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Scientists find key to 'turbo-charging' immune system to kill all cancers

RL_sparky

Senior Member
Messages
379
Location
California
Article Excerpts:

"A protein which ‘turbo-charges’ the immune system so that it can fight off any cancer or virus has been discovered by scientists.
In a breakthrough described as a ‘game-changer’ for cancer treatment, researchers at Imperial College found a previously unknown molecule which boosts the body’s ability to fight off chronic illnesses.
Scientists at Imperial College London, who led the study, are now developing a gene therapy based on the protein and hope to begin human trials in three years".

“This is a completely unknown protein. Nobody had ever seen it before or was even aware that it existed. It looks and acts like no other protein.”
The protein – named lymphocyte expansion molecule, or LEM, promotes the spread of cancer killing ‘T cells’ by generating large amounts of energy.
Normally when the immune system detects cancer it goes into overdrive trying to fight the disease, flooding the body with T cells. But it quickly runs out of steam."

"However the new protein causes a massive energy boost which makes T cells in such great numbers that the cancer cannot fight them off.
It also causes a boost of immune memory cells which are able to recognise tumours and viruses they have encountered previously so there is less chance that they will return."

http://www.telegraph.co.uk/news/sci...arging-immune-system-to-kill-all-cancers.html
 

drob31

Senior Member
Messages
1,487
It sounds like the immune system is dropping nuclear bombs. Like alex said, i wouldn't want to see an autoimmune side to that either.
 

lansbergen

Senior Member
Messages
2,512
http://www.sciencemag.org/content/early/2015/04/15/science.aaa7516.abstract

Protective CD8+ T cell–mediated immunity requires a massive expansion in cell number and the development of long-lived memory cells. Using forward genetics in mice, we identified an orphan protein named Lymphocyte Expansion Molecule (LEM) that promoted antigen-dependent CD8+ T cell proliferation, effector function, and memory cell generation in response to infection with lymphocytic choriomeningitis virus. Generation of LEM-deficient mice confirmed these results. Through interaction with CR6 interacting factor (CRIF1), LEM controlled the levels of oxidative phosphorylation (OXPHOS) complexes and respiration resulting in the production of pro-proliferative mitochondrial Reactive Oxygen Species (mROS). LEM provides a link between immune activation and the expansion of protective CD8+ T cells driven by OXPHOS and represents a pathway for the restoration of long-term protective immunity based on metabolically modified CTL.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
I don't really see how this could be used as a cancer therapy on its own, as it does not exploit any specific aspects to target cancer cells directly. I think it is more likely to be used as part of combination therapies, if it is to be used.

But that is if it actually works and is safe. They haven't yet shown whether it is worthwhile as a therapy in mice, let alone safety in humans. Wait a decade or two and we'll see.

Otherwise, it is also vaguely possible that it could be helpful for other diseases. Or as an adjuvant in vaccines...

See also:
http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_16-4-2015-14-51-47
 
Last edited:

heapsreal

iherb 10% discount code OPA989,
Messages
10,103
Location
australia (brisbane)
It sounds similar to the ms treatment where they increase t cell response to ebv. Expose t cells to an ebv vaccine and re infuse it back into the patient.

interesting research seems to be happening with different T cell treatments.

Would like to seem them improve nk cells.
 

Valentijn

Senior Member
Messages
15,786
LEM is created by the gene at C1orf177 (Chromosome 1 open reading frame 177 - doesn't have a proper name yet). 23andMe tests for 18 SNPs on C1orf177. rs9782980 is a missense mutation, C1orf177 G126C, with two very common possible alleles.

The minor allele frequency of T is 49.8%, meaning a calculated 24.8% of the population should have TT, though actual rates of TT are at about 30% for Europeans. For the 31 ME/SEID patients I have 23andMe data for, 48.4% have TT, which is quite a bit higher. 29% of the 31 controls have TT, in line with larger European samples.

There's not enough data regarding the protein for mutation modeling programs to determine the impact of the mutation. However under BLOSUM62 scoring, Glycine->Cysteine rates a -3 (worst possible is -4) which indicates a high likelihood of the substitution impacting the integrity of the protein.

So it might be having an impact, despite being very common, if the impact is triggered by certain events. Or it might just be random chance that our group has a higher frequency. And, of course, there are many coding SNPs on the gene which aren't tested by 23andMe, so there's no guessing what might or might not be going on with those.