Washington: Scientists have discovered a gene that carries a protein linked to liver cancer, paving the way for treatment targeting the pro-inflammatory protein.
Researchers from the Georgia Health Sciences University Cancer Center found that laboratory mice bred without the gene lacked a protein called TREM-1 which protected them from developing liver cancer after exposure to carcinogens.
"We have long suspected that chronic inflammation is a very powerful tool in the initiation of cancer, and also in the progression or metastasis of cancer," lead researcher Dr Anatolij Horuzsko, said.
"We [looked] at the molecules that control inflammatory responses to gain a better understanding of how this process works. One important triggering receptor for inflammation is TREM-1," Horuzsko said in a statement.
TREM-1`s role in promoting inflammation is useful in cases such as battling viral or bacterial infections and in maintaining normal tissue function.
Horuzsko`s team discovered that in abnormal conditions such as liver damage due to alcohol abuse or other irritants production of TREM-1 goes haywire.
A chronic, low-level state of inflammation is produced as TREM-1 leads to the development of other inflammatory agents, which causes more damage, increases cell production and creates mutated cells.
These mutated cells then reproduce planting the seeds that can lead to cancer.
The researchers used mouse studies to gather data on the effect of TREM-1 in the liver cells and identify potential sources for therapies.
Two sets of mice one with the TREM-1 gene removed were exposed to the cancer-causing agent diethylnitrosamine, or DEN, which is present in tobacco smoke, chemicals and other products.
Within just 48 hours of DEN injection, the control mice were already showing signs of liver cell injury and death and high levels of TREM-1 expression in the liver`s Kupffer cells.
These specialised liver cells normally destroy bacteria and worn-out red blood cells. Eight months later, these mice also showed massive liver tumours.
The mice with the gene removed remained healthy, showing very few changes?and very small, if any, tumours after eight months. The only difference between the two groups was the appearance of TREM-1 in the Kupffer cells.
The team hopes the findings and their potential in TREM-1-related cancer treatment?will be applicable to other cancers as well.
"TREM-1 could be a target for any inflammation-associated cancer," Horuzsko said.
The study was published in journal Cancer Research.