Talks
Presenting Author Academic/Professional Position
Melina J Sedano
Academic Level (Author 1)
Staff
Discipline/Specialty (Author 1)
Cancer and Immunology
Academic Level (Author 2)
Faculty
Discipline/Specialty (Author 2)
Cancer and Immunology
Academic Level (Author 3)
Faculty
Discipline/Specialty (Author 3)
Cancer and Immunology
Academic Level (Author 4)
Faculty
Discipline/Specialty (Author 4)
Cancer and Immunology
Academic Level (Author 5)
Faculty
Discipline/Specialty (Author 5)
Cancer and Immunology
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: Triple-negative breast cancer (TNBC) is projected to make up about 10–15% of all new breast cancer cases in 2025, with poorer outcomes than other subtypes. An estimated 42,170 women will die from breast cancer this year. TNBC often involves larger, higher-grade tumors, leading to lower survival and recurrence-free rates. Chemotherapy, especially anthracyclines like doxorubicin, is commonly used, but its efficacy is limited by drug resistance. The mechanisms behind this resistance are unclear, possibly involving changes in cellular pathways, interactions with the extracellular matrix, or epigenetic modifications.
Methods: To study resistance, two TNBC cell lines were gradually exposed to increasing doxorubicin concentrations to induce resistance. We performed integrative genomic analyses that uncovered pathways involved in cancer progression and factors driving the resistant phenotype.
Results: Findings showed many transcripts that have evolved recently with coding or limited coding potential are differentially expressed in resistant cells versus non-resistant ones. Genes with altered expression are linked to cellular plasticity, suggesting cancer cells may adapt to doxorubicin through transcriptional reprogramming.
Conclusions: The study examines genetic and epigenetic changes that lead to doxorubicin resistance in TNBC cells, correlating these findings with patient data to better understand prognosis. Ultimately, understanding resistance mechanisms aims to reveal new therapeutic targets and strategies.
Presentation Type
Talk
Recommended Citation
Sedano, Melina J.; Dhandayuthapani, Subramanian; Yallapu, Murali; Chauhan, Subhash; and Gadad, Shrikanth, "Developing a TNBC resistance model and identifying unique molecular pathways related to drug resistance" (2025). Research Colloquium. 9.
https://scholarworks.utrgv.edu/colloquium/2025/talks/9
Included in
Developing a TNBC resistance model and identifying unique molecular pathways related to drug resistance
Background: Triple-negative breast cancer (TNBC) is projected to make up about 10–15% of all new breast cancer cases in 2025, with poorer outcomes than other subtypes. An estimated 42,170 women will die from breast cancer this year. TNBC often involves larger, higher-grade tumors, leading to lower survival and recurrence-free rates. Chemotherapy, especially anthracyclines like doxorubicin, is commonly used, but its efficacy is limited by drug resistance. The mechanisms behind this resistance are unclear, possibly involving changes in cellular pathways, interactions with the extracellular matrix, or epigenetic modifications.
Methods: To study resistance, two TNBC cell lines were gradually exposed to increasing doxorubicin concentrations to induce resistance. We performed integrative genomic analyses that uncovered pathways involved in cancer progression and factors driving the resistant phenotype.
Results: Findings showed many transcripts that have evolved recently with coding or limited coding potential are differentially expressed in resistant cells versus non-resistant ones. Genes with altered expression are linked to cellular plasticity, suggesting cancer cells may adapt to doxorubicin through transcriptional reprogramming.
Conclusions: The study examines genetic and epigenetic changes that lead to doxorubicin resistance in TNBC cells, correlating these findings with patient data to better understand prognosis. Ultimately, understanding resistance mechanisms aims to reveal new therapeutic targets and strategies.
