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Objective: Gliomas are the most common primary brain tumors, and have been ranked as the fourth leading cause of cancer death. Tumor mesenchymal-like stem cells [tMSCs] contribute to the aggressive behavior of glial tumors by providing a favorable microenvironment for the malignant cells. The aim of our study was to identify differential proteome of tMSCs derived from low vs. high grade glioma tumors
Materials and Methods: Patients with newly diagnosed low and high grade gliomas were included in this case control study. tMSCs were isolated from tumors using enzymatic digestion validated by flow cytometer analysis after sub-culturing. Differential proteomic analysis of tMSCs derived from low and high grade tumors was performed by two-dimensional gel electrophoresis and mass spectrometry. Protein spots with more than two fold differences and P values below 0.05 were considered as differentially expressed ones
Results: In tMSCs isolated from low and high grade gliomas, different isoforms of mesenchymal- related proteins vimentin and transgelin were differentially expressed. Overexpressed proteins in tMSCs isolated from low grade gliomas were mitochondrial manganese-containing superoxide dismutase [Mn-SOD], 40S ribosomal protein SA, and GTP-binding nuclear protein, while in tMSCs isolated from high grade gliomas, cathepsin B, endoplasmin, ezrin, peroxiredoxin1, and pyruvate kinase [PK] were found to be significantly overexpressed
Conclusion: For the first time, we analyzed the differential proteomic profiles of tMSCs isolated from glioma tumors with different grades. It was found that molecules related to mesenchymal cells [vimentin and transglin], in addition to those related to tumor aggressiveness with potential secretory behavior [e.g. cathepsin B] were among differentially expressed proteins
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Background: salivary gland tumors are among malignancies that have high recurrence rate. Immune responses in salivary gland tumors have not been well elucidated. T helper type 1 [Th1] and Th2 cytokines have been reported to play a role in the outcome of head and neck cancers
Objective: to evaluate the serum levels of interferon gamma [IFN- [gamma]], as the hallmark of Th1 cytokines, and interleukin-4 [IL-4], as the hallmark of Th2 cytokines, in patients with benign and malignant salivary gland tumors in comparison with healthy controls
Methods: fifty patients with benign and 14 patients with malignant salivary gland tumors, as well as 23 healthy individuals were recruited. Serum levels of IFN-[gamma] and IL-4 were measured using ELISA method. Nonparametric tests were used for data analysis
Results: serum levels of IFN-[gamma] and IL-4 were found not to be significantly different in patients compared to the control group [0.68 +/- 0.29 vs. 1.03 +/- 0.57 pg/ml, p=0.58 for IFN-[gamma], 4.57 +/- 1.57 vs. 4.41 +/- 1.31 pg/ml, p=0.28 for IL-4]. IFN-[gamma] and IL-4 serum levels were also not significantly different between patients with benign and malignant salivary gland tumors [p=0.54 and p=0.86, respectively]
Conclusion: the systemic levels of IL-4 and IFN-[gamma] seem not to be associated with salivary gland tumor in our study. Investigation of other cytokines produced by Th1 and Th2 cells are warranted
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Background: Colorectal cancer [CRC] is one of the most common causes of cancer-related death in the world. The expression of N-myc downstream-regulated gene 2 [NDRG2] is down-regulated in CRC. The aim of this study was to investigate the effect of NDRG2 overexpression on cell proliferation and invasive potential of SW48 cells
Methods: SW48 cells were transfected with a plasmid overexpressing NDRG2. After stable transfection, the effect of NDRG2 overexpression on cell proliferation was evaluated by MTT assay. The effects of NDRG2 overexpression on cell migration, invasion and cell motility and matrix metalloproteinase 9 [MMP9] activities were also investigated using matrigel transwell assay, wound healing assay and gelatin zymography, respectively
Results: MTT assay showed that overexpression of NDRG2 caused attenuation of SW48 cell proliferation. Transwell and wound healing assay revealed that NDRG2 overexpression led to inhibition of migration, invasion, and motility of SW48 cells. The overexpression of NDRG2 also reduced the activity of secreted MMP-9
Conclusions: The results of this study suggest that NDRG2 overexpression inhibits proliferation and invasive potential of SW48 cells, which likely occurs via suppression of MMP-9 activity
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Background: An association between lung cancer and chemokines has been advocated in the recent years. This study aims at investigating the association between lung cancer and 16C/A single nucleotide polymorphism [SNP] [rs. 4359426] in C-C motif chemokine 22 [CCL22] as well as C1014T SNP [rs. 2228428] in C-C chemokine receptor type 4 [CCR4], which serves as the receptor for CCL22
Methods: Genotyping was performed in 148 lung cancer patients and 148 normal controls using Polymerase Chain Reaction- Restriction-Fragment Length Polymorphism [PCR-RFLP]. The data were verified by direct automated sequencing
Results: Frequencies of CC, CA and AA genotypes of 16C/A SNP in CCL22 gene were 112 [75.7%], 33 [22.3%] and 3 [2.0%] in patients, and 119 [80.4%], 24 [16.2%] and 5 [3.4%] in controls respectively. No significant differences were observed in genotype frequencies at this position between cases and controls [P=0.34]. Moreover, there was no significant association between CCL22 polymorphism and types of lung cancer in patients. The distribution of CC, CT and TT genotypes of C1014T SNP in CCR4 gene, was 76 [51.4%], 60 [40.5%] and 12 [8.1%] in patients, and 80 [54.1%], 49 [33.1%] and 19 [12.8%] in controls respectively. No statistically significant differences were observed in genotypes frequencies of CCR4 gene between patients and controls [P=0.24]. The genotype inherited by patients observed not to be associated with the type of lung cancer [P>0.05]
Conclusion: Results reveal that CCL22 gene polymorphism at position 16C/A and CCR4 gene polymorphism at position C1014T, appear not to be associated with susceptibility to lung cancer
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The alteration of Thl and Th2 cytokine levels is the subject of controversy in pleural effusions caused by malignancy, a situation that favors a Th2 immune response. To examine the different levels of IL-4 and IL-10 [Th2 cytokines], and IL-2 and interferon-y [IFN-gamma] [Thl cytokines] in malignant and non-malignant pleural effusions. The cytokine levels in pleural fluid of 62 patients with malignant pleural effusion [44 with lung cancer and 18 with extrathoracic tumors], 8 with tuberculous and 8 with congestive heart failure pleural effusion were analysed using enzyme-linked immunosorbent assays. IL-2 was below the detectable concentration of the assay. A significant decrease in IFN-gamma level was observed in malignant but not in congestive heart failure cases compared to tuberculous cases. IL-10 levels were higher in malignant and tuberculous pleural effusions than in congestive heart failure pleural effusions, however, this difference did not reach the significant level. IL-4 levels were also increased non-significantly in lung cancer pleural effusions compared to the other groups. Our results show a wide variation in IL-4, IL-10, and IFN-gamma levels in malignant pleural effusions, a pattern which was not convincing enough to differentiate the cause of effusion
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The proto-oncogene HER2 plays a key role in the control of cellular proliferation. Its overexpression has been reported to be associated with a poor prognosis in cancer, particularly in breast cancer. In the present study, serum HER2 levels were investigated in patients diagnosed with epithelial ovarian cancer. Serum HER2 levels were detected by an ELISA commercial kit in 51 patients and 33 healthy individuals. The mean serum HER2 level was found to be significantly higher in patients than healthy controls [P=0.005]. In 29% of patients, serum HER2 levels were higher than the cut-off value. HER2 serum level was not associated with tumor stage at diagnosis. Elevation of HER2 in a high proportion of patients with epithelial ovarian cancer further strengthens the importance of this molecule in the pathogenesis of ovarian cancer