T
Teresa C. Dugger
Researcher at Vanderbilt University
Publications - 29
Citations - 3187
Teresa C. Dugger is an academic researcher from Vanderbilt University. The author has contributed to research in topics: Cancer cell & Transforming growth factor. The author has an hindex of 18, co-authored 29 publications receiving 2806 citations. Previous affiliations of Teresa C. Dugger include Vanderbilt University Medical Center & Veterans Health Administration.
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Journal ArticleDOI
Blockade of TGF-β inhibits mammary tumor cell viability, migration, and metastases
Rebecca S. Muraoka,Nancy Dumont,Christoph A. Ritter,Teresa C. Dugger,Dana M. Brantley,Jin Chen,Evangeline Easterly,L. Renee Roebuck,Sarah Ryan,Philip Gotwals,Victor Koteliansky,Carlos L. Arteaga +11 more
TL;DR: Blockade of TGF-β signaling may reduce tumor cell viability and migratory potential and represents a testable therapeutic approach against metastatic carcinomas.
Journal ArticleDOI
Human breast cancer cells selected for resistance to trastuzumab in vivo overexpress epidermal growth factor receptor and ErbB ligands and remain dependent on the ErbB receptor network.
Christoph A. Ritter,Marianela Perez-Torres,Cammie Rinehart,Marta Guix,Teresa C. Dugger,Jeffrey A. Engelman,Carlos L. Arteaga +6 more
TL;DR: The results are consistent with the inability of trastuzumab to block the heterodimerization of HER2 and suggest that amplification of ligand-induced activation of ErbB receptors is a plausible mechanism of acquired resistance to trastzumab that should be investigated in primary mammary cancers.
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TGF-β inhibition enhances chemotherapy action against triple-negative breast cancer
Neil E. Bhola,Justin M. Balko,Teresa C. Dugger,Maria G. Kuba,Violeta Sanchez,Melinda E. Sanders,Jamie C. Stanford,Rebecca S. Cook,Carlos L. Arteaga +8 more
TL;DR: Analysis of RNA expression in matched pairs of primary breast cancer biopsies before and after chemotherapy suggests that chemotherapy-induced TGF-β signaling enhances tumor recurrence through IL-8-dependent expansion of CSCs and that T GF-β pathway inhibitors prevent the development of drug-resistant C SCs.
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Inhibition of TGF-β with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression
Swati Biswas,Marta Guix,Cammie Rinehart,Teresa C. Dugger,Anna Chytil,Harold L. Moses,Michael L. Freeman,Carlos L. Arteaga +7 more
TL;DR: Analysis of the MMTV/PyVmT transgenic model of metastatic breast cancer shows that administration of ionizing radiation or doxorubicin caused increased circulating levels of TGF-beta1 as well as increased circulating tumor cells and lung metastases, which implicate T GF-beta induced by anticancer therapy as a pro-metastatic signal in tumor cells.
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Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER+ breast cancer
Luigi Formisano,Yao Lu,Alberto Servetto,Ariella B. Hanker,Ariella B. Hanker,Valerie M. Jansen,Joshua A. Bauer,Dhivya R. Sudhan,Dhivya R. Sudhan,Angel Guerrero-Zotano,Sarah Croessmann,Yan Guo,Paula Gonzalez Ericsson,Kyungmin Lee,Mellissa J. Nixon,Luis J. Schwarz,Melinda E. Sanders,Teresa C. Dugger,Marcelo Rocha Cruz,Amir Behdad,Massimo Cristofanilli,Aditya Bardia,Joyce O'Shaughnessy,Rebecca J. Nagy,Richard B. Lanman,Nadia Solovieff,Wei He,Michelle Miller,Fei Su,Yu Shyr,Ingrid A. Mayer,Justin M. Balko,Carlos L. Arteaga,Carlos L. Arteaga +33 more
TL;DR: It is shown that FGFR1 amplification is a resistance mechanism to CDK4/6 inhibitor and endocrine therapy and that combined treatment with FGFR, CDK 4/6, and anti-estrogens is a potential therapeutic strategy in Era+ breast cancer tumors.