Researchers at Stanford University, CA, have taken the first step in developing a tool that can trace the origin of certain types of cancer from the biological signature of their mutated cells. They believe the tool will help doctors decide the best treatments for their patients.
The interdisciplinary team of chemists, oncologists and one statistician describes how it created and tested the tool on a cancer gene related to lymphoma in the Proceedings of the National Academy of Sciences.
This gives extra information that could be prognostic.
The research team explains that while different genes can give rise to the same cancer, in some cases, the aggressiveness and type of treatment will depend on which particular cancer gene - called oncogene - triggered it in the first place.
Team investigated a cancer gene known to trigger half of all human cancers
An oncogene is a normal gene that has mutated - its DNA has been disrupted in some way - causing cells to dysfunction and become cancerous.
An oncogene is a normal gene that has mutated, causing cells to dysfunction and become cancerous.
For their study, the researchers decided to investigate MYC, an oncogene that is related to lymphoma and is known to trigger around half of all human cancers.
The oncogene is known to regulate many biological functions in cancer cells - including glucose and glutamine metabolism.
When cancer takes place, the cell loves to gobble up glucose - that's a sugar - and glutamine. It takes those and makes different lipids - different fatty molecules than what it normally makes.
The researchers used a combination of sophisticated statistical tools and "desorption electrospray ionization mass spectrometry imaging (DESI-MSI)" to investigate changes in fatty molecules in MYC-induced lymphoma in animal models and cell samples.
New tool traced 86 fatty molecules back to the cancer gene
Using the new method, they managed to trace not just one, but 86 fatty molecules or lipids back to the oncogene.
Then using human lymphoma samples with varying expression levels of MYC oncoprotein, they showed that lymphomas with high MYC expression had a distinct lipid profile compared to those with low expression.
They also found that the lipid profiles of the human lymphoma samples contained many lipids that were also significant in MYC-induced animal lymphomas.
The researchers say the next step will be to work out what the causal mechanism is - while we now have a much clearer picture of the link between cancer cells and their origin, the actual biological trigger that pushes the cancer to progress is still somewhat of a mystery.
Meanwhile, researchers recently reported how a team in the UK discovered how to map a cell's DNA history to its embryonic origin. By looking at the numbers and types of mutations in a cell's DNA, the team found they could detect the imprints or "signatures" of DNA damage that the cell had undergone over the life of the organism.
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