The Science Dragon

Let’s make clear what these studies mean. These are Genome-Wide Association Studies (’GWAS’ as they tend to be shortened to). What they do is analyze the genetics of a large group of control people who are non-sufferers of the conditions (almost 11,000 people in this study) and then they analyze the genetics of a large pool of people who suffer from the condition (around 3500 in this case). They then run that data through complicated programs that compare the two sets of data, looking for mutations/specific sequences/alleles in the sufferers and seeing whether the probability of those being present in the sufferers of the condition is higher than that in the general population (the control group). It can be areas of protein-coding DNA and it can be in non-coding DNA so it is not necessarily a mutated protein you are looking at but may well be involved in regulation of protein production, in chromosomal packaging, in protein-DNA binding, in the splicing of RNA, pretty much anything to do with DNA running your cells.

Scarring basically occurs because of extensive healing processes become harder the larger/more serious the wound. If you get a paper cut, the skin and fibroblasts can migrate and plug the hole in your skin without too much difficulty. However when larger damage is done, say during surgery, the healing process is much more difficult. There are more layers to fix, greater distances to migrate, a far larger disruption in the extracellular matrix (the area that surrounds the cells within your body and keeps them ‘happy’ and behaving how you would like) which affects how the cells and structures within that wound respond. Because of this, the body can struggle to heal these big wounds properly. You get a battle for power between an inflammatory, protective response at the site of a large wound and a healing response. In large wounds with a big inflammatory/immune response, you get improper collagen reformation and scarring.

Although this method is far from being adopted as a treatment, technique devised here by the group seems to be incredibly promising and, at the very least, it has shown that developing methods to re-introduce insulin-producing cells back into the body of Type 1 diabetes sufferers is not only possible on paper but is possible with today’s technology. By using a unique ‘gel’, the group has found a way to introduce these homogenized, engineered cells without causing the typically seen inflammatory response, reducing the need for inflammation suppressive drugs and reducing the chance of inflammation caused damage. Engineering the cells and growing them with the patient’s own plasma has limited the chance for rejection as well making this a viable long term solution. This group has even shown that it works long term with a trial patient to the point of not needing to depend on insulin injections over the course of the 12-month follow-up study.

Obviously, this will only work in Type 1 diabetes as Type 2 sufferers are not insulin-sensitive any longer and still have their beta Islet of Langerhan pancreas cells (the ones that produce insulin).

I got an email from tumblr the other day telling me that my blog recently turned 2! It seems crazy to think it’s been that long and even stranger to think I’ve spent a lot of that time too busy to update but I’m looking to find more time to get back into updating it. My master’s degree is winding up in about a month and so I’ve been pulling extra time in the lab to try and wrap things up which has been taking most of my time. I will be going almost immediately onto a PhD project starting this summer that I’m very excited about but it also means I don’t have a huge amount of time to prepare (no doubt that will add to my workload and slow updates). But the good news is that all of the extra bits of coursework for my master’s degree is now completed meaning that I should be a little less busy for the time being and can back to giving updates on the world of science. I’ve missed sharing so much good science while I was away but I will do my best to make up for it!

IMM-101 is a suspension of heat-inactivated Mycobacterium obuense. Cancers, especially solid tumors, create an environment inside of themselves which suppresses the immune response by releasing and presenting chemicals that tell the immune system to stop responding effectively; chemicals we have naturally to stop our immune system getting out of control when fighting normal infections. This means that cancer-specific immune cells target the tumor but are quickly ‘switched off’ when they arrive there. This new treatment aims to switch them back on so that the immune system can fight the tumor rather than relying on damaging drugs like we currently do. 

Although the cells that respond to the Mycobacterium obuense are not the same cells that are fighting the cancer, they produce chemokines (chemical signals) that alert surrounding cells of the infection and so activates them in preparation for fighting an infection. This process is unspecific and so the immune system responding strongly to the Mycobacterium infection has the knock-on effect of creating more effective cancer-fighting immune cells by overcoming the suppression signal that they are getting from the tumor cells.

In this trial the IMM-101 was also given alongside Gemcitabine; a nucelotide mimic which kills cells faster the quicker they divide. As cancers are fast growing, the Gemcitabine kills cancer cells more readily than other body cells and when these cells die, they release cancer-defining proteins that the immune system can use to identify and then target the rest of the cells. This propagates the immune response.