Lymph nodes, essential components of the body's immune defense, paradoxically become the first stop for most metastatic breast cancers, according to researchers from Cold Spring Harbor Laboratory who investigated this phenomenon, discovering that breast cancer cells manipulate the immune system with the help of a molecule called MHC-II. Targeting this molecule with future therapeutics could potentially slow cancer spread and improve patient outcomes.
MHC-II acts as a "passport" for breast cancer cells, convincing the lymph node to let them in and protect them from immune attacks. However, breast cancer's version of MHC-II lacks the red flags that immune cells recognize, causing the lymph node to treat it as a false alarm. This manipulation allows cancer cells to bribe neighboring cells, promoting growth and metastasis in the lymph node.
In mice, the team observed that higher levels of MHC-II on cancer cells led to increased immune suppression in lymph nodes, resulting in worse metastasis and shorter survival. When MHC-II production was switched off in cancer cells, the lymph nodes responded to the threat, reducing cancer spread and extending the mice's lifespan.
The team aims to uncover the exact mechanisms behind cancer adaptation and spread to develop new therapeutics that block metastasis. However, they acknowledge that the effectiveness of potential drugs will depend on the specific location of cancer development. The study, published in the Journal of Experimental Medicine, offers promising insights into potential clinical implications, leading to improved therapies and better patient outcomes in breast cancer cases.