α-1-antitrypsin (also named serpin), and HRS possess a binding affinity for plasmin and thrombin [76].…”