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The authors looked at genes and pathways that are enriched in glioblastoma multiforme.

With herbal plants providing an address to the adverse effects of oxidative stress found within the body, the authors of this article develop and assess a novel compound (“MAT20”) that blends three herbal plants for optimal oxidative stress relief.

In this article, the authors analyzed ribosome profiling data from amino acid-starved pancreatic cancer cells to explore whether the pattern of ribosome distribution along transcripts under normal conditions can predict the degree of ribosome stalling under stress. The authors found that ribosomes in amino acid-deprived cells stalled more along elongation-limited transcripts. By contrast, they observed no relationship between read density near start and stop and disparities between mRNA sequencing reads and ribosome profiling reads. This research identifies an important relationship between read distribution and propensity for ribosomes to stall, although more work is needed to fully understand the patterns of ribosome distribution along transcripts in ribosome profiling data.

Polo-like kinase 1 (Plk1) is a master regulator of mitosis, initiating key steps of cell cycle regulation, and its overexpression is associated with certain types of cancer. In this study, the authors carefully designed peptides that were able to bind to Plk1 at a location that is important for its proper localization and function. Future studies could further develop these peptides to selectively target Plk1 in cancer cells and induce mitotic arrest.

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.

In this work the authors investigate new possible treatment methods for gastric and bladder cancers. They specifically targeted the transient receptor potential cation subfamily M member 7 (TRPM7), an ion channel that plays an important role in the survival of both of these cancers, and extracellular regulated kinases (ERKs),which contributes to the carcinogenesis of many cancers including gastric cancer. As a result, the authors consider the effects of Ginsenoside Rd, NS8593, curcumin, and icariin , known to inhibit TRPM7 and ERK. The authors found that these treatments decrease proliferation and induce apoptosis in studies of gastric and bladder cancer cells.

In this study, the authors looked at a proto-oncogene, KRAS, and searched for molecules that are predicted to be able to bind to the inactive form of KRAS. They found that a modified version of Irbesartan, a derivative of benzimidazole, showed the best binding to inactive KRAS.

Although the 5-year survival rate for colorectal cancer is below 10%, it increases to greater than 90% if it is diagnosed early. We hypothesized from our research that analyzing non-synonymous single nucleotide variants (SNVs) in a patient's exome sequence would be an indicator for high genetic risk of developing colorectal cancer.

Cancer is often caused by improper function of a few proteins, and sometimes it takes only a few proteins to malfunction to cause drastic changes in cells. Here the authors look at the genes that were mutated in patients with a type of pancreatic cancer to identify proteins that are important in causing cancer. They also determined which proteins currently lack effective treatment, and suggest that certain proteins (named KRAS, CDKN2A, and RBBP8) are the most important candidates for developing drugs to treat pancreatic cancer.

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.