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274 results on '"Lange, Carol"'

5. Blockade of tumor cell-intrinsic PD-L1 signaling enhances AURKA-targeted therapy in triple negative breast cancer.

Author

Takchi, Andrew, Zhang, Minzhi, Jalalirad, Mohammad, Ferre, Roberto Leon, Shrestha, Royal, Haddad, Tufia, Sarkaria, Jann, Tuma, Ann, Carter, Jodi, David, Hillman, Giridhar, Karthik, Wang, Liewei, Lange, Carol, Lendahl, Urban, Ingle, James, Goetz, Matthew, and D'Assoro, Antonino Bonaventura

Subjects
TRIPLE-negative breast cancer, PROGRAMMED death-ligand 1, CANCER stem cells, HORMONE receptor positive breast cancer, EPITHELIAL-mesenchymal transition, CANCER cell growth, DISEASE relapse
Abstract

Triple negative breast cancer (TNBC) accounts for 15-20% of all breast cancers and mainly affects pre-menopausal and minority women. Because of the lack of ER, PR or HER2 expression in TNBC, there are limited options for tailored therapies. While TNBCs respond initially to standard of care chemotherapy, tumor recurrence commonly occurs within 1 to 3 years post-chemotherapy and is associated with early organ metastasis and a high incidence of mortality. One of the major mechanisms responsible for drug resistance and emergence of organ metastasis is activation of epithelial to mesenchymal transition (EMT) reprogramming. EMT-mediated cancer cell plasticity also promotes the enrichment of cancer cells with a CD44high/CD24low and/or ALDHhigh cancer stem-like phenotype [cancer stem cells (CSCs)], characterized by an increased capacity for tumor self-renewal, intrinsic drug resistance, immune evasion and metastasis. In this study we demonstrate for the first time a positive feedback loop between AURKA and intra-tumoral PD-L1 oncogenic pathways in TNBC. Genetic targeting of intra-tumoral PD-L1 expression impairs the enrichment of ALDHhigh CSCs and enhances the therapeutic efficacy of AURKA-targeted therapy. Moreover, dual AURKA and PD-L1 pharmacological blockade resulted in the strongest inhibition of tumor growth and organ metastatic burden. Taken together, our findings provide a compelling preclinical rationale for the development of novel combinatorial therapeutic strategies aimed to inhibit cancer cell plasticity, immune evasion capacity and organ metastasis in patients with advanced TNBC. [ABSTRACT FROM AUTHOR]

Published
2024
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6. A functional signal profiling test for identifying a subset of HER2-negative breast cancers with abnormally amplified HER2 signaling activity

Author

Huang, Yao, Burns, David J, Rich, Benjamin E, MacNeil, Ian A, Dandapat, Abhijit, Soltani, Sajjad M, Myhre, Samantha, Sullivan, Brian F, Furcht, Leo T, Lange, Carol A, Hurvitz, Sara A, and Laing, Lance G

Subjects
Cancer, Clinical Research, Breast Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Adult, Aged, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Immunological, Biosensing Techniques, Breast Neoplasms, Case-Control Studies, Cell Adhesion, Cell Line, Tumor, Dose-Response Relationship, Drug, Epidermal Growth Factor, Female, Humans, Middle Aged, Receptor, ErbB-2, Receptors, Estrogen, Receptors, Progesterone, Reproducibility of Results, Signal Transduction, Tumor Cells, Cultured, HER2 negative, HER2 signaling, targeted therapy, CELx HSP test, tumor primary cells, Receptor, erbB-2, Oncology and Carcinogenesis
Abstract

The results of clinical trials evaluating the efficacy of HER2 inhibitors in patients with breast cancer indicate that the correlation between HER2 receptor levels and patient outcomes is as low as 50%. The relatively weak correlation between HER2 status and response to HER2-targeting drugs suggests that measurement of HER2 signaling activity, rather than absolute HER2 levels, may more accurately diagnose HER2-driven breast cancer. A new diagnostic test, the CELx HER2 Signaling Profile (CELx HSP) test, is demonstrated to measure real-time HER2 signaling function in live primary cells. In the present study, epithelial cells extracted fresh from breast cancer patient tumors classified as HER2 negative (HER2-, n = 34 of which 33 were estrogen receptor positive) and healthy subjects (n = 16) were evaluated along with reference breast cancer cell lines (n = 19). Live cell response to specific HER2 agonists (NRG1b and EGF) and antagonist (pertuzumab) was measured. Of the HER2- breast tumor cell samples tested, 7 of 34 patients (20.5%; 95% CI = 10%-37%) had HER2 signaling activity that was characterized as abnormally high. Amongst the tumor samples there was no correlation between HER2 protein status (by cell cytometry) and HER2 signaling activity (hyperactive or normal) (Regression analysis P = 0.144, R2 = 0.068). One conclusion is that measurement of HER2 signaling activity can identify a subset of breast cancers with normal HER2 receptor levels with abnormally high levels of HER2 signaling. This result constitutes a new subtype of breast cancer that should be considered for treatment with HER2 pathway inhibitors.

Published
2016

12. International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily—Update 2023

Author

Burris, Thomas P., primary, de Vera, Ian Mitchelle S., additional, Cote, Isabelle, additional, Flaveny, Colin A., additional, Wanninayake, Udayanga S., additional, Chatterjee, Arindam, additional, Walker, John K., additional, Steinauer, Nickolas, additional, Zhang, Jinsong, additional, Coons, Laurel A., additional, Korach, Kenneth S., additional, Cain, Derek W., additional, Hollenberg, Anthony N., additional, Webb, Paul, additional, Forrest, Douglas, additional, Jetten, Anton M., additional, Edwards, Dean P., additional, Grimm, Sandra L., additional, Hartig, Sean, additional, Lange, Carol A., additional, Richer, Jennifer K., additional, Sartorius, Carol A., additional, Tetel, Marc, additional, Billon, Cyrielle, additional, Elgendy, Bahaa, additional, Hegazy, Lamees, additional, Griffett, Kristine, additional, Peinetti, Nahuel, additional, Burnstein, Kerry L., additional, Hughes, Travis S., additional, Sitaula, Sadichha, additional, Stayrook, Keitch R., additional, Culver, Alexander, additional, Murray, Meghan H., additional, Finck, Brian N., additional, and Cidlowski, John A., additional

Published
2023
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15. 3C. 3-Ketosteroid receptors in GtoPdb v.2023.1

Author

Cain, Derek, primary, Cidlowski, John, primary, Edwards, Dean P., primary, Fuller, Peter, primary, Grimm, Sandra L., primary, Hartig, Sean, primary, Lange, Carol A., primary, Oakley, Robert H., primary, Richer, Jennifer K., primary, Sartorius, Carol A., primary, Tetel, Marc, primary, Weigel, Nancy, primary, and Young, Morag J., primary

Published
2023
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16. Receptor for hyaluronan‐mediated motility (RHAMM) defines an invasive niche associated with tumor progression and predicts poor outcomes in breast cancer patients

Author

Tarullo, Sarah E, primary, He, Yuyu, additional, Daughters, Claire, additional, Knutson, Todd P, additional, Henzler, Christine M, additional, Price, Matthew A, additional, Shanley, Ryan, additional, Witschen, Patrice, additional, Tolg, Cornelia, additional, Kaspar, Rachael E, additional, Hallstrom, Caroline, additional, Gittsovich, Lyubov, additional, Sulciner, Megan L, additional, Zhang, Xihong, additional, Forster, Colleen L, additional, Lange, Carol A, additional, Shats, Oleg, additional, Desler, Michelle, additional, Cowan, Kenneth H, additional, Yee, Douglas, additional, Schwertfeger, Kathryn L, additional, Turley, Eva A, additional, McCarthy, James B, additional, and Nelson, Andrew C, additional

Published
2023
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17. Data from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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19. Supplementary figure legends from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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20. Data from Breast Tumor Kinase (Brk/PTK6) Mediates Advanced Cancer Phenotypes via SH2-Domain Dependent Activation of RhoA and Aryl Hydrocarbon Receptor (AhR) Signaling

Author

Dwyer, Amy R., primary, Kerkvliet, Carlos Perez, primary, Krutilina, Raisa I., primary, Playa, Hilaire C., primary, Parke, Deanna N., primary, Thomas, Warner A., primary, Smeester, Branden A., primary, Moriarity, Branden S., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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21. Supplemental Methods including references, Supplemental Table 1, and Supplemental Figures 1-5 from Breast Tumor Kinase (Brk/PTK6) Mediates Advanced Cancer Phenotypes via SH2-Domain Dependent Activation of RhoA and Aryl Hydrocarbon Receptor (AhR) Signaling

Author

Dwyer, Amy R., primary, Kerkvliet, Carlos Perez, primary, Krutilina, Raisa I., primary, Playa, Hilaire C., primary, Parke, Deanna N., primary, Thomas, Warner A., primary, Smeester, Branden A., primary, Moriarity, Branden S., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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26. Supplementary Figure 3 from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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27. Supplementary Figure 4 from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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28. Supplementary Figure 5 from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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32. Supplementary Figure 1 from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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33. Supplementary Figure 2 from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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35. Supplementary Figure 6 from Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF–driven Signaling Axis

Author

Regan Anderson, Tarah M., primary, Ma, Shihong, primary, Perez Kerkvliet, Carlos, primary, Peng, Yan, primary, Helle, Taylor M., primary, Krutilina, Raisa I., primary, Raj, Ganesh V., primary, Cidlowski, John A., primary, Ostrander, Julie H., primary, Schwertfeger, Kathryn L., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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37. Supplementary Figure 2 from Breast Tumor Kinase (Brk/PTK6) Is a Mediator of Hypoxia-Associated Breast Cancer Progression

Author

Regan Anderson, Tarah M., primary, Peacock, Danielle L., primary, Daniel, Andrea R., primary, Hubbard, Gregory K., primary, Lofgren, Kristopher A., primary, Girard, Brian J., primary, Schörg, Alexandra, primary, Hoogewijs, David, primary, Wenger, Roland H., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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40. Supplementary Table from Breast Tumor Kinase (Brk/PTK6) Is a Mediator of Hypoxia-Associated Breast Cancer Progression

Author

Regan Anderson, Tarah M., primary, Peacock, Danielle L., primary, Daniel, Andrea R., primary, Hubbard, Gregory K., primary, Lofgren, Kristopher A., primary, Girard, Brian J., primary, Schörg, Alexandra, primary, Hoogewijs, David, primary, Wenger, Roland H., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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43. Supplementary Figure 1 from Breast Tumor Kinase (Brk/PTK6) Is a Mediator of Hypoxia-Associated Breast Cancer Progression

Author

Regan Anderson, Tarah M., primary, Peacock, Danielle L., primary, Daniel, Andrea R., primary, Hubbard, Gregory K., primary, Lofgren, Kristopher A., primary, Girard, Brian J., primary, Schörg, Alexandra, primary, Hoogewijs, David, primary, Wenger, Roland H., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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45. Supplementary Figure 3 from Breast Tumor Kinase (Brk/PTK6) Is a Mediator of Hypoxia-Associated Breast Cancer Progression

Author

Regan Anderson, Tarah M., primary, Peacock, Danielle L., primary, Daniel, Andrea R., primary, Hubbard, Gregory K., primary, Lofgren, Kristopher A., primary, Girard, Brian J., primary, Schörg, Alexandra, primary, Hoogewijs, David, primary, Wenger, Roland H., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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47. Supplementary Methods from Breast Tumor Kinase (Brk/PTK6) Is a Mediator of Hypoxia-Associated Breast Cancer Progression

Author

Regan Anderson, Tarah M., primary, Peacock, Danielle L., primary, Daniel, Andrea R., primary, Hubbard, Gregory K., primary, Lofgren, Kristopher A., primary, Girard, Brian J., primary, Schörg, Alexandra, primary, Hoogewijs, David, primary, Wenger, Roland H., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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48. Abstract OT2-01-02: The SMILE Study: A phase II trial of onapristone in combination with fulvestrant for patients with ER-positive and HER2-negative metastatic breast cancer after progression on endocrine therapy and CDK 4/6 inhibitors

Author

Kamaraju, Sailaja, primary, Fowler, Amy, additional, Chaudhary, Lubna N., additional, Burkard, Mark, additional, Giever, Thomas, additional, Hegeman, Robert N, additional, Pipp-Dahm, Michele, additional, Cheng, Yee Chung, additional, Lange, Carol, additional, Jorns, Julie M., additional, Stella, Amy, additional, Siddiqui, Nauman, additional, Zurbriggen, Luke, additional, Rajguru, Saurabh, additional, Tarima, Sergey, additional, Sriram, Deepika, additional, Retseck, Janet, additional, Rui, Hallgeir, additional, Sahmoud, Tarek, additional, and Wisinski, Kari B., additional

Published
2023
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