Eric A. Armstrong

University of Wisconsin–Madison

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Paul M. Harari

University of Wisconsin Carbone Cancer Center

179

Shyhmin Huang

University of Wisconsin–Madison

134

Lauryn R. Werner

University of Kansas Medical Center

Chunrong Li

University of Wisconsin–Madison

Zachary S. Morris

University of Wisconsin–Madison

Deric L. Wheeler

Wisconsin Institutes for Discovery

Chunrong Li

Guigang City People's Hospital

Randall J. Kimple

University of Wisconsin–Madison

Mark X. Sliwkowski

Molecular Oncology (United States)

Gopal Iyer

National Cancer Centre Singapore

Cooperative Institutions

University of Wisconsin–Madison

133

University of Wisconsin Carbone Cancer Center

Istituti di Ricovero e Cura a Carattere Scientifico

Madison Group (United States)

Wisconsin Institutes for Discovery

UW Health University Hospital

Harvard University

Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale"

National Institutes of Health

Azienda Sanitaria Ospedaliera S.Croce e Carle Cuneo

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Bacterial Analogs of Plant Tetrahydropyridine Alkaloids Mediate Microbial Interactions in a Rhizosphere Model System

Applied and Environmental Microbiology (2019)

Gabriel L. Lozano Hyun Bong Park Juan I. Bravo Eric A. Armstrong John M. Denu

The microbiomes of plants are critical to host physiology and development. Microbes are attracted to the rhizosphere due to massive secretion of plant photosynthates from roots. Microorganisms that successfully join the rhizosphere community from bulk soil have access to more abundant and diverse molecules, producing a highly competitive and selective environment. In the rhizosphere, as in other microbiomes, little is known about the genetic basis for individual species’ behaviors within the community. In this study, we characterized competition between Pseudomonas koreensis and Flavobacterium johnsoniae , two common rhizosphere inhabitants. We identified a widespread gene cluster in several Pseudomonas spp. that is necessary for the production of a novel family of tetrahydropyridine alkaloids that are structural analogs of plant alkaloids. We expand the known repertoire of antibiotics produced by Pseudomonas in the rhizosphere and demonstrate the role of the metabolites in interactions with other rhizosphere bacteria.

10.1128/aem.03058-18

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Citations (31)

Supplemental Figure 4 from In Situ Tumor Vaccination by Combining Local Radiation and Tumor-Specific Antibody or Immunocytokine Treatments

Zachary S. Morris Emily I. Guy David M. Francis Monica M. Gressett Lauryn R. Werner

Hu14.18K322A and hu14.18-IL2 do not impact intrinsic cell sensitivity to radiation in vitro and radiation does not impact GD2 expression but GD2-expression is required for the cooperative in vivo interaction of radiation with hu14.18K322A or hu14.18-IL2.

10.1158/0008-5472.22409708

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Supplemental Figure 6 from In Situ Tumor Vaccination by Combining Local Radiation and Tumor-Specific Antibody or Immunocytokine Treatments

Zachary S. Morris Emily I. Guy David M. Francis Monica M. Gressett Lauryn R. Werner

The time-sensitivity of combined radiation and hu14.18-IL2 is not observed with radiation and hu14.18K322A and radiation induces a dose-dependent increase in Fas/CD95 expression.

10.1158/0008-5472.22409702

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Supplementary Methods and Materials from Dual Targeting of EGFR and HER3 with MEHD7945A Overcomes Acquired Resistance to EGFR Inhibitors and Radiation

Shyhmin Huang Chunrong Li Eric A. Armstrong Chimera R. Peet Jarob Saker

PDF file- 63KB, Supplementary Materials and Methods

EGFR Inhibitors

10.1158/0008-5472.22398876

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Data from Antitumor Effects of MEHD7945A, a Dual-Specific Antibody against EGFR and HER3, in Combination with Radiation in Lung and Head and Neck Cancers

Chunrong Li Shyhmin Huang Eric A. Armstrong David M. Francis Lauryn R. Werner

<div>AbstractHuman epidermal growth factor receptor family members (EGFR, HER2, HER3, and HER4) play important roles in tumorigenesis and response to cancer therapeutics. In this study, we evaluated the capacity of the dual-target antibody MEHD7945A that simultaneously targets EGFR and HER3 to modulate radiation response in lung and head and neck cancer models. Antitumor effects of MEHD7945A in combination with radiation were evaluated in cell culture and tumor xenograft models. Mechanisms that may contribute to increased radiation killing by MEHD7945A, including DNA damage and inhibition of EGFR–HER signaling pathways, were analyzed. Immunohistochemical analysis of tumor xenografts was conducted to evaluate the effect of MEHD7945A in combination with radiation on tumor growth and microenvironment. MEHD7945A inhibited basal and radiation-induced EGFR and HER3 activation resulting in the inhibition of tumor cell growth and enhanced radiosensitivity. MEHD7945A was more effective in augmenting radiation response than treatment with individual anti-EGFR or anti-HER3 antibodies. An increase in DNA double-strand breaks associated γ-H2AX was observed in cells receiving combined treatment with MEHD7945A and radiation. Immunohistochemical staining evaluation in human tumor xenografts showed that MEHD7945A combined with radiation significantly reduced the expression of markers of tumor proliferation and tumor vasculature. These findings reveal the capacity of MEHD7945A to augment radiation response in lung and head and neck cancers. The dual EGFR/HER3–targeting action of MEHD7945A merits further investigation and clinical trial evaluation as a radiation sensitizer in cancer therapy. Mol Cancer Ther; 14(9); 2049–59. ©2015 AACR.</div>

Radiosensitivity

EGFR Inhibitors

10.1158/1535-7163.c.6538522.v1

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Panitumumab, a Fully Human Anti-EGFR Monoclonal Antibody, Augments Radiation Response in Xenograft Models of Upper Aerodigestive Tract Cancers

International Journal of Radiation Oncology*Biology*Physics (2007)

Tim J. Kruser Eric A. Armstrong S. Huang Robert Radinsky Charlie Starnes

Panitumumab

EGFR Inhibitors

10.1016/j.ijrobp.2007.07.1934

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Supplementary Figure Legends from Dual Targeting of EGFR and HER3 with MEHD7945A Overcomes Acquired Resistance to EGFR Inhibitors and Radiation

Shyhmin Huang Chunrong Li Eric A. Armstrong Chimera R. Peet Jarob Saker

PDF file - 63KB, Supplementary Figure Legends

EGFR Inhibitors

10.1158/0008-5472.22398879.v1

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Data from Establishment and Characterization of a Model of Acquired Resistance to Epidermal Growth Factor Receptor Targeting Agents in Human Cancer Cells

Sergio Benavente Shyhmin Huang Eric A. Armstrong Alexander Chi Kun-Tai Hsu

<div>AbstractPurpose: The epidermal growth factor receptor (EGFR) is recognized as a key mediator of proliferation and progression in many human tumors. A series of EGFR-specific inhibitors have recently gained Food and Drug Administration approval in oncology. These strategies of EGFR inhibition have shown major tumor regressions in approximately 10% to 20% of advanced cancer patients. Many tumors, however, eventually manifest resistance to treatment. Efforts to better understand the underlying mechanisms of acquired resistance to EGFR inhibitors, and potential strategies to overcome resistance, are greatly needed.Experimental Design: To develop cell lines with acquired resistance to EGFR inhibitors we utilized the human head and neck squamous cell carcinoma tumor cell line SCC-1. Cells were treated with increasing concentrations of cetuximab, gefitinib, or erlotinib, and characterized for the molecular changes in the EGFR inhibitor–resistant lines relative to the EGFR inhibitor–sensitive lines.Results: EGFR inhibitor–resistant lines were able to maintain their resistant phenotype in both drug-free medium and in athymic nude mouse xenografts. In addition, EGFR inhibitor–resistant lines showed a markedly increased proliferation rate. EGFR inhibitor–resistant lines had elevated levels of phosphorylated EGFR, mitogen-activated protein kinase, AKT, and signal transducer and activator of transcription 3, which were associated with reduced apoptotic capacity. Subsequent in vivo experiments indicated enhanced angiogenic potential in EGFR inhibitor–resistant lines. Finally, EGFR inhibitor–resistant lines showed cross-resistance to ionizing radiation.Conclusions: We have developed EGFR inhibitor–resistant human head and neck squamous cell carcinoma cell lines. This model provides a valuable preclinical tool to investigate molecular mechanisms of acquired resistance to EGFR blockade.</div>

EGFR Inhibitors

Growth inhibition

Erlotinib Hydrochloride

10.1158/1078-0432.c.6517899

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Data from p53 Modulates Acquired Resistance to EGFR Inhibitors and Radiation

Shyhmin Huang Sergio Benavente Eric A. Armstrong Chunrong Li Deric L. Wheeler

<div>AbstractThere is presently great interest in mechanisms of acquired resistance to epidermal growth factor receptor (EGFR) inhibitors that are now being used widely in the treatment of a variety of common human cancers. To investigate these mechanisms, we established EGFR inhibitor–resistant clones from non–small cell lung cancer cells. A comparative analysis revealed that acquired resistance to EGFR inhibitors was associated consistently with the loss of p53 and cross-resistance to radiation. To examine the role of p53, we first knocked down p53 in sensitive parental cells and found a reduction in sensitivity to both EGFR inhibitors and radiation. Conversely, restoration of functional p53 in EGFR inhibitor–resistant cells was sufficient to resensitize them to EGFR inhibitors or radiation in vitro and in vivo. Further studies indicate that p53 may enhance sensitivity to EGFR inhibitors and radiation via induction of cell-cycle arrest, apoptosis, and DNA damage repair. Taken together, these findings suggest a central role of p53 in the development of acquired resistance to EGFR inhibitors and prompt consideration to apply p53 restoration strategies in future clinical trials that combine EGFR inhibitors and radiation. Cancer Res; 71(22); 7071–9. ©2011 AACR.</div>

EGFR Inhibitors

Acquired resistance

10.1158/0008-5472.c.6503190.v1

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Insulin-like Growth Factor-I Receptor Signaling Blockade Combined with Radiation

Cancer Research (2007)

Gregory W. Allen Corey Saba Eric A. Armstrong Shyhmin Huang Sergio Benavente

Abstract Signaling through the insulin-like growth factor-I receptor (IGF-IR) is implicated in cellular proliferation, apoptosis, carcinogenesis, metastasis, and resistance to cytotoxic cancer therapies. Targeted disruption of IGF-IR signaling combined with cytotoxic therapy may therefore yield improved anticancer efficacy over conventional treatments alone. In this study, a fully human anti–IGF-IR monoclonal antibody A12 (ImClone Systems, Inc., New York, NY) is examined as an adjunct to radiation therapy. IGF-IR expression is shown for a diverse cohort of cell lines, whereas targeted IGF-IR blockade by A12 inhibits IGF-IR phosphorylation and activation of the downstream effectors Akt and mitogen-activated protein kinase. Anchorage-dependent proliferation and xenograft growth is inhibited by A12 in a dose-dependent manner, particularly for non–small cell lung cancer lines. Clonogenic radiation survival of H226 and H460 cells grown under anchorage-dependent conditions is impaired by A12, demonstrating a radiation dose-enhancing effect for IGF-IR blockade. Postradiation anchorage-independent colony formation is inhibited by A12 in A549 and H460 cells. In the H460 xenograft model, combining A12 and radiation significantly enhances antitumor efficacy compared with either modality alone. These effects may be mediated by promotion of radiation-induced, double-stranded DNA damage and apoptosis as observed in cell culture. In summary, these results validate IGF-IR signal transduction blockade as a promising strategy to improve radiation therapy efficacy in human tumors, forming a basis for future clinical trials. [Cancer Res 2007;67(3):1155–62]

Clonogenic assay

10.1158/0008-5472.can-06-2000

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Citations (93)