scholarly journals Duodenogastric refluх: a look at the problem in terms of carcinogenesis

2019 ◽  
pp. 108-111
Author(s):  
Z. M. Galeeva ◽  
R. G. Toukhbatullina ◽  
A. I. Gaisina

The role of duodenogastric reflux (DGR) in malignant degeneration of the gastric mucosa. It was demonstrated by immunohistochemistry using monoclonal antibodies to p53, PCNA, CD10, MUC2, MUC5AC, MUC6, CD31 and the polymerase chain reaction to detect CDX1, CDX2, FXR genes. The main carcinogenic components of bile are lysolecithin and conjugated bile acids. Biliary reflux increases the risk of malignant tumors in combination with Helicobacter pylori. DGR is one of the etiological factors for gastric cancer, so it determines the necessity for detailed diagnosis in clinical practice.

2020 ◽  
Vol 12 (4) ◽  
pp. 498-505
Author(s):  
Dan Zhang ◽  
Zhaoxi Lu ◽  
Bing Sun

Gastric cancer is a malignant tumor that is originated from the epithelia of the gastric mucosa. Although the gastroscopic biopsy of suspicious gastric areas can provide better early-warning opportunities for patients with malignant tumors that result in achieving early diagnosis and treatment, many malignant tumors are still excluded due to atypical histology, sampling errors, nonspecific antibodies, and other reasons, which pose a threat to the physical and mental health of patients. Therefore, more sensitive and specific detection methods of gastric cancer are needed to improve the screening efficiency of gastroscopic biopsy. The sensitivity of nano PCR was 10 times higher than that of conventional PCR. In comparison with the conventional RT-PCR method, nano PCR technology can amplify brighter bands and identify higher gene expression levels for ALK weak positive gastric cancer in IHC, and improve the detection rate of clinical specimens with lower ALK staining. Therefore, nano-gold polymerase chain reaction used gold nanoparticle (nano-gold PCR) has high sensitivity and positive detection rate for ALK-positive gastric cancer identified by gastroscopy. When a low concentration was observed for the amplified gene, especially when the biopsy tissue was too small to carry out IHC staining, the target gene could be amplified more effectively. Therefore, nano PCR technology is proposed to be widely used in target gene detection of biopsy tissue to achieve better tumor screening.


2020 ◽  
Author(s):  
Ran Cui ◽  
Ludi Yang ◽  
Yiwei Wang ◽  
Ming Zhong ◽  
Minhao Yu ◽  
...  

Abstract Background: Colorectal cancer is one of the most common malignant tumors worldwide. ASXL2 is an enhancer of trithorax and polycomb gene, which have been proved to act in many tumor types. The role of ASXL2 in the occurrence and development of tumors have been extensively studied in recent years. However the relationship between ASXL2 and the prognosis of CRC is still unclear.Methods: In this study, quantitative real-time polymerase chain reaction (qRT-PCR), Western blot analysis and immunohistochemistry (IHC) were used to examine the expression of ASXL2 in CRC tissues. Cells were transfected with siRNAs or lentivirus to regulate the expression of ASXL2. The effects of ASXL2 on proliferation of CRC cells were determined by CCK8 assay.Results: This study demonstrated that ASXL2 was significantly more expressed in CRC specimens relative to the normal adjacent tissues. The upregulation of ASXL2 was related to advanced clinical stages. Patients who exhibited high expression levels of ASXL2 had poorer overall survival, whereas those with low expression of ASXL2 survived longer. Multivariate Cox regression analysis revealed ASXL2 expression could be considered as an independent prognostic factor for CRC. Inhibition or overexpression of ASXL2 markedly influenced the proliferation of CRC cells.Conclusion: These results showed that ASXL2 could induce cell proliferation which is associated with poor prognosis of CRC patients and might be a new therapeutic target for CRC.


2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Raquel Weber ◽  
Ana Paula Santin Bertoni ◽  
Laura Walter Bessestil ◽  
Ilma Simoni Brum ◽  
Tania Weber Furlanetto

Goiter is more common in women, suggesting that estrogen could be involved in its physiopathology. The presence of classical estrogen receptors (ERαand ERβ) has been described in thyroid tissue, suggesting a direct effect of estrogen on the gland. A nonclassic estrogen receptor, the G-protein-coupled estrogen receptor (GPER1), has been described recently in several tissues. However, in goiter, the presence of this receptor has not been studied yet. We investigated GPER1 gene and protein expressions in normal thyroid and goiter using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. In normal thyroid (n=16) and goiter (n=19), GPER1 gene was expressed in all samples, while GPER1 protein was expressed in all samples of normal thyroid (n=15) but in only 72% of goiter samples (n=13). When comparing GPER1 gene and protein levels in both conditions, gene expression and protein levels were higher in normal thyroid than in goiter, suggesting a role of this receptor in this condition. Further studies are needed to elucidate the role of GPER1 in normal thyroid and goiter.


2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Ming Liu ◽  
Zikun Xie ◽  
Guang Sun ◽  
Liujun Chen ◽  
Dake Qi ◽  
...  

Abstract Background Osteoarthritis (OA) is the most prevalent form of arthritis and the major cause of disability and overall diminution of quality of life in the elderly population. Currently there is no cure for OA, partly due to the large gaps in our understanding of its underlying molecular and cellular mechanisms. Macrophage migration inhibitory factor (MIF) is a procytokine that mediates pleiotropic inflammatory effects in inflammatory diseases such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, data on the role of MIF in OA is limited with conflicting results. We undertook this study to investigate the role of MIF in OA by examining MIF genotype, mRNA expression, and protein levels in the Newfoundland Osteoarthritis Study. Methods One hundred nineteen end-stage knee/hip OA patients, 16 RA patients, and 113 healthy controls were included in the study. Two polymorphisms in the MIF gene, rs755622, and -794 CATT5-8, were genotyped using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) and PCR followed by automated capillary electrophoresis, respectively. MIF mRNA levels in articular cartilage and subchondral bone were measured by quantitative polymerase chain reaction. Plasma concentrations of MIF, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) were measured by enzyme-linked immunosorbent assay. Results rs755622 and -794 CATT5-8 genotypes were not associated with MIF mRNA or protein levels or OA (all p ≥ 0.19). MIF mRNA level in cartilage was lower in OA patients than in controls (p = 0.028) and RA patients (p = 0.004), while the levels in bone were comparable between OA patients and controls (p = 0.165). MIF protein level in plasma was lower in OA patients than in controls (p = 3.01 × 10−10), while the levels of TNF-α, IL-6 and IL-1β in plasma were all significantly higher in OA patients than in controls (all p ≤ 0.0007). Multivariable logistic regression showed lower MIF and higher IL-1β protein levels in plasma were independently associated with OA (OR per SD increase = 0.10 and 8.08; 95% CI = 0.04–0.19 and 4.42–16.82, respectively), but TNF-α and IL-6 became non-significant. Conclusions Reduced MIF mRNA and protein expression in OA patients suggested MIF might have a protective role in OA and could serve as a biomarker to differentiate OA from other joint disorders.


2018 ◽  
Vol 16 ◽  
pp. 205873921876729
Author(s):  
An Wan ◽  
Daodong Liu

Osteoporosis is a chronic multifactorial disease characterized by deterioration of bone mass and is vulnerable to bone fracture. Plasminogen activator inhibitor-1 (PAI-1) is an important molecule for maintenance of optimum bone mass. Several single-nucleotide polymorphisms (SNPs) in PAI-1 have been reported to alter PAI-1 expression and/or the translational level. In this report, we explored the possible role of common PAI-1 gene polymorphisms on predisposition to osteoporosis in a Chinese cohort. A total of 364 post-menopausal Chinese women diagnosed of having osteoporosis and 350 healthy females hailing from similar areas were enrolled in this study. Five common SNPs (−844G > A, −6754G/5G, +43G > A, +9785G > A and +11053T > G) were genotyped by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP). Relative expression of PAI-1 mRNA and plasma PAI-1 levels were quantified by reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Prevalence of homozygous mutant (5G/5G) and minor allele (5G) of PAI-1 (−675 4G/5G) polymorphism was significantly more frequent in patients than in healthy controls (5G/5G: P < 0.0001, odds ratio (OR) = 3.18; 5G: P < 0.0001, OR = 1.65). Both plasma PAI-1 and relative mRNA expression levels were significantly lower in patients compared to healthy controls. Interestingly, the quantity of plasma PAI-1 and mRNA expression was correlated with PAI-1 (−675 4G/5G) polymorphism: subjects with 4G/4G genotype had elevated PAI-1 in comparison to homozygous mutant, and displayed lower quantity of PAI-1 protein and mRNA values. PAI-1 (−675 4G/5G) mutant is associated with susceptibility to development of osteoporosis in post-menopausal Chinese women. Furthermore, this variant in the promoter region alters plasma protein levels and relative expression of PAI-1.


2017 ◽  
Vol 16 (4) ◽  
pp. 38-45
Author(s):  
D. A. Ryabchikov ◽  
I. K. Vorotnikov ◽  
T. P. Kazubskaya ◽  
S. S. Lukina ◽  
E. A. Filippova ◽  
...  

Background. Epigenetic changes of TSG are supposed as the most fine and active genes regulation mechanism in particular breast cancer (BC) genes pathway development. The most valuable results are awaited for methylation role of genes located on the short arm of chromosome 3 with also MGMT gene (10q26) in BC pathogenesis because of their ambiguous data for methylation status in tumors. Objective: to illustrate the specific methylation role of the RASSF1A, SEMA3B, RARß2, RHOA, GPX1, USP4, DAG1, NKIRAS1 and MGMT genes promoter regions in BC pathogenesis. Materials and methods. Sample set of 174 BC patients consists of tumor and surrounding histologically normal tissue that were collected and clinically characterized in the N.N. Blokhin National Medical Research Center of Oncology. Two substantive methods were used to evaluate DNA methylation status. To analyse RASSF1A, SEMA3B, RARß2 and MGMT genes methylation we used polymerase chain reaction specific for the methylated allele. Whereas for analyses RHOA, GPX1, USP4, DAG1, NKIRAS1 promoter regions genes methylation status was used methyl sensitive restriction analyses with 2 methyl sensitive endonuclaeses HpaII and HhaI with subsequent polymerase chain reaction. Results. A statistically significant high frequency of RASSF1A, SEMA3B, RARß2, and MGMT genes methylation in epithelial breast tumors compared with histologically normal tissue from the same patients was shown. Significant correlation of RARß2 and MGMT genes methylation frequency considering the different clinical and morphological characteristics of the malignant process was revealed. The statistically significant relationship between methylation of RASSF1A, RARß2 and MGMT genes and patient survival is shown for the first time. Conclusion. The findings of epigenetic changes in the luminal BC supplement the “molecular picture” of this cancer and contribute to an understanding of its pathogenesis. The revealed features of investigated genes methylation can find clinical application for the development of modern approaches to prognosis, prevention and choice of tactics for treatment of BC in females of the Moscow region.


Author(s):  
Sima SHAHROKHZADEH ◽  
Azam SOLEIMANI ◽  
Dor-Mohammad KORDI-TAMANDANI ◽  
Mohammad Hossein SANGTARASH ◽  
Omid NEJATI ◽  
...  

Background: Vesicoureteral reflux (VUR) disease is the most common type of urinary tract anomalies in children. Genetic risk factors may be associated with the etiology of VUR. The role of the Glutathione S-transferases (GSTs) as multifunctional enzymes is cellular oxidative stress handling. This is the first study aimed at evaluating the relative risk of GSTP1, GSTM1, and GSTT1 polymorphisms in VUR susceptibility in children and provides new important insights into the genetics of affected children. Methods: The study was done in 2013 in Sistan and Baluchestan University, eastern Iran. Genotyping of three GSTP1, GSTM1, and GSTT1 genes were determined using the multiplex polymerase chain reaction assay in 216 reactions for 72 VUR children and 312 reactions for 104 healthy controls. Results: The presence of GSTT1 deletion was associated with high risk of VUR in children, whereas GSTP1 and GSTM1 genotypes did not show the same effect. Furthermore, the combination of GSTT1/GSTM1 and GSTT1/ GSTP1 genotypes showed a significant influence on lower risk of VUR in children. Conclusion: Deletion of GSTT1 functional gene is a genetic risk factor causing VUR in children. Interestingly, the combination of GSTM1 and GSTP1 null genotypes with GSTT1 has shown a protective role against risk of GSTT1 deletion.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Anahita Rahmani ◽  
Danial Kheradmand ◽  
Peyman Keyhanvar ◽  
Alireza Shoae-Hassani ◽  
Amir Darbandi-Azar

Fluoxetine (FLX) is a selective serotonin reuptake inhibitor (SSRI). Its action is possibly through an increase in neural cell survival. The mechanism of improved survival rate of neurons by FLX may relate to the overexpression of some kinases such as Akt protein. Akt1 (a serine/threonine kinase) plays a key role in the modulation of cell proliferation and survival. Our study evaluated the effects of FLX on mesenchymal stem cell (MSC) fate and Akt1 phosphorylation levels in MSCs. Evaluation tests included reverse transcriptase polymerase chain reaction, western blot, and immunocytochemistry assays. Nestin, MAP-2, andβ-tubulin were detected after neurogenesis as neural markers. TenμM of FLX upregulated phosphorylation of Akt1 protein in induced hEnSC significantly. Also FLX did increase viability of these MSCs. Continuous FLX treatment after neurogenesis elevated the survival rate of differentiated neural cells probably by enhanced induction of Akt1 phosphorylation. This study addresses a novel role of FLX in neurogenesis and differentiated neural cell survival that may contribute to explaining the therapeutic action of fluoxetine in regenerative pharmacology.


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