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Start Over Author "Schwarz LJ" Journal cancer research
8 results on '"Schwarz LJ"'

1. Abstract P4-01-09: Combined analysis of tissue and blood biopsies by NGS in patients with advanced breast cancer identifies targetable molecular alterations

Author

Salvador, JF, primary, Pinto, JA, additional, Araujo, JM, additional, Tirado-Hurtado, I, additional, Flores, CJ, additional, Chirinos, LA, additional, Requena, MC, additional, Carpio, S, additional, Finzel Pérez, A, additional, Aguilar, A, additional, Demol, F, additional, and Schwarz, LJ, additional

Published
2019
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2. Abstract PD5-02: Not presented

Author

Guerrero-Zotano, AL, primary, Stricker, TP, additional, Hutchinson, KE, additional, Stover, DG, additional, Formisano, L, additional, Lee, K-M, additional, Schwarz, LJ, additional, Giltnane, JM, additional, Jansen, VM, additional, Gavila, J, additional, Perez-Fidalgo, A, additional, Lluch, A, additional, Llombart, A, additional, Bayar, MA, additional, Michiels, S, additional, André, F, additional, Arnedos, M, additional, Ruiz, A, additional, and Arteaga, CL, additional

Published
2018
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3. Abstract GS6-05: Gain-of-function kinase library screen identifies FGFR1 amplification as a mechanism of resistance to antiestrogens and CDK4/6 inhibitors in ER+ breast cancer

Author

Formisano, L, primary, Lu, Y, additional, Jansen, VM, additional, Bauer, JA, additional, Hanker, A, additional, Gonzalez Ericsson, P, additional, Lee, K-M, additional, Nixon, MJ, additional, Guerrero-Zotano, AL, additional, Schwarz, LJ, additional, Sanders, M, additional, Sudhan, D, additional, Dugger, TC, additional, Cruz, MR, additional, Behdad, A, additional, Cristofanilli, M, additional, Bardia, A, additional, O'Shaughnessy, J, additional, Mayer, IA, additional, and Arteaga, CL, additional

Published
2018
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4. Abstract P1-13-08: Extended adjuvant neratinib/fulvestrant blocks ER/HER2 crosstalk and maintains complete responses of ER+/HER2+ tumors following treatment with chemotherapy and anti-HER2 therapy

Author

Sudhan, DR, primary, Schwarz, LJ, additional, Guerrero-Zotano, AL, additional, Nixon, M, additional, Formisano, L, additional, Croessmann, S, additional, Gonzalez Ericsson, PI, additional, Sanders, ME, additional, Balko, JM, additional, Avogadri-Connors, F, additional, Cutler, RE, additional, Lalani, AS, additional, Bryce, R, additional, Auerbach, A, additional, and Arteaga, CL, additional

Published
2018
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5. Abstract P6-12-09: Pan-HER, an antibody mixture with antitumor activity against drug-resistant HER2-overexpressing breast cancers with high ERBB ligand expression

Author

Schwarz, LJ, primary, Hutchinson, KE, additional, Estrada, MV, additional, Sanders, ME, additional, Dugger, TC, additional, Formisano, L, additional, Guerrero, AL, additional, Red-Brewer, M, additional, Young, CD, additional, Lantto, J, additional, Pedersen, MW, additional, Kragh, M, additional, Horak, ID, additional, and Arteaga, CL, additional

Published
2017
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6. Abstract S6-01: JAK2 amplifications are enriched in triple negative breast cancers (TNBCs) after neoadjuvant chemotherapy and predict poor prognosis

Author

Balko, JM, primary, Giltnane, JM, additional, Schwarz, LJ, additional, Sanders, ME, additional, Wang, K, additional, Harris, LN, additional, Lin, NU, additional, Miller, VA, additional, Stephens, PJ, additional, Yelensky, R, additional, Pinto, JA, additional, Gomez, H, additional, and Arteaga, CL, additional

Published
2013
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8. Activation of MAPK pathways due to DUSP4 loss promotes cancer stem cell-like phenotypes in basal-like breast cancer.

Author

Balko JM, Schwarz LJ, Bhola NE, Kurupi R, Owens P, Miller TW, Gómez H, Cook RS, and Arteaga CL

Subjects
Animals, Breast Neoplasms genetics, Breast Neoplasms metabolism, Cell Culture Techniques, Dual-Specificity Phosphatases genetics, Dual-Specificity Phosphatases metabolism, Female, Heterografts, Humans, Mice, Mice, Nude, Mitogen-Activated Protein Kinase Phosphatases genetics, Mitogen-Activated Protein Kinase Phosphatases metabolism, Mitogen-Activated Protein Kinases metabolism, Neoplastic Stem Cells metabolism, Neoplastic Stem Cells pathology, Phenotype, Transfection, Breast Neoplasms enzymology, Breast Neoplasms pathology, Dual-Specificity Phosphatases deficiency, MAP Kinase Signaling System physiology, Mitogen-Activated Protein Kinase Phosphatases deficiency, Mitogen-Activated Protein Kinases genetics
Abstract

Basal-like breast cancer (BLBC) is an aggressive disease that lacks a clinically approved targeted therapy. Traditional chemotherapy is effective in BLBC, but it spares the cancer stem cell (CSC)-like population, which is likely to contribute to cancer recurrence after the initial treatment. Dual specificity phosphatase-4 (DUSP4) is a negative regulator of the mitogen-activated protein kinase (MAPK) pathway that is deficient in highly aggressive BLBCs treated with chemotherapy, leading to aberrant MAPK activation and resistance to taxane-induced apoptosis. Herein, we investigated how DUSP4 regulates the MAP-ERK kinase (MEK) and c-jun-NH2-kinase (JNK) pathways in modifying CSC-like behavior. DUSP4 loss increased mammosphere formation and the expression of the CSC-promoting cytokines interleukin (IL)-6 and IL-8. These effects were caused in part by loss of control of the MEK and JNK pathways and involved downstream activation of the ETS-1 and c-JUN transcription factors. Enforced expression of DUSP4 reduced the CD44(+)/CD24(-) population in multiple BLBC cell lines in a MEK-dependent manner, limiting tumor formation of claudin-low SUM159PT cells in mice. Our findings support the evaluation of MEK and JNK pathway inhibitors as therapeutic agents in BLBC to eliminate the CSC population., (©2013 AACR.)

Published
2013
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