Treatments inhibiting Notch signaling pathways have been explored by researchers as a new approach for the treatment of glioblastoma tumors, which is a fast-growing and aggressive brain tumor. Recently, retinoic acid (RA) therapy, which inhibits Notch signaling, has shown a promising effect on inhibiting glioblastoma progression. RA, which is a metabolite of vitamin A, is very important in embryonic cellular development, which includes the regulation of multiple developmental processes, such as brain neurogenesis. However, high doses of RA treatment caused many side effects such as headaches, nausea, redness around the injection site, or allergic reactions. Therefore, we hypothesized that a combination treatment of RA and siRNA targeting NOTCH1 (siNOTCH1), the essential gene that activates Notch signaling, would effectively inhibit brain cancer cell proliferation. The aim of the study was to determine whether inhibiting NOTCH1 would inhibit the growth of brain cancer cells by cell viability assay. We found that the combination treatment of siNOTCH1 and RA in low concentration effectively decreased the NOTCH1 expression level compared to the individual treatments. However, the combination treatment condition significantly decreased the number of live brain cancer cells only at a low concentration of RA. We anticipate that this novel combination treatment can provide a solution to the side effects of chemotherapy.

The authors looked at how a 3D bioprinter could be used to model the blood brain barrier.

Disruption of the blood-brain barrier (BBB) is related to many neurological disorders, and can be caused by oxidative stress to cerebral microvascular endothelial cells (CMECs) composing the BBB. The authors of the paper investigated the protective effects of the total saponins in the leaves of Panax notoginseng (LPNS) on oxidative-stress-induced damage in a mouse cerebral microvascular endothelial cell line.

This study hypothesizes that nanoparticles derived from corn (cNPs)may have anti-proliferative effects on bone cancer and metastasized bone cancer. It finds that human osteosarcoma and human lung carcinoma metastasized to bone marrow cell viability decreased to 0% when treated with cNPs. Overall, these results indicate that cNPs have anti-proliferative effects on bone cancer cells and cancer cells that metastasize to the bone.

In this study, we aimed to characterize CD44-mediated regulation of the Wnt/β-catenin signaling pathway, which promotes cancer invasion and metastasis. We hypothesized that CD44 down-regulation will inhibit gastric cancer cell migration and invasion by leading to down-regulation of Wnt/β-catenin signaling. We found that CD44 up-regulation was significantly related to poor prognosis in gastric cancer patients. We demonstrated the CD44 down-regulation decreased β-catenin protein expression level. Our results suggest that CD44 down-regulation inhibits cell migration and invasion by down-regulating β-catenin expression level.

This paper hypothesized that the tumor microenvironment mediates cancer’s response to oxidative stress by delivering extracellular vesicles to cancer cells. Breast and lung cancer cells were treated with EVs, reavealing that EVs extracted from oxidatively stressed adipocytes increased the cell proliferation of breast cancer cells. These findings present a novel way that the TME influences cancer progression.

With disruption of DNA repair pathways pertinent to the timeline of cancer, thorough evaluation of mutations relevant to DNA repair proteins is crucial within cancer research. One such mutation includes S815L PMS2 - a mutation that results in significant decrease of DNA repair function by PMS2 protein. While mutation of PMS2 is associated with significantly increased colorectal and endometrial cancer risk, much work is left to do to establish the functional effects of the S815L PMS2 mutation in ovarian cancer progression. In this article, researchers contribute to this essential area of research by uncovering the tumor-progressive effects of the S815L PMS2 mutation in the context of ovarian cancer cell lines.

Wang and Gong developed a novel dynamic gene-searching algorithm called Dynamic Gene Search (DyGS) to create a gene panel for each of the 12 cancers with the highest annual incidence and death rate. The 12 gene panels the DyGS algorithm selected used only 3.5% of the original gene mutation pool, while covering every patient sample. About 40% of each gene panel is druggable, which indicates that the DyGS-generated gene panels can be used for early cancer detection as well as therapeutic targets in treatment methods.

Since cancer cells inhibit T-cell activity, the authors investigated a method to reverse T-cell disfunction with gene therapy, so that the T-cells would become effective once again in fighting cancer cells. They used the inhibition of proprotein convertases (PCSK1) in T cells and programmed death-ligand 1 (CD274) in cancer cells. They observed the recovery of IL-2 expression in Jurkat cells, with increased recovery noted in a co-culture sample. This study suggests a novel strategy to reactivate T cells.

A significant percentage of cancer survivors develop a second primary cancer. Using data of deceased patients provided by the Peninsula Regional Medical Center, Li and Holdai conducted a retrospective statistical analysis to investigate whether the type of the first cancer affects the occurrence time and type of the second primary cancer.