Authors:

Cristina Ball

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About Paper:

Breast cancer cells often depend on multiple survival pathways, which can limit the effectiveness of single-drug treatments. MEK inhibitors target the MAPK signaling pathway, but resistance commonly develops when they are used alone. To improve therapeutic response, our lab investigates combination treatments that simultaneously target complementary survival mechanisms.Preliminary combination drug screening revealed subtype-specific synergy patterns in inflammatory breast cancer (IBC) and non-IBC cell lines. Using combination index models to quantify drug interactions, we observed strong synergy between MEK and BCL-2 inhibitors in IBC models, while MEK and HDAC inhibitors demonstrated significant synergy in non-IBC cell lines. In both cases, combination treatments reduced cell viability more effectively than either drug alone, with combination index values below 1 across multiple dose levels, indicating synergistic interactions. These findings suggest that IBC and non-IBC subtypes rely on distinct survival pathways, making them differentially sensitive to targeted drug combinations. Building on these preliminary results, our current work tests whether these vulnerabilities persist when the inhibitor pairings are reversed (MEK plus BCL-2 in non-IBC and MEK plus HDAC in IBC). Ongoing screening will determine whether synergy is conserved or subtype-specific.Overall, this study advances understanding of how breast cancer subtypes respond to rationally designed combination therapies. Identifying consistent and subtype-dependent drug synergies may help guide more effective, precision-based treatment strategies and improve therapeutic outcomes.

Source:

Chicago Area Undergraduate Research Symposium

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Co-authors:

Cristina Ball