Establishing and Characterizing Patient-Derived Breast Cancer Cell Lines

Commercial cancer cell lines have long been extensively used as an important platform to study cancer. They have contributed to a plethora of discoveries in the field of cancer research. However, there are limitations with using these cell lines, such as induced mutations over the long-term in vitro culture. These mutations cause incorrect exhibition of the in vivo characteristics of the cancer cells. Here, we focused on establishing Patient-derived breast cancer cell lines and attempted to characterize them in terms of several biomarkers that are shown to be overexpressed in breast cancer cells. Patient-derived breast cancer cell lines are more reliable tools to study the molecular and cellular processes taking place in vivo, since they are freshly isolated from the tumor biopsy and do not undergo induced immortalization. We explored the CK19, Ki67, vimentin, EpCAM, E-cadherin, and N-cadherin expression in three successfully established patient-derived breast cancer cell lines

Oncolytic paramyxoviruses-induced autophagy; A prudent weapon for cancer therapy

Oncolytic virotherapy has currently emerged as a promising approach upon which scientists have been able to induce tumor-specific cell death in a broad spectrum of malignancies. Paramyxoviruses represent intrinsic oncolytic capability, which makes them excellent candidates to be widely used in oncolytic virotherapy. The mechanisms through which these viruses destroy the cancerous cells involve triggering the autophagic machinery and apoptosis in target cells. Interestingly, oncolytic paramyxoviruses have been found to induce autophagy and lead to tumor cells death rather than their survival. Indeed, the induction of autophagy has been revealed to enhance the immunogenicity of tumor cells via the release of damage-associated molecular patterns (DAMPs) and the activation of autophagy-related immunogenic cell death (ICD). Subsequent cross-presentation of tumor-associated antigens (TAA) through the MHC-I complex to CD8+ T cells results in the productive priming of the tumor-specific immune response. In this review, we first briefly discuss autophagy and explain the process of viral xenophagy. Finally, we focus on the interactions between virus and autophagy proteins, elaborating on the global preclinical studies on oncolytic paramyxoviruse

Correction: Oncolytic paramyxoviruses-induced autophagy; A prudent weapon for cancer therapy (Journal of Biomedical Science (2019) 26 (48) DOI: 10.1186/s12929-019-0542-9)

After publication of this article [1], it was brought to our attention that there are some errors in the section of 'Authors' contributions'. The correct Authors' contributions should be: MK, FS, and AG collected literature, designed and wrote the manuscript. FS and MM edited and prepared the manuscript for submission. All authors read and approved the final manuscrip

Association between Epstein-Barr virus infection and gastric cancer: A systematic review and meta-analysis

Background: Numerous studies conducted over the past 30 years have pointed to the presence of Epstein-Barr virus (EBV) in gastric cancer samples. This study was aimed to provide a meta-analytic review of the prevalence of EBV in gastric cancer patients, and to clarify the relationship between EBV infection and gastric cancer. Methods: A literature search was performed electronically using online databases for English language publications until July 1, 2019. The pooled EBV prevalence and 95 confidence intervals (CIs) were estimated using a random-effects model. To determine the association between EBV and gastric cancer, pooled odds ratio (OR) and its 95 CI were computed for case-control studies. Two separate analyses were performed on data from case-control studies with matched and non-match pairs designs to calculate the pooled estimates of ORs. Results: The pooled prevalence of EBV in 20,361 gastric cancer patients was 8.77 (95 CI: 7.73-9.92; I2 = 83.2). There were 20 studies with matched pairs design, including tumor and tumor-adjacent normal tissue pairs from 4116 gastric cancer patients. The pooled ORs were 18.56 (95 CI: 15.68-21.97; I2 = 55.4) for studies with matched pairs design and 3.31 (95 CI: 0.95-11.54; I2 = 55.0) for studies with non-matched pairs design. The proportion of EBV-associated gastric cancer among male cases was significantly higher than among female cases (10.83, vs. 5.72) (P < 0.0001). However, the pooled OR estimate for EBV-associated gastric cancer was significantly higher among females (21.47; 95 CI: 15.55-29.63; I2 = 0) than in males (14.07; 95 CI: 10.46-18.93; I2 = 49.0) (P = 0.06). EBV was more prevalent in the cardia (12.47) and the body (11.68) compared to the antrum (6.29) (P = 0.0002). Conclusions: EBV infection is associated with more than 18 times increase the risk of gastric cancer. Although the prevalence of EBV was higher in male patients than in female patients with gastric cancer, women are more likely than men to develop EBV-associated gastric cancer. Our findings showed that using tumor-adjacent normal tissues as the control group provides more robust and accurate results regarding the relationship between EBV infection and gastric cancer. © 2020 The Author(s)

Metabolic host response and therapeutic approaches to influenza infection

Based on available metabolomic studies, influenza infection affects a variety of cellular metabolic pathways to ensure an optimal environment for its replication and production of viral particles. Following infection, glucose uptake and aerobic glycolysis increase in infected cells continually, which results in higher glucose consumption. The pentose phosphate shunt, as another glucose-consuming pathway, is enhanced by influenza infection to help produce more nucleotides, especially ATP. Regarding lipid species, following infection, levels of triglycerides, phospholipids, and several lipid derivatives undergo perturbations, some of which are associated with inflammatory responses. Also, mitochondrial fatty acid β-oxidation decreases significantly simultaneously with an increase in biosynthesis of fatty acids and membrane lipids. Moreover, essential amino acids are demonstrated to decline in infected tissues due to the production of large amounts of viral and cellular proteins. Immune responses against influenza infection, on the other hand, could significantly affect metabolic pathways. Mainly, interferon (IFN) production following viral infection affects cell function via alteration in amino acid synthesis, membrane composition, and lipid metabolism. Understanding metabolic alterations required for influenza virus replication has revealed novel therapeutic methods based on targeted inhibition of these cellular metabolic pathways

Balantidiasis in the gastric lymph nodes of Barbary sheep (Ammotragus lervia): an incidental finding

A 4-year-old female Barbary sheep (Ammotragus lervia) was found dead in the Gwangju Uchi Park Zoo. The animal had previously exhibited weakness and lethargy, but no signs of diarrhea. The carcass was emaciated upon presentation. The main gross lesion was characterized by severe serous atrophy of the fat tissues of the coronary and left ventricular grooves, resulting in the transformation of the fat to a gelatinous material. The rumen was fully distended with food, while the abomasum evidenced mucosal corrugation with slight congestion. Microscopic examination revealed the presence of Balantidium coli trophozoites within the lymphatic ducts of the gastric lymph node and the abdominal submucosa. On rare occasions, these organisms may invade extra-intestinal organs, in this case the gastric lymph nodes and abomasum

Deciphering the complex signalling systems that regulate intestinal epithelial cell death processes and shedding

Intestinal epithelial cells play a fundamental role in maintaining homeostasis. Shedding of intestinal cells in a controlled manner is critical to maintenance of barrier function. Barrier function is maintained during this shedding process by a redistribution of tight junctional proteins to facilitate closure of the gap left by the shedding cell. However, despite the obvious importance of epithelial cell shedding to gut health a central question is how the extrusion of epithelial cells is achieved, enabling barrier integrity to be maintained in the healthy gut and restored during inflammation remains largely unanswered. Recent studies have provided evidence that excessive epithelial cell shedding and loss of epithelial barrier integrity is triggered by exposure to lipopolysaccharide (LPS) or tumour necrosis factor (TNF). Subsequent studies have provided evidence of the involvement of specific cellular components and signalling mechanisms as well as the functionality of microbiota that can be either detrimental or beneficial for intestinal barrier integrity. This review, will focus on the evidence and decipher how the signalling systems through which the mucosal immune system and microbiota can regulate epithelial cell shedding and how these mechanisms interact to preserve the viability of the epithelium

Tissue Invasion by Entamoeba histolytica: Evidence of Genetic Selection and/or DNA Reorganization Events in Organ Tropism

Entamoeba histolytica infection may have various clinical manifestations. Nine out of ten E. histolytica infections remain asymptomatic, while the remainder become invasive and cause disease. The most common form of invasive infection is amebic diarrhea and colitis, whereas the most common extra-intestinal disease is amebic liver abscess. The underlying reasons for the different outcomes are unclear, but a recent study has shown that the parasite genotype is a contributor. To investigate this link further we have examined the genotypes of E. histolytica in stool- and liver abscess-derived samples from the same patients. Analysis of all 18 paired samples (16 from Bangladesh, one from the United States of America, and one from Italy) revealed that the intestinal and liver abscess amebae are genetically distinct. The results suggest either that E. histolytica subpopulations in the same infection show varying organ tropism, or that a DNA reorganization event takes place prior to or during metastasis from intestine to liver