biostudies-literatureJallow FU.S. Department of Health & Human Services | Administration for Children & Families | U.S. Children's BureauUniversity of Wisconsin Carbone Cancer CenterNICHD NIH HHSU.S. Department of Health & Human Services | NIH | National Cancer InstituteNCI NIH HHSNIGMS NIH HHSU.S. Department of Health & Human Services | National Institutes of HealthU.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development6913-6925https://www.ebi.ac.uk/biostudies/studies/S-EPMC6814534biostudies-literatureUnknown38(43)Metastatic, antiestrogen resistant estrogen receptor α positive (ER+) breast cancer is the leading cause of breast cancer deaths in USA women. While studies have demonstrated the importance of the stromal tumor microenvironment in cancer progression and therapeutic responses, effects on the responses of ER+ cancers to estrogen and antiestrogens are poorly understood, particularly in the complex in vivo environment. In this study, we used an estrogen responsive syngeneic mouse model to interrogate how a COL1A1-enriched fibrotic ECM modulates integrated hormonal responses in cancer progression. We orthotopically transplanted the ER+ TC11 cell line into wild-type (WT) or collagen-dense (Col1a1^tm1Jae/+, mCol1a1) syngeneic FVB/N female mice. Once tumors were established, recipients wOncogeneDynamic interactions between the extracellular matrix and estrogen activity in progression of ER+ breast cancer.PMC6814534R01 CA206458P30 Ca014520R01 CA179556R01 CA157675R25 GM083252P30 CA014520T32 HD041921Jallow FSchuler LAO'Leary KAPonik SMGuerrero JFRugowski DEfalseDynamic interactions between the extracellular matrix and estrogen activity in progression of ER+ breast cancer.Metastatic, antiestrogen resistant estrogen receptor α positive (ER+) breast cancer is the leading cause of breast cancer deaths in USA women. While studies have demonstrated the importance of the stromal tumor microenvironment in cancer progression and therapeutic responses, effects on the responses of ER+ cancers to estrogen and antiestrogens are poorly understood, particularly in the complex in vivo environment. In this study, we used an estrogen responsive syngeneic mouse model to interrogate how a COL1A1-enriched fibrotic ECM modulates integrated hormonal responses in cancer progression. We orthotopically transplanted the ER+ TC11 cell line into wild-type (WT) or collagen-dense (Col1a1^tm1Jae/+, mCol1a1) syngeneic FVB/N female mice. Once tumors were established, recipients w2019-01-01T00:00:00Z2019 Oct2025-04-05T13:50:46.871Z2020-05-22T09:47:32ZS-EPMC68145343140625110.1038/s41388-019-0941-0