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INTRODUCTION: Oral squamous cell carcinoma (OSCC) is the commonest malignancy in oral cavity. Dysregulated inflammatory processes could impose a cancer risk. Cytokines are inflammatory mediators that can induce cell proliferation. Interleukin-10 is a pleiotropic cytokine which has a dual role in cancer pathogenesis. It contributes to tumor growth and in other cases to tumor rejection. OBJECTIVES: To evaluate and correlate the expression of IL-10 in different histopathological grades of OSCC, as well as to assess its serum and salivary levels. MATERIALS AND METHODS: Immunohistochemical (IHC) study using the IL-10 antibody was done on 20 surgical specimens and 5 normal mucosal tissues taken from OSCC patients and healthy individuals, respectively. Serum and salivary levels of IL-10 were also measured with a human IL-10 ELISA Kit in both patients and controls. RESULTS: OSCC biopsies showed immunoreactivity to IL-10, while normal tissues were immunonegative. The IHC staining intensity was directly proportional to the grading of OSCC. Conversely, it showed no significant correlation to the disease stage. The difference in the serum and salivary IL-10 levels in patients and controls was not statistically significant. However, there was a significant correlation between IL-10 tissue expression and its serum and salivary levels in OSCC patients. CONCLUSIONS: IL-10 is expressed in OSCC biopsies. Additionally, the levels of IL-10 in tissue, serum and saliva were correlated to each other. This could reflect the same way of regulation of IL-10 in different parts of the body.

BackgroundHead and neck cancer is a major health problem. Recent studies on the pathobiology of oral squamous cell carcinoma (OSCC) have led to the discovery of a small population of cancer cells with a consistent behavior with the features of cancer stem cells (CSCs).  CSCs are required and responsible for initiation, maintenance and recurrence of disease. Molecular markers are commonly used for the identification of CSCs. CD44 is the most reported CSC marker in OSCC.The aim of the study was to evaluate and correlate the expression of CD44 in different histopathological grades of OSCC, as well as to assess the diagnostic and prognostic value of soluble CD44 (CD44sol) in peripheral blood of patients.Materials and methodsFifteen patients with OSCC were included; biopsies were histologically evaluated using haematoxylin and eosin. Serial sections were immunohistochemically stained by monoclonal antibody to CD44. The intensity of immunostaining of CD44 was calculated. Enzyme-linked immunosorbent assay (ELISA) method was used to determine the concentration of CD44sol in the blood serum.ResultsAll grades of OSCC showed membranous immunosignaling of CD44. The well, moderately and poorly differentiated OSCC cases showed weak, moderate and intense positive membranous immunosignaling of CD44 respectively.CD44sol levels were significantly higher in OSCC patients than they were in control groups. Soluble CD44 serum levels were significantly higher in poorly differentiated than they were in moderately and well differentiated.ConclusionCSCs detection in fixed human tissue and CD44sol detection in peripheral blood using ELISA seemed to be a promising method and may have a diagnostic and prognostic value in management of OSCC.

Background: Adipose tissue (AT) is a rich source of mesenchymal stem cells (MSCs), however, there is no standardized protocol for stem cell isolation and culture. This leads to inconsistency of the results and limits the comparison of the data from different laboratories. Our aim was to provide an applied protocol for ASCS isolation and expansion, study the cell behavior and define their cellular surface markers. ASCs were cultured from both resected adipose tissue (RAT) obtained following abdominoplasty or breast reduction and lipoaspirates (LPA) following laser-free liposuction. Method: the protocol entailed coculturing of stromal vascular fraction (SVF) with RAT as raw pieces using DMEM medium with varying glucose concentration. The coculture protocol aimed to mimic the normal physiological conditions required for cell growth. ASCs were immunophenotyped to define their MSCs surface markers by flowcytometry. Results: ASCs were isolated from coculturing RAT with SVF with fibroblast-like adherent cells morphology. The ASCs yield isolated from LPA was significantly greater than from RAT on day 14 and 28 (p = 0.002, <0.001, respectively). Significant increase in ASCs proliferation rate was detected when ASCs were cultured under high glucose (4.5 g/L) compared to low glucose (1 g/ L) condition on day 7 and 14 (p = 0.04, 0.015, respectively). ASCs isolated from both protocols were positive for CD34, CD49d, CD73, CD90 and CD105 and negative for CD3, CD14, CD19, CD45 and HLA-DR. Conclusion: We concluded that the cells harvested by our protocol were ASCs. Hence, our method can be an efficient isolation tool to obtain primary ASCs under culture conditions mimicking normal physiological status. This will help in providing ASCs which can be similar to cells in human tissue for further study.

Background: Chronic inflammation with sustained unregulated immune stimulation in autoimmune rheumatic diseases (ARD) may be a risk factor for developing lymphoproliferative disorders (LPD). Markers of ARD activity as high erythrocyte sedimentation rate or erosive joint diseases and the development of B-symptoms were accounted as risk factors for LPD development. We investigated the association of five inflammatory cytokine genes single nucleotide polymorphisms (SNPs): TNF-α-308G>A; TGF-β1 gene codon 10 T>C and 25 G>C; IL-10 promoter SNPs-1082 A>G,-819T>C, and-592A>C; IL-6-174G>C; and IFN-γ 874 T>A with the risk of LPD development in ARD patients. The study was conducted on 70 patients divided into group I, 25 ARD patients diagnosed as RA (n = 15) and SLE (n = 10) and with no history of malignancy; group II, 25 patients diagnosed with LPD and had no ARD; and group III, 20 patients diagnosed with both diseases: ARD and LPD. Cytokine genotyping was analyzed by PCRsequence-specific primer (PCR-SSP). Results: ARD+LPD patients had significantly higher frequency of TNF-α-308A allele and AA+AG genotype (high TNF-α producers) and IL-10-1082A allele and AA genotype (low IL-10 producers) than ARD patients (p = 0.003, p = 0.024, p = 0.003, p = 0.03, respectively) with a significantly increased risk of LPD development in ARD patients expressing the corresponding alleles and genotypes. No significant differences were detected in the distribution frequency of either TGF-β1, IL-6, or IFN-γ SNPs between groups I and III or any of the studied SNPs between groups II and III. The distribution frequency of IL-10 ATA haplotype was significantly increased in group III as compared to group I (p = 0.037). Conclusion: The significantly increased frequency of the high-TNF-α-and low-IL-10-producing alleles and genotypes in ARD patients may participate in the provision of a proinflammatory milieu that eventually increases the risk of LPD development.