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Your search keyword '"Hirsch, Heather A."' showing total 11 results
Start Over Author "Hirsch, Heather A." Publisher american association for cancer research
11 results on '"Hirsch, Heather A."'

1. Abstract 4053: Genetic and molecular profiling of ICOS hi CD4 T cells demonstrates clonal expansion of Th1 effector cells following JTX-2011 treatment in subjects with solid tumors

Author

Harvey, Christopher, primary, Hanson, Amanda, additional, Fan, Martin, additional, McGrath, Lara, additional, Felitsky, Daniel, additional, Johnson, Calvin, additional, Lacey, Sean, additional, Hirsch, Heather, additional, Hooper, Ellen, additional, McClure, Ty, additional, Trehu, Elizabeth, additional, Law, Deborah, additional, and Laken, Haley, additional

Published
2019
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2. Abstract 1678: Integrated genomics and histology based studies of triple negative breast cancer identify ICOS as potential target for therapeutic intervention

Author

Hirsch, Heather A., primary, Zi, Tong, additional, Fontana, Rachel, additional, Wu, Yun, additional, Reeves, Jason, additional, Needham, Alexander, additional, Stack, Edward, additional, Lee, David, additional, Lees, Emma, additional, Law, Deborah A., additional, Trehu, Elizabeth, additional, and Mittendorf, Elizabeth A., additional

Published
2018
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5. Abstract 543: Preclinical combination strategies to enhance the efficacy of the anti-PD-1 antibody pembrolizumab

Author

Pinheiro, Elaine M., primary, Hinton, Marlene, additional, Mangadu, Ruban, additional, Cai, Mingmei, additional, Phan, Uyen, additional, Nebozhyn, Michael, additional, Hirsch, Heather, additional, Loboda, Andrey, additional, Javaid, Sarah, additional, Wang, Yaolin, additional, Sriram, Venkataraman, additional, Phillips, Joseph H., additional, McClanahan, Terri, additional, and Long, Brian, additional

Published
2016
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7. Abstract 1307: Assessment of gene expression in peripheral blood from patients with advanced melanoma using RNA-seq before and after treatment with anti-PD-1 therapy with pembrolizumab (MK-3475)

Author

Ayers, Mark D., primary, Nebozhyn, Michael, additional, Hirsch, Heather A., additional, Cristescu, Razvan, additional, Murphy, Erin E., additional, Kang, S. Peter, additional, Ebbinghaus, Scot W., additional, McClanahan, Terrill K., additional, Loboda, Andrey, additional, and Lunceford, Jared K., additional

Published
2015
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9. Abstract 269: Evaluation of the antitumor activity of anti-PD-1 immunotherapy as a single agent and in combination with approved agents in preclinical tumor models

Author

Pinheiro, Elaine M., primary, Mangadu, Ruban, additional, Phan, Uyen T., additional, Cai, Mingmei, additional, Ma, Yanhong, additional, Hirsch, Heather A., additional, McClanahan, Terrill K., additional, Moniz, Raymond J., additional, Al-Assaad, Ali-Samer, additional, Basu, Samik, additional, Wang, Yaolin, additional, Sriram, Venkataraman, additional, Phillips, Joseph H., additional, and Long, Brian J., additional

Published
2015
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10. Metformin decreases the dose of chemotherapy for prolonging tumor remission in mouse xenografts involving multiple cancer cell types.

Author

Iliopoulos D, Hirsch HA, and Struhl K

Subjects
Administration, Oral, Animals, Breast Neoplasms drug therapy, Carboplatin administration & dosage, Carcinoma, Ductal, Breast drug therapy, Cell Line, Tumor, Dose-Response Relationship, Drug, Doxorubicin administration & dosage, Drug Synergism, Female, Humans, Injections, Intraperitoneal, Lung Neoplasms drug therapy, Male, Metformin administration & dosage, Mice, Mice, Nude, Paclitaxel administration & dosage, Prostatic Neoplasms drug therapy, Xenograft Model Antitumor Assays, Antineoplastic Combined Chemotherapy Protocols pharmacology, Metformin pharmacology, Neoplasms drug therapy
Abstract

Metformin, the first-line drug for treating diabetes, selectively kills the chemotherapy resistant subpopulation of cancer stem cells (CSC) in genetically distinct types of breast cancer cell lines. In mouse xenografts, injection of metformin and the chemotherapeutic drug doxorubicin near the tumor is more effective than either drug alone in blocking tumor growth and preventing relapse. Here, we show that metformin is equally effective when given orally together with paclitaxel, carboplatin, and doxorubicin, indicating that metformin works together with a variety of standard chemotherapeutic agents. In addition, metformin has comparable effects on tumor regression and preventing relapse when combined with a four-fold reduced dose of doxorubicin that is not effective as a monotherapy. Finally, the combination of metformin and doxorubicin prevents relapse in xenografts generated with prostate and lung cancer cell lines. These observations provide further evidence for the CSC hypothesis for cancer relapse, an experimental rationale for using metformin as part of combinatorial therapy in a variety of clinical settings, and for reducing the chemotherapy dose in cancer patients.

Published
2011
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11. Metformin selectively targets cancer stem cells, and acts together with chemotherapy to block tumor growth and prolong remission.

Author

Hirsch HA, Iliopoulos D, Tsichlis PN, and Struhl K

Subjects
Adult, Animals, Antineoplastic Combined Chemotherapy Protocols pharmacology, Breast drug effects, Breast pathology, Breast Neoplasms pathology, Cell Growth Processes drug effects, Cell Line, Tumor, Cell Transformation, Neoplastic drug effects, Cell Transformation, Neoplastic pathology, Doxorubicin administration & dosage, Doxorubicin pharmacology, Female, Humans, Metformin administration & dosage, Mice, Mice, Nude, Neoplastic Stem Cells pathology, Random Allocation, Xenograft Model Antitumor Assays, Breast Neoplasms drug therapy, Metformin pharmacology, Neoplastic Stem Cells drug effects
Abstract

The cancer stem cell hypothesis suggests that, unlike most cancer cells within a tumor, cancer stem cells resist chemotherapeutic drugs and can regenerate the various cell types in the tumor, thereby causing relapse of the disease. Thus, drugs that selectively target cancer stem cells offer great promise for cancer treatment, particularly in combination with chemotherapy. Here, we show that low doses of metformin, a standard drug for diabetes, inhibits cellular transformation and selectively kills cancer stem cells in four genetically different types of breast cancer. The combination of metformin and a well-defined chemotherapeutic agent, doxorubicin, kills both cancer stem cells and non-stem cancer cells in culture. Furthermore, this combinatorial therapy reduces tumor mass and prevents relapse much more effectively than either drug alone in a xenograft mouse model. Mice seem to remain tumor-free for at least 2 months after combinatorial therapy with metformin and doxorubicin is ended. These results provide further evidence supporting the cancer stem cell hypothesis, and they provide a rationale and experimental basis for using the combination of metformin and chemotherapeutic drugs to improve treatment of patients with breast (and possibly other) cancers.

Published
2009
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