Science Bites seeks to compile the latest scientific research updates in bite-sized forms.

1. Cells for forming blood vessels can also produce tumours and facilitate their spread

Scientists have now proven that tumour production and their spread can stem from cells that are key to blood vessel formation.

Dr Lan Ko, a cancer biologist at Augusta University said, “Today we actually propose that blood vessels can form tumours and then the whole picture becomes a cycle.” She is a corresponding author of the study that offers some of the initial clues of the vicious cycle. It also serves as a potential new target for intervention.

Pericytes, contractile cells forming the blood vessel outer layer, are known to have properties similar to stem cells as they are able to form various tissue types. The gene, GT198, is known for its DNA repairing and stem cell regulating abilities. Usually, it is expressed in low levels in the body but, when mutated, could become an oncogene.

In pericytes of vascular networks supporting many human tumours like cancer in the brain, lung, kidney and prostate, researchers have discovered unusually high levels of GT198 in the cell cytoplasm. In human oral cancer, it was found that pericytes proliferated into tumour cells and detached from blood vessels to allow for spread.

“Blood vessels can actually make tumours. This is a bit of a new idea that does not negate the fact that tumours also make blood vessels. But we believe instead provides the other half of the story,” explained Ko.

Upon administering a vaccine against GT198 in mice, tumour growth was slowed and mouse survival was prolonged. Hence, GT198 could serve as an efficient and effective cancer treatment target, according to Ko.

2. New insulin-producing cell discovered in pancreas

Mark Huising from the University of California worked as a lead researcher with a team to study diabetes by dissecting and observing pancreatic cells and their reactions from tissue in the lab.

“We've seen phenomenal advances in the management of diabetes, but we cannot cure it. If you want to cure the disease, you have to understand how it works in the normal situation,” he said.

As the main issue in Type 1 diabetes is the knock-off of pancreatic beta cells, scientists have tried to find a treatment and assumed that the division of other adult beta cells was the one main way for the production of beta cells. However, Huising and his team have found a novel cell type around the islet cell edges. They appear similar to immature beta cells.

Upon examining, these virgin beta cells can make insulin but could not serve as mature beta cells due to the lack of glucose receptors. Not only that, the team observed the unexpected transition of some mature beta cells into alpha cells.

“There's much more plasticity in the system than was thought,” said Huising.

Huising explains that there is cause to be thrilled from this as it marks a discovery of a new beta cell population in both humans and mice that was previously unknown. Also, a possible new source of beta cells for diabetic treatment could be found here.

He adds, “Finally, understanding how these cells mature into functioning beta cells could help in developing stem cell therapies for diabetes.”

3. Rab32 found to play a role in multiple sclerosis development

The cause of multiple sclerosis has always been poorly understood. Nevertheless, mitochondria, the cellular “powerhouse”, have been thought to play a role in causing this debilitating disease.

Researchers from the Universities of Exeter and Alberta used human brain tissue samples and discovered that a protein, Rab32, is abundantly present in the brains of those diagnosed with multiple sclerosis, while in healthy brain cells, they are almost undetectable.

These scientists found that the part of cell that stores calcium gets too near the mitochondria in cells where there is Rab32. Subsequently, the miscommunication with the calcium supply causes the mitochondria to misbehave. This leads to brain cell toxicity in patients with multiple sclerosis.

The reason for Rab32 influx into the cell is not yet known, but scientists suspect there could be a defect stemming from the cellular base.

Results from this study will aid in discovering effective treatments for the disease that target Rab32 and pave the way for investigating other proteins linked to the disease. Professor Paul Eggleton from the University of Exeter noted the severity of multiple sclerosis and its devastating effects.

He added, “Our exciting new findings have uncovered a new avenue for researchers to explore. It is a critical step, and in time, we hope it might lead to effective new treatments for MS.” MIMS

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