They discover the cells that act as the Trojan horse in metastasis

by time news

2023-07-31 20:00:00

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Los lymph nodes They are one of the body’s first lines of defense against disease. The cells of our immune system leave from these “biological police stations” to fight off intruders. Yet somehow, the lymph nodes are also the first stop for most metastatic cancers.

“It’s paradoxical,” says the assistant professor at the Cold Spring Harbor Laboratory -CSHL- Semir White. “Cancer immediately affects the lymphatic system, which is in charge of protecting us, but the immune cells do nothing. This is an extremely important mechanism to understand, because what is happening is that cancer is taking our entire body hostage.”

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To try to figure out what was going on, Beyaz joined a team of scientists at Massachusetts General Hospital. During his investigation, whose results recently published in the magazine Journal of Experimental Medicinediscovered that, for example in breast cancer, lCancer cells tricked the immune system with the help of a molecule called MHC-II.

“MHC-II acts as the passport from breast cancer to the organism”, explains Beyaz. “It’s like a kind of Trojan horse. It convinces the lymph node to let the cancer in and protect it; and from there everything is a chaos”.

The mechanism is paradoxical, since in other places, such as the intestine, MHC-II helps kill cancer cells before they become a problem. But in cancers like breast immune cells are unable to recognize the alert, and the lymph node treats it as a false alarm.

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Continuing his analogy, Beyaz explains that: “cancer hijacks the lymph node: the police station. The detectives simply say: Welcome! Here is a comfortable sofa. Here is a cafe. Then the cancer “bribes” neighboring cells and grows. This is what MHC-II is doing in lymph node metastasis.”

In other of their mouse experiments, Beyaz’s team also found that higher levels of MHC-II in a subset of cancer cells led to greater immune suppression in lymph nodes. This caused a more aggressive metastasis, decreasing the survival rate of the affected cells.

However, chen they inhibited the production of MHC-II in cancer cells, the lymph nodes sensed the threat. As a result, the cancer could not spread as quickly and the mice lived longer. “If you remove MHC-II from cancer cells, you stop the invasion,” Beyaz continues. “The lymph nodes stop suppressing the immune response and reduce the ability of cancer to colonize.”

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In consecutive investigations, Beyaz and his team hope to reveal exactly how cancer adapts and spreads, for which understanding this type of mechanism could be essential in the development of new therapies against metastasis. However, he cautions: “The efficacy of any potential drug will depend on where the cancer first develops. For example, in the intestine we see the opposite of what happens in breast cancer,” explains Beyaz. “There are specific rules context, and this tells us that there is no panacea”.

Despite this, Beyaz believes that this research could one day have big and positive clinical implications that lead to better therapies against metastasis since future study therapies targeting this molecule could help slow the spread of cancer and improve the results of the patients.

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