The Next Generation of Inflammatory Breast Cancer Research at SABCS

The San Antonio Breast Cancer Symposia is an exciting time for providers and advocates around the world. Every year, nearly approximately 2,000 abstracts are presented with posters revealing the latest findings on research in all aspects of breast cancer. It’s truly a blend of experience and innovation. The place where seasoned experts building on years of progress are found right alongside emerging researchers bringing fresh ideas and new technologies to the table. Together, they push the field forward, learning from past data, questioning old assumptions, and exploring new ways to improve outcomes for patients.

There is never enough funding for research, especially inflammatory breast cancer.

This conference is where the breast cancer research community comes together to share insights, challenge each other, and imagine what’s possible next.

This year, The IBC Network Foundation was excited to partner with American Association for Cancer Research (AACR) to support the next generation of researchers. Five early-career researchers were granted $1,000 in seed money for their work at SABCS. This funding allows these researchers to build a foundation to receive more grant money from the NIH and make discoveries that may one day change patient care.

Here are the recipients and the results of their work:

• Mohd Mughees, PhD.
  

UT MD Anderson Cancer CenterAbstract: Combination of a novel MELK inhibitor with standard of care treatment results in tumor regression and improved survival in a triple-negative inflammatory breast cancer xenograft model.

Researchers have been looking at a protein called MELK, which shows up a lot in aggressive breast cancers like triple-negative breast cancer (TNBC) and inflammatory breast cancer (IBC). When MELK is active, tumors tend to grow faster and spread more easily.

This study tested a new idea in mice: What if we block MELK and use the current standard treatment at the same time? Using a MELK-blocking drug called MELK-In-30e together with eribulin, a chemotherapy often used for aggressive breast cancers, Mughees and his team learned this combination of treatment was more effective than either treatment alone. Tumor growth slowed and the combination therapy slowed the cancer's ability to spread. They also learned that the markers linked to rapid growth and metastasis were turned off.

While the study was done in mice, the results are promising and suggest that combining a MELK inhibitor with standard therapy could one day become a new strategy to treat TNBC and potentially IBC. In their next steps, Mughees hopes to receive additional funding to investigate if these findings are consistent in human tissue samples.

• Tanu Sharma
  

UT MD Anderson Cancer CenterAbstract: Aurora Kinase A (AURKA) a new druggable target in ER+ Inflammatory Breast Cancer 

This study looked at a new combination treatment approach for ER-positive inflammatory breast cancer (ER+ IBC), a subtype of ER+ breast cancer that unfortunately hasn’t received nearly enough research attention. Even though ER+ breast cancers are often considered less aggressive, ER+ IBC is a very different story. Patients are treated the same way as those with high-risk, non-IBC ER+ disease, yet their long-term survival is much shorter, often looking more like outcomes seen in triple-negative IBC.

Because of this gap, Dr. Sharma and her team set out to explore whether blocking a protein called Aurora Kinase A (AURKA) could offer a new, more effective treatment path for ER+ IBC. Their idea was simple: if AURKA helps IBC cells grow, then shutting it down might slow the cancer or stop it altogether.

In the study, they tested the drugs alisertib, navitoclax, and fulvestrant alone and in different combinations. Alisertib on its own was able to push cancer cells into senescence, or “sleep mode” where the cells stop dividing. When combined with navitoclax, that senescence effect didn’t hold, but alisertib paired with fulvestrant, a standard ER-targeting drug, showed promising effectiveness.

In plain terms:

·      Alisertib alone slowed down or stopped ER+ IBC cell growth.

·      Alisertib and fulvestrant attacks ER+ IBC from two angles: the hormone and the protein.

This suggests a possible new combination therapy worth developing.

This is early research, but it’s an exciting step forward for a subtype of IBC that urgently needs more treatment options and more attention.

• Christophe Van Berckelaer, MD
  

University of AntwerpAbstract: Spatial Immune Profiling in Inflammatory Breast Cancer Reveals a Central Role for Tumor-Associated Macrophages and a Spatial Context-Dependent Negative Prognostic Impact of B Cells

Van Berckelaer has been very busy. He did not have just one poster to present, he had two! His innovative ideas bring artificial intelligence (AI) to help scientists look at breast cancer in a brand new way. Instead of looking at tiny pieces of a tumor like we usually do, his study looked at the whole of the tumor at once, not just a section.

The resulting data found that IBC tumors had more of certain immune cell called CD163+ macrophages. These are cells that work to help but the body, however, in the case of IBC, they tell the immune system to stay quiet, allowing the cancer to grow. This indicates that IBC is more immunosuppressive.

This study also found that it wasn’t just the number of immune cells that predicted outcomes, but their location and proximity to the cancer. For example, B-cells clustering near IBC tumor cells was linked to poorer prognosis. These insights point toward new therapeutic possibilities that specifically target the IBC microenvironment, including reprogramming macrophages, modifying B-cell activity, or interrupting cytokine pathways that help the tumor thrive.

• Ekene Onwubiko

  
  

MD Anderson Cancer CenterAbstract: Outcome After Locoregional Recurrences For Definitively Treated Non-Metastatic Inflammatory Breast Cancer

This study looked at one of the tougher situations in inflammatory breast cancer: what happens when the cancer comes back in the breast area or nearby lymph nodes after a patient has already gone through the full standard treatment—medicine, mastectomy, and radiation. This type of recurrence, called locoregional recurrence (LRR), is thankfully uncommon, but when it happens, it’s important to understand why.

Out of 140 IBC patients who received trimodality therapy, only 9 experienced an LRR. Most recurrences happened on the chest wall, some in nearby lymph nodes, and they typically appeared about 17 months after treatment.

Unfortunately, survival after an LRR was low, highlighting how serious these recurrences are. Only about 14% of patients were still alive five years later, though one patient lived more than seven years without the cancer spreading. The research team’s next step is to review the original radiation plans to see whether certain areas may not have received enough coverage. This could help identify ways to improve treatment and hopefully reduce recurrences for future IBC patients.

• Caroline Sabotta, BS
  

Baylor College of Medicine Abstract: Mechanisms of resistance to anti-HER2 therapies in brain metastatic derivatives of inflammatory HER2-positive breast cancer models

One of the standout presentations this year came from Sabotta and Baylor College of Medicine, who explored why some HER2-positive inflammatory breast cancers stop responding to treatments like tucatinib and T-DXd (medicine that acts like a homing device to help cancer drugs find the HER2+ cells), especially after the cancer spreads to the brain. HER2-positive disease is already an aggressive subtype, and up to half of patients with metastatic disease develop brain metastases, so understanding resistance is critical.

Sabotta’s study looked at cancer cells that had become resistant to tucatinib, a drug that normally works well in HER2-positive IBC. What she found was surprisingly clear: once the cancer became resistant, a growth signal called EGFR was turned on at very high levels. In simple terms, when one growth “switch” was blocked, the cancer just flipped on another one to keep going. These high-EGFR cells were found to be less sensitive to T-DXd, meaning they needed more of the drug to work.

The promising part is that adding EGFR inhibitors helped restore the effectiveness of T-DXd in these resistant models. Drugs like neratinib and capivasertib also showed activity against the resistant cells, giving researchers new paths to explore.

Caroline’s work suggests that for HER2-positive IBC, especially when it spreads to the brain, treatment may need to target both HER2 and EGFR (or the PI3K pathway) to stay ahead of resistance. Her findings are an important step toward combination strategies that could help overcome treatment failure and improve outcomes for this very aggressive form of breast cancer.

These studies are opening doors in breast cancer research and bringing new ideas to the table. The next phase for these researchers is to continue their work, expand their research, and confirm their findings. This requires funding. NIH grant money is critical for continue research but often, more funding is needed. This is why agencies such as The IBC Network Foundation are so important. All of the money raised by The IBC Network Foundation is channeled into these research projects. These studies are delivering the promise of hope to all of patients who are currently fighting IBC.

2025 SABCS posters and presenters with the latest findings in breast cancer research.

Remember, IBC is rare and it is aggressive. Because of this, it is understudied and often unappreciated. Worse, it's frequently misunderstood and misdiagnosed, delaying lifesaving interventions. Healthcare needs more studies such as these five that focus on learning this disease, how effective our current treatment methods are, and looking for more effective methods.

This year’s SABCS made one thing clear: the momentum behind inflammatory breast cancer research is growing and the next generation of scientists is stepping up in powerful ways. From uncovering new treatment targets in TNBC and ER+ IBC, to exploring the tumor’s immune “neighborhood,” to understanding why HER2 therapies sometimes fail, each project adds an important piece to the larger puzzle of IBC. Thanks to our partnership with AACR, these young investigators were able to bring fresh ideas, new tools, and bold questions to the stage. Their work gives us hope—not just for better treatments, but for a future where IBC is understood earlier, treated smarter, and faced with far more options than we have today.

Research like this does not move forward without support. Seed funding gives investigators the ability to ask bold questions, gather preliminary data, and compete for larger federal grants that can ultimately change patient care. If you believe inflammatory breast cancer deserves focused attention, better treatments, and earlier diagnosis, I encourage you to support this work. Donations to The IBC Network Foundation go directly toward funding IBC-specific research and supporting the scientists committed to improving outcomes for patients facing this aggressive disease. Together, we can turn promising ideas into real progress.