NERDG 2026
Poster 10 Abstract
The Synergistic Inhibitory Effect of Targeting CCL5 and Endoglin
Phani Vatsavai and Kideok Jin
Albany College of Pharmacy and Health Sciences
Presenting Author: Phani Vatsavai
Corresponding Author: Kideok Jin, [email protected]
Abstract
Endocrine resistance remains a major clinical challenge for patients with estrogen receptor–positive (ER⁺) breast cancer, often leading to therapeutic failure and disease progression. Prior studies in our laboratory identified two stromal-associated factors—CCL5 and Endoglin (CD105)—as consistently upregulated in tumor–stromal co-culture systems representing endocrine-resistant breast cancer. These molecules are linked to enhanced angiogenesis, immune modulation, tumor–stromal crosstalk, and metastatic behavior, suggesting a potential role in supporting resistance mechanisms. In this study, we established endocrine-resistant variants of the murine ER⁺ EO771 mammary carcinoma line through chronic exposure to 4-hydroxytamoxifen, fulvestrant, and the CDK4/6 inhibitor palbociclib. All resistant models demonstrated stable long-term proliferation under drug pressure, distinct morphological alterations, and significantly reduced drug sensitivity compared with parental cells, confirming successful induction of resistance. These resistant cell lines provide a biologically relevant platform for examining the expression and functional contribution of CCL5 and Endoglin in endocrine resistance. By integrating prior mechanistic findings with an immunocompetent murine model, this study establishes a foundation for investigating how microenvironmental cytokine and angiogenic signaling pathways support resistance, with the long-term goal of identifying therapeutic strategies that target CCL5- and CD105-mediated pathways in endocrine-resistant breast cancer.
Keywords
Endocrine Resistance, ER positive breast cancer, CCL5 and CD105
Poster 10 Abstract
The Synergistic Inhibitory Effect of Targeting CCL5 and Endoglin
Phani Vatsavai and Kideok Jin
Albany College of Pharmacy and Health Sciences
Presenting Author: Phani Vatsavai
Corresponding Author: Kideok Jin, [email protected]
Abstract
Endocrine resistance remains a major clinical challenge for patients with estrogen receptor–positive (ER⁺) breast cancer, often leading to therapeutic failure and disease progression. Prior studies in our laboratory identified two stromal-associated factors—CCL5 and Endoglin (CD105)—as consistently upregulated in tumor–stromal co-culture systems representing endocrine-resistant breast cancer. These molecules are linked to enhanced angiogenesis, immune modulation, tumor–stromal crosstalk, and metastatic behavior, suggesting a potential role in supporting resistance mechanisms. In this study, we established endocrine-resistant variants of the murine ER⁺ EO771 mammary carcinoma line through chronic exposure to 4-hydroxytamoxifen, fulvestrant, and the CDK4/6 inhibitor palbociclib. All resistant models demonstrated stable long-term proliferation under drug pressure, distinct morphological alterations, and significantly reduced drug sensitivity compared with parental cells, confirming successful induction of resistance. These resistant cell lines provide a biologically relevant platform for examining the expression and functional contribution of CCL5 and Endoglin in endocrine resistance. By integrating prior mechanistic findings with an immunocompetent murine model, this study establishes a foundation for investigating how microenvironmental cytokine and angiogenic signaling pathways support resistance, with the long-term goal of identifying therapeutic strategies that target CCL5- and CD105-mediated pathways in endocrine-resistant breast cancer.
Keywords
Endocrine Resistance, ER positive breast cancer, CCL5 and CD105
