Prevalence of Hepatitis B Virus Markers among the Women with Breast Cancer.

INTRODUCTION: Breast cancer represents a formidable peril to the female populace on a worldwide level. The association between breast cancer and various factors, including viral infections, has been extensively investigated. Recently, the link between HBV infection and breast cancer patients has garnered attention. The present research aims to assess the prevalence of HBV markers among women diagnosed with breast cancer in Ahvaz city, Iran. MATERIALS AND METHODS: Serum specimens were procured from 90 patients who had been clinically diagnosed with breast cancer. The age of the patients ranged from 29 to 80 years, with a mean age of 49.42±10.7. Histological examination of biopsy specimens revealed that 75 (83.33%) were ductal, 11 (8.88%) lobular, 2 (2.22%) mucinous, 1 (1.11%) medullary, and 1 (1.11%) was metastatic. The serum samples were subjected to initial HBsAg and anti-HBc testing via ELISA. Samples that tested seropositive (HBsAg + anti-HBc) were subsequently analyzed for the S region of HBV through nested PCR and DNA sequencing. Finally, a phylogenetic tree was constructed for positive HBV DNA tests. RESULTS: Among the 5/90 (5.55%) cancer patients, it was found that 3 (3.33%) cases of ductal carcinoma and one (1.11%) lobular carcinoma displayed positivity for HBV markers (HBsAg, anti-HBc, HBV PCR). Notably, one (1.11%) patient with ductal carcinoma solely demonstrated anti-HBc positivity. The phylogenetic tree analysis of the S region revealed that all HBV strains identified were categorized as genotype D. CONCLUSION: The statistical analysis did not reveal any significant findings (p= 0.315) in the distribution of cancer types across different age groups. Among patients diagnosed with breast cancer, a notable prevalence of 5.5% was observed in HBV markers. The dominant HBV genotype among breast cancer patients was identified as genotype D.

Long non-coding RNA signatures and related signaling pathway in T-cell acute lymphoblastic leukemia.

T-cell acute lymphoblastic leukemia (T-ALL) is a malignancy caused by clonal proliferation of T-cell pre-cursors arising from the thymus. Although the optimized chemotherapy regimen could improve the outcome of such patients, some challenges such as higher risk for induction failure, early relapse and isolated central nervous system (CNS) relapse occurring in T-ALL patients are of great significance, leading to increased mortality rates. Long non-coding RNA (lncRNA) is a key component involved in cell signaling through a variety of mechanisms in regulating gene expression. Oncogenes and tumor suppressors are no exception and their expression can be affected by lncRNAs. In addition, accumulating researches in samples from T-ALL patients as well as pre-clinical studies in mice suggest that the expression profile of lncRNAs in T-ALL could be aberrant, resulting in deregulation of target genes and downstream signaling pathways. In addition, accumulating researches in samples from T-ALL patients as well as pre-clinical studies in mice suggest that the expression profile of lncRNAs in T-ALL could be aberrant, resulting in deregulation of target genes and downstream signaling pathways. These lncRNAs may be determinants of proliferation, apoptosis, and drug resistance observed in T-ALL. Thus, lncRNAs can be a good tool to develop novel strategies against cancer cells in the treatment of relapsed and refractory T-ALL. They can also act as promoting biomarkers in assessing T-ALL and differentiating between patients with poor prognosis and good prognosis.

The role of inflammatory mediators in the pathogenesis of periodic fever, aphthous stomatitis, pharyngitis and cervical adenitis (PFAPA) syndrome.

INTRODUCTION: As a recurrent disease, periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis (PFAPA) syndrome is characterized by episodes of febrile attacks and is often prominent in children under five years of age. However, the etiology of this condition has not been fully understood yet. MATERIALS AND METHODS: The search in the extensive literature of peer-reviewed articles published from the inception to December 2021 was conducted to identify the relevant studies, using the electronic databases of MEDLINE/PubMed, Embase, Scopus, the Cochrane Library, and the Web of Science. RESULTS: The analysis of complex relationships indicates that inflammatory factors, such as various cytokines and acute-phase proteins (APPs), play leading roles in the pathogenesis of this disease. Accordingly, this article summarizes the current state of knowledge to explain the mechanisms involved in inflammatory responses among patients with PFAPA syndrome and investigate its role in the pathogenesis of this disease. Moreover, the possibilities for further implementation of new therapeutic strategies are pointed out. CONCLUSION: It is concluded that some pathophysiological processes are associated with immune dysregulation, which itself may be secondary to environmental factors, genetic background, and underlying diseases, including latent infections that multiply inflammatory mediators. elevated inflammatory markers similarly play a significant part in the clinical outcomes of this condition, whose pyrogenic nature is the reason for the development of episodes of febrile attacks in the population of patients suffering from PFAPA syndrome.

Carcinogenic Risk Assessment among Children and Adult due to Exposure to Toxic Air Pollutants.

Health endpoint and risk of carcinogenic among people enhancement due to Exposures to toxic air pollutants. The purpose of this study was investigation of a carcinogenic risk assessment among children and adults due to exposure to toxic pollutants. A review study of literature was performed with seven hundred and twenty-six articles were retrieved based on Google Scholar, Web of Science, PubMed, Elsevier, and Springer databases. Studies reporting data on predetermined consequences potential toxic air pollutants and related to lifetime cancer risk (LCR) and hazard quotient (HQ) were used to assess carcinogenic and non-carcinogenic risk. The literature signs a notable undesirable affect from potential toxic air pollutants related to carcinogenic risk assessment among children and adult. Based on Result this study, the toxic air pollutants can endanger health of children and adult exposure to this pollutant and increase lifetime cancer risk number and carcinogenic risk among exposed people. Useful for health policymaker in order to cope with the incidence of cancer among citizenship Can be the main application the results of this study. Increasing the level of public awareness, especially of sensitive groups, about the incidence of cancer and its important factors and reduce exposures to toxic air pollutants are the main vital government actions for decrease the prevalence of cancer. Further research using more sophisticated methodology is warranted.

Impact of COVID-19 acute respiratory disease on the risk factors attributed to cancer patients.

Communicable diseases (CDs) based on Health organization reported are one of the most threat for human health. SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is the main pandemic that nowadays it threatens the health of people around the world, especially cancer patients. The purpose of this study was to investigate the effects of COVID-19 acute respiratory disease (COVID-19 ARD) on risk factors related to health of cancer patients. A review study of was conducted to base on results of various studies published. Nine hundred and eighty articles were retrieved based on various databases: Science Direct, Taylor & Francis, Google Scholar, Elsevier, PubMed and BMJ. In this study, were used the results of research on COVID-19 and its effects on risk factors attributed to cancer patients. The literature signs a notable undesirable affect from COVID-19 on risk factors attributed to health of cancer patients. Result showed that transfer SARS-CoV-2 viruses can endanger health of cancer patients due to interruption of the disease treatment process and increase number of deaths between in this patents. The survey requires the need to act creating healthy conditions to continue the treatment process and vaccination coverage among these patients in order to decrease the transmission of COVID-19 acute respiratory disease and increase the success rate of cancer treatment.

Introducing GATA3 as a prominent player in Crohn's disease.

AIM: This study was aimed at gene assessment of Crohn's disease (CD) through protein-protein interaction (PPI) network analysis to find crucial genes. BACKGROUND: CD is a major subtype of inflammatory bowel diseases (IBD), which affects gastrointestinal tract. PPI network analysis is a suitable tool to clarify a critical gene as a drug target or diagnostic biomarker for these types of diseases. METHODS: Gene expression profile GSE126124 of 20 CD patients and 20 healthy controls was obtained from the Gene Expression Omnibus (GEO) database. RNA profile of peripheral blood mononuclear cells (PBMCs) and colon biopsy samples of the studied groups was investigated. Crucial genes were selected and analyzed via the PPI network by Cytoscape software. Gene ontology enrichment for the hubs, bottlenecks, and hub-bottlenecks was performed via CluGO plugin of Cytoscape software. RESULTS: Eighty-one differentially expressed genes (DEGs) among 250 initial DEGs were highlighted as significant by FC>2 and p-value ≤ 0.05, and 69 significant DEGs were used for PPI network construction. The network was characterized by poor connections, so 20 top neighbors were added to form a scale-free network. The main connected component included 39 query DEGs and 20 added first neighbors. Three clusters of biological processes associated with crucial genes were identified and discussed. CONCLUSION: The results of this study indicated that GATA3 has a key role in CD pathogenesis and could be a possible drug target or diagnostic biomarker for Crohn's disease.