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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.

The authors found that treatment with AS20 suppressed phorbol 12-myristate 13-acetate (PMA) and 5-flurouracil (5-FU) induction of COX2 expression. We also observed AS20 treated cells showed DNA fragmentation in HeLa cells.

The independent effects of metastasis-promoting gene CD151 in the process of metastasis are not known. This study aimed to isolate CD151 to discover what its role in metastasis would be uninfluenced by potential interactions with other components and pathways in human cells. Results showed that CD151 significantly increased the adhesion of the cells and decreased their motility. Thus, it may be that CD151 is upregulated in cancer cells for the last step of metastasis, and it increases the chances of success of metastasis by aiding in implantation of the cancer cells. Targeting CD151 in chemotherapeutic modalities could therefore potentially slow or prevent metastasis.

The authors test the antiproliferative and apoptosis-inducing properties of an extract created from a traditional Indian medicinal plant of the Amaranthus genus.

In this study, the authors investigate the effect of a herbal formulation on Cyclooxygenase-2 (COX-2) expression in cancer cells. High levels of COX-2 correlates with worsened cancer outcomes and the authors hypothesize that the formulation will inhibit COX-2 levels.