Three-fourths of all breast cancer cases are influenced by the hormone estrogen.
These cases are often treated with medications designed to block estrogen receptor activity.
But here’s the problem – these treatments don’t work for at least half of the patients, leaving them to deal with drug-resistant tumors and very few treatment choices.
In a recent scientific breakthrough, researchers discovered that two molecules from our immune system might be the culprits behind the development of drug resistance in estrogen-driven breast cancers.
This finding is super important because it could lead to new treatments and change the way we approach these types of breast cancers, which affect tens of thousands of patients.
These two immune system molecules are known as interleukin 1 beta (IL1β) and tumor necrosis factor alpha (TNFα).
They are types of cytokines, which are like messengers in our immune system. They’ve been connected to drug-resistant cancer in the past, but until now, scientists weren’t exactly sure how these molecules caused drug resistance.
Published in the journal Molecular Cell, the new study shows that IL1β and TNFα kick-start processes that actually change the shape of the estrogen receptor. This shape-shifting appears to be what causes resistance to a common anti-cancer drug called tamoxifen.
In a heroic attempt to fight back against drug resistance, researchers used a mix of techniques to show how these cytokines change the estrogen receptor enough to encourage the growth of breast cancer cells.
This change doesn’t just counteract the effects of tamoxifen, it also makes a specific type of human breast cancer cell, known as MCF-7, more invasive.
Using a technique called x-ray crystallography, like a super high-tech microscope, the researchers took a close-up picture of the estrogen receptor. This helped them see how these shape changes happen and how they might be stopped.
One interesting point the researchers made is that both inflammation (swelling and redness in the body) and immune cells can lead to drug resistance. But if we could block that inflammation, we might be able to reduce or even get rid of drug resistance.
The researchers explained, “These tumors can trick the immune cells to work in their favor, helping the tumor grow.
We believe we can create hormone therapies that could ‘un-trick’ the immune system or stop it from altering the receptor in the first place, which could prevent these negative effects.” This discovery is a major step forward in the fight against drug-resistant breast cancer!
