Evolution has driven organisms to develop a wide range of biological mechanisms to protect against cancer. Some organisms, including the sponge Tethya wilhelma and the Placozoa Trichoplax adhaerens have developed particularly effective mechanisms to suppress cancer and repair DNA damage. While these mechanisms are rooted in DNA damage repair and prevention, evidence of bacteria may suggest that endosymbionts living within the organisms may plays a role as well. Likewise, other organisms, such as the flatworm Macrostomum lignano, are proven model organisms whose extensive documentation enables more in-depth analysis of biological mechanisms associated with cancer. Sponges, flatworms, and Placozoa were exposed to X-ray radiation totaling 600 Gy, 25 Gy, and up to 240 Gy, respectively. RNA sequencing and bioinformatics analyses were undergone to determine the differential gene expression of the animals at different time points. No common response to the X-ray radiation was discovered amongst all organisms. Instead, sponges showed evidence of tumor suppression and DNA repair gene upregulation including CUBN, bacterial endosymbionts showed evidence of lateral gene transfer and different DNA repair genes including FH, and flatworms showed evidence of allelic and mutational shifts in which tumorous populations became more reliant on alternate alleles and a single variant signature. This study highlights the varying mechanisms that have evolved in different organisms and the importance of studying these novel model organisms further.

An immune regulatory network was constructed for the purpose of identifying target regulators in malignant pleural mesothelioma for therapies. An identified causal flow linked a mutation of D-dopachrome tautomerase to a heightened expression of regulator ASH1L and consequent down regulation of chemokine CCL5 and invasion of CD8+ T cells. Experimental validation of this initial use case indicates mRNA expression of CCL5 within the tumor cells and subsequent protein expression and secretion. Further analyses will explore the migration of CD8+ T cells in response to the chemotactic CCL5.

Obesity increases the risk for colorectal cancer. In mice, a pro-obesity high-fat-diet (HFD) leads to an intestinal phenotype characterized by enhanced proliferation, numbers, function and tumor-initiating capacity of stem cells, the cell-of-origin for many intestinal cancers. This phenotype is driven by a lipid metabolism program facilitated by an intrinsic Peroxisome Proliferator-Activated Receptor/Fatty Acid Oxidation (PPAR/FAO) axis that senses and utilizes cellular lipids. However, the microbiome is a known regulator of lipid metabolism in the gut, but little is understood about how the gut commensals affect access to the lipids and alter stem cell function. Here, we use the long term HFD-fed mouse model to analyze the phenotypic changes in the intestinal stem cells (ISCs) after depletion of the gut microbiota. We find that the loss of the gut microbiome after four weeks of antibiotic treatment imposes significant changes in ISC function leading to reduced HFD ISC regenerative potential. These results indicate that the gut microbiome plays a crucial role in the lipid metabolic process which regulates and maintains the HFD ISC phenotype, and further suggests that the gut microbiome may augment the diet-induced tumor initiating capacity by altering the stem cell function.

This paper examines the physics behind cancer treatment and more specifically radiation therapy. A phenomenon known as Compton scattering has played a substantial role in the treatment of breast cancer and improvement of lives of women around the world. Through Compton scattering, radiation therapy has been tremendously improved and has allowed for the most accurate and effective treatment in breast cancer patients today.