Expression level of quiescin sulfhydryl oxidase 1 (QSOX1) in neuroblastomas

Abstract

Neuroblastoma is the most common extracranial solid malignant tumor observed during childhood. Although these tumors can sometimes regress spontaneously or respond well to treatment in infants, genetic alterations that influence apoptosis can, in some cases, confer resistance to chemotherapy or result in relapses and adversely affect prognosis for these patients. The aim of this study was to correlate immunohistochemical expression of the protein quiescin sulfhydryl oxidase 1 (QSOX1) in samples obtained from untreated neuroblastomas with the patients’ clinical and pathological prognostic factors and clinical course. Neuroblastoma samples (n=23) obtained from histology blocks were arrayed into tissue microarrays and analysed by immunohistochemistry. The cases were classified according to the following clinical and pathological prognostic factors: age at diagnosis greater or less than/equal to 18 months; location of the lesion at diagnosis (abdominal or extra-abdominal); presence or absence of bone-marrow infiltration; tumor differentiation (well or poorly differentiated); Shimada histopathologic classification (favourable or unfavourable); state of the tumor extracellular matrix (Schwannian-stroma rich or poor); amplification of the MYCN oncogene; and clinical course (dead or alive with or without relapses/residual lesions). Twelve of the cases were female, 9 children were over 18 months old, 9 cases presented with extra-abdominal tumors and 9 cases exhibited tumors with unfavourable histologies. Fifteen patients underwent bone-marrow biopsy, and 4 of these were positive for metastasis. Nine patients died. The higher immunohistochemical expression of QSOX1 was more common in well-differentiated samples (P=0.029), in stroma-rich samples (P=0.029) and in samples from patients with a high prevalence of relapses/residual disease. The functions of QSOX1 include extracellular matrix maturation and the induction of apoptosis. Therefore, QSOX1 may be involved in neuroblastoma differentiation and regression and may thus function as a biomarker for identifying risk groups for this neoplasm.

Microarray Analysis of the Molecular Mechanism Involved in Parkinson’s Disease

“…GATA3 , a member of the GATA family, is a regulator of T-cell development and plays roles in endothelial cells [ 68 , 69 ]. TFDP1 is involved in the cell cycle and contributes to hepatocellular carcinomas [ 70 , 71 ], SMAD1 is involved in multiple pathways [ 72 , 73 ], and QSOX1 plays roles in some cancers such as breast cancer and neuroblastoma [ 74 – 76 ]. However, there are few reports regarding the involvement of these TFs in PD.…”

Effect of <i>QSOX1</i> on cattle carcass traits as well as apoptosis and triglyceride production in bovine fetal fibroblasts and mammary epithelial cells

“…In fibroblasts and mesenchymal stem cells, QSOX1 functions as an immune response modifier to prevent tissue inflammation and fibrosis in the lungs [ 17 ]. QSOX1 might also be involved in the differentiation and regression of neuroblastomas through extracellular maturation and apoptosis induction [ 2 ]. It is suggested that QSOX1 could be a potential biomarker for acute decompensated heart failure [ 9 ].…”

“…QSOX1 is overexpressed in diverse tumor types and hence, might be involved in promoting the growth and invasion of tumor cells and altering the composition of the extracellular matrix [ 11 ]. It was suggested that QSOX1 could be a biomarker for identifying individuals with higher risk for certain types of cancer, including neural tumors, pancreatic cancer, and breast cancer [ 2 , 8 , 12 ]. Site-directed mutagenesis suggested that the C449-C452 motif is essential for the activity of QSOX1 ; the C70-C73 motif is fundamental in the transfer of electrons from thiol-containing substrates, including the reduced proteins DTT (DL-Dithiothreitol) and GSH (glutathione), to the C449-C452 motif; and the C509-C512 motif is not involved in electron transfer during disulphide formation [ 20 ].…”

Is there still room for novelty, in histochemical papers?

“…In most of the published papers on Tumor biology & markers , 4-21 the expression of specific protein has been investigated (in hepatocellular carcinoma, 4-6 uterine lesions, 7,8 colorectal carcinoma, 9,10 and other neoplasms 11,15,21 ). The aim was either to originally define new diagnostic/prognostic markers, 4,6,8,10-12 or to identify proteins involved in tumor onset 7 or progression, 5,21 or to evaluate the effect of therapy.…”