Vitamin D and cancer

Vitamin D is correlated with many health benefits, including lower cancer risk; but until now, the link has always been unclear. McGill researchers have uncovered a piece of the puzzle, explaining how the vitamin may help to prevent cancer.

In a recent study published in the Proceedings of the National Academy of Sciences, researchers from the departments of medicine and physiology, John White, and David Goltzman, discovered a mechanism in vitamin D that slows the multiplication of cancer cells. Previously, researchers saw a relationship between consumption of vitamin D supplements and a reduced risk of certain cancers, but the omplete reasons for this relationship are still not well understood.

Vitamin D plays a role in controlling epidermal differentiation and cell proliferation— two processes that run rampant in cancerous cells. Specifically, it controls a protein called cMYC—a transcription factor or protein that controls genetic expression.

When White and Goltzman applied vitamin D to human cancer cells, they saw a reduction in cMYC, and cell multiplication slowed. The vitamin played two roles: it reduced the production of cMYC, and caused the cells to manufacture a protein that destroyed cMYC. Applying vitamin D to the skin of mice yielded similar results.

These findings may be of particular interest to residents of northern climates, as sun exposure is a major source of vitamin D replenishment. Indeed, the Canadian Cancer Society recommends a supplement of 1000 IU per day for the average adult.

Hydrogen embrittlement

In high-performance metals, there is a delicate balance between bending and breaking. Ductile metals, like copper, can be easily bent and worked; brittle metals like cast iron are stronger, but break more easily. One unexplained problem that has plagued metallurgists is that of ‘hydrogen embrittlement.’ In this process, hydrogen atoms penetrate the structure of the metal and cause it to lose ductility and fracture easily.

In certain materials, like high-strength steel, hydrogen embrittlement is more common. This is also the case in metals with more exposure to the element. For example, zirconium alloys, high-performance metals used in nuclear reactors, are susceptible to hydrogen embrittlement during cooling accidents. Hot steam reacts with the metal to form hydrogen gas, which in turn, leaches into the zirconium alloy, weakening the metal, and causing it to corrode.

A new study, published last month in Nature Materials, may shed light on the causes of hydrogen embrittlement. The study, conducted by Assistant Professor Jun Song of McGill materials engineering, and Professor William Curtin, director of mechanical engineering at École Polytechnique Fédérale de Lausanne, used a combination of computer models and experiments to create a method for predicting the phenomenon. It turns out, that the process is likely due to hydrogen, filling miniscule spaces in the metallic structure that normally give leeway for movement.

The researchers hope that this study will open new avenues for embrittlement-proof materials.

Autism spectrum disorders

Autism spectrum disorders (ASDs) encompass a variety of neurodevelopmental diseases including autism, Asperger syndrome, and Rett’s disorder. Essentially, ASDs affect the development of the brain.

Professor Nahum Sonenberg of McGill’s department of biochemistry, faculty of medicine, and researcher at the Goodman Cancer Research Centre, recently uncovered a new avenue of research that may lead to further understanding ASDs.

Sonenberg’s lab focuses on clarifying the role of dysregulated protein synthesis in cancer. They were surprised to discover that there are similarities between the irregular protein synthesis in cancer and that in ASD. Using a model mouse, they showed that irregular protein synthesis, resembling that of ASD patients, have an increased production of compounds, known as neurologins.

Neurologins are important for transferring information in the body through neurons—cells that send electrical signals. Using computer modeling, the team was able to identify the unique structures of mRNA—molecules that transfer genetic information from DNA to form proteins—of the neurologins that could be responsible for causing their irregular behaviour.

They found that dysregulated synthesis of neurologins increases cell signaling in the brain. This increase seems to result in an imbalance between excitation and inhibition of single brain cells. Although there is much more progress to be made in the treatment of ASD, these findings may be of particular interest to autism research, as they open up a new area of study that has yet to be fully explored.