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Flood Kuhn posted an update a month ago
Currently, the immunotherapy approved for gastric cancer is immune checkpoint blockade( ICB) therapy. The effects of ICB depend on the T cell-mediated immune response elicited at the cancer site. Adenosine disodium triphosphate clinical trial Based on the results of previous clinical trials, it is clear that an enhanced immune response to cancer improves prognosis. Thus, the development of biomarkers to predict local immune responses may increase the significance of future immunotherapy for gastric cancer. Biomarker research has clearly progressed with the rapid development of genetic analysis technologies, enabling the analysis of data from clinical trials. Not only the molecular biomarkers known to date for ICB biomarkers, but immune cells that influence ICB therapy are also reviewed in this article.There have been many reports on the association between tumor infiltrating lymphocytes and cancer prognosis. It is known that tumor infiltrating lymphocytes contain not only cytotoxic T lymphocytes but also bystander lymphocytes and immunosuppressive cells. In most of previous reports, tumor infiltrating lymphocytes were defined as CD3 or CD8 T cells. It is generally thought that patients with cancer rich in tumor infiltrating lymphocytes have a good prognosis. Most tumor infiltrating lymphocytes are thought to be cytotoxic T lymphocytes. It is also reported that cancer rich in tumor infiltrating lymphocytes is responsive to immune checkpoint inhibitors. In recent years, several reports revealed clonal replacement in tumor infiltrating lymphocytes after administration of immune checkpoint inhibitors. This change was also detectable in peripheral blood. From the viewpoint of lung cancer treatment, combination of immune checkpoint inhibitors and chemotherapy became the standard therapy. We need to understand the tumor immune microenvironment in order to select the best treatment regimen for each patient. However, it is often difficult to obtain an adequate amount of tissue biopsy sample in standard of care. It is hoped that we can understand the tumor immune microenvironment using the peripheral blood. Thus, studying the association between treatment response, tumor infiltrating lymphocytes, and peripheral blood is considered to be important to research and develop peripheral blood biomarkers in lung cancer.Advances in sequencing technology have been reported to show cancer driver mutations with aging in a variety of normal tissues at very small clone sizes. In the normal esophagus, prior to carcinogenesis, clones that had acquired driver mutations in esophageal cancer, mainly NOTCH1 mutations, during early life appeared multi-centrically. With aging, the number of driver mutations increased and the clones expanded. In the elderly, most of the normal esophagus was replaced by clones with driver mutations. In contrast, in normal colorectal epithelium, about 1% of crypts contain driver mutations even in the 50s. In normal hepatocytes, age-related mutations are rarely detected. These results suggest that the frequency of detection of driver mutations in normal tissues varies greatly among tissues. The panorama of aging and cancer remains veiled.
Coma is the most serious disturbance of consciousness, which affects the life quality of patients and increases the burden of their family. Studies to assess the prognostic value of neuron-specific enolase (NSE) in patients with coma have not led to precise, generally accepted prognostic rules. The study aims to assess the correlation between NSE and prognosis of coma and the predictive value of NSE for clinical prognosis.
A search was conducted using PubMed, Web of Science, EMBASE, Cochrane Library, China National Knowledge Infrastructure (CNKI), and WanFang Data from the establishment time of databases to December 2019. This analysis included patients with coma, regardless of how long the coma was. In total, 26 articles were retrieved and included in the review.
The meta-analysis revealed the NSE concentration of patients with coma is significantly higher than that of the control group (standard mean difference = 0.88, 95% confidence interval 0.63-1.12, p < 0.05). The pooled sensitivity and specificity of NSE in coma diagnosis was 0.5 (95% CI 0.39-0.61) and 0.86 (95% CI 0.71-0.94).
The NSE concentration of patients with poor coma prognosis is significantly higher than that of the control group. The high NSE concentration is not necessarily a poor prognosis for coma, but low NSE concentration indicates a high probability of a good prognosis for coma.
The NSE concentration of patients with poor coma prognosis is significantly higher than that of the control group. The high NSE concentration is not necessarily a poor prognosis for coma, but low NSE concentration indicates a high probability of a good prognosis for coma.According to the 2018 GLOBOCAN database, colorectal cancer is one of the most common malignancies and leading causes of cancer-related death worldwide. During the last decades, considerable progress has been made in understanding the complex pathogenetic mechanisms involved in this neoplastic disease. Due to the need to improve treatment responses and clinical outcomes of colorectal cancer patients, the identification of new molecular biomarkers became a crucial spot in clinical oncology. As biological indicators of a specific pathological or physiological process, molecular markers play a central role in cancer detection, diagnosis, outcome prediction, and treatment choice. Considering the existing evidence that malignancies originating from distinct colonic regions behave differently, it is clear that specific biomarkers can be associated to right- or left-sided colon carcinomas, reflecting the distinct molecular signatures of these different tumor entities. The aim of this review is to summarize the main differences among tumors arising from proximal and distal colon in terms of current and emerging biomarkers.
Recent reports have corroborated that micro-RNAs (miRs) are related to the pathological changes of cerebral ischemia-reperfusion (CIR) induced injury. This work aimed to unearth the role and potential mechanism of miR-325-3p in regulating neuronal survival in CIR injury.
To conduct this investigation, we established an in vitro model of CIR injury by subjecting neurons to oxygen-glucose deprivation and reoxygenation (OGD/R). Gain and loss of function of miR-325-3p and receptor-interacting serine-threonine kinase 3 (RIP3) in neurons were performed to observe its effect on cell apoptosis and the release of lactate dehydrogenase. The levels of miR-325-3p and RIP3 in neurons were detected by qRT-PCR. Western blot was employed to inspect the levels of caspase3, Bax, and Bcl-2, as well as p38 and JNK phosphorylation. The relationship between miR-325-3p and RIP3 was detected by TargetScan and validated by dual-luciferase reporter assay.
Firstly, miR-325-3p expression was obviously downregulated while RIP3 expression was upregulated in neurons following OGD/R treatment.