New Study Discovered Why Chemo And Immunotherapies Do Not Work On Difficult-To-Treat Breast Cancer Cases
Breast cancer is the second most common cancer type diagnosed among women, following skin cancer.
In 2022, an estimated 288,000 cases were diagnosed in the United States alone.
Despite the high volume of cases, though, many forms of breast cancer are actually very treatable– especially when diagnosed during the earlier stages.
For instance, the most common type of noninvasive breast cancer– ductal carcinoma in situ (DCIS)– has a long-term survival rate of nearly 100%.
Still, there are some outlier cases in which breast cancer cannot be treated via hormone therapies or targeted therapies and does not respond to chemotherapy.
These particular cases remain the most challenging to treat and wind up being the deadliest.
Recently, though, researchers from Tulane University in New Orleans, Louisiana, conducted a study that, for the first time, discovered how it is possible for cancers to persist following chemotherapy and why cancers do not respond well to immunotherapies– which are designed to ramp up the immune system.
Essentially, the team found that after surviving chemotherapy, a host of immune checkpoints are triggered.
These checkpoints then actually shield breast cancer against the immune system’s various lines of attack.
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In turn, a problem akin to “whack-a-mole” is created for immunotherapy drugs– or checkpoint inhibitors– since they may eliminate tumor cells that express one checkpoint but miss other tumor cells that have various checkpoints.
“We found that they [breast cancers] avoid immune clearance by expressing a complex, redundant program of checkpoint genes and immune modulatory genes. The tumor completely changes after chemotherapy treatment into this thing that is essentially built to block the immune system,” explained James Jackson, a corresponding author of the study.
Then, following this discovery, the team studied this process in mouse models as well as human breast tumors. The researchers ultimately identified 16 immune checkpoint genes that are responsible for encoding proteins designed to disable T-cells– which help protect the body from infection and fight off cancer.
Additionally, the tumors that do not respond to chemotherapy– and survive rather than die after treatment– then enter a dormancy state known as cellular senescence. The team found two distinct major populations of these senescent tumor cells. Each of the populations expressed differing immune checkpoints, which are activated via specific signal pathways.
The researchers did also test a combination of drug therapies in hopes of targeting the various immune checkpoints. Unfortunately, though, the strategy was still unable to completely eradicate most of the tumors– underscoring how personalized these therapies need to become for patient care.
“Our findings reveal the challenge of eliminating residual disease populated by senescent cells that activate complex immune inhibitory programs,” Jackson concluded.
“Breast cancer patients will need rational, personalized strategies that target the specific checkpoints induced by the chemotherapy treatment.”
To read the study’s complete findings, which have since been published in Nature Cancer, visit the link here.
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