by Association of Basic Medical Sciences of FBIH

Credit: Association of Basic Medical Sciences of FBIH

Diffuse large B-cell lymphoma (DLBCL) is the most common and fast-growing type of non-Hodgkin lymphoma, a cancer that affects the lymphatic system. It makes up around 30–40% of adult non-Hodgkin lymphoma cases worldwide. DLBCL can appear in lymph nodes or other parts of the body and often progresses quickly.

While some patients respond well to standard treatments, others experience relapse or resistance to therapy, which makes long-term recovery more difficult. These challenges have increased interest in identifying new treatment targets that can help improve outcomes for patients with aggressive or treatment-resistant forms of the disease.

The standard approach to treating DLBCL is a combination drug therapy known as R-CHOP. Although this regimen has helped improve survival rates, it does not work for everyone. Around one-third of patients either do not respond to treatment or experience a return of the disease after an initial response. This has led scientists to explore the underlying biology of DLBCL more closely.

A recent study has identified a new potential target—Apolipoprotein C1 (APOC1)—which may offer a new way to treat the disease more effectively. The research is published in the journal Biomolecules and Biomedicine.

APOC1 is a small protein best known for its role in managing how the body processes fats. However, recent evidence suggests it may also contribute to cancer progression. Researchers studying DLBCL found that APOC1 levels are significantly higher in tumor tissues than in normal ones. They also observed a link between high APOC1 levels and lower survival rates, suggesting this protein may be involved in making the disease more aggressive.

Further experiments showed that APOC1 actively supports cancer cell survival. When researchers used gene-silencing techniques to reduce APOC1 in DLBCL cells, the cells stopped growing and began to die. These results suggest that APOC1 is not just a marker of disease but a potential driver of cancer growth, making it a promising target for future therapies.

The study also found that APOC1 helps support angiogenesis, the process by which tumors build new blood vessels to supply themselves with oxygen and nutrients. When APOC1 was blocked in lab models, not only did tumor cells stop dividing, but the formation of new blood vessels also decreased. This was partly due to lower levels of VEGFA, a protein that stimulates blood vessel growth. Without VEGFA, tumors had a harder time building the networks they need to grow and survive.

These findings suggest that targeting APOC1 could slow tumor growth and limit its blood supply, potentially making cancer cells more sensitive to other forms of treatment.

A potential shift in treatment strategy

While there are currently no approved therapies that target APOC1, this research highlights several promising directions. Future treatment strategies might include:

These approaches could offer better options for patients who do not respond well to standard therapies, especially those with tumors that show high APOC1 activity.

This study adds to the growing understanding of how DLBCL develops and spreads. More research is needed to confirm these findings in clinical settings and to design therapies that can safely and effectively block APOC1. Still, the results offer a new pathway for developing personalized treatments for a disease that remains difficult to treat in many patients.

By uncovering APOC1's role in lymphoma, this research opens the door to more targeted and potentially more effective therapies in the future.

More information: Jing Gao et al, APOC1 knockdown induces apoptosis and decreases angiogenesis in diffuse large B-cell lymphoma cells through blocking the PI3K/AKT/mTOR pathway, Biomolecules and Biomedicine (2025). DOI: 10.17305/bb.2024.11550