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3. Activation of ERBB4 in Glioblastoma Can Contribute to Increased Tumorigenicity and Influence Therapeutic Response.

Author

Donoghue, Jacqueline F, Kerr, Lauren T, Alexander, Naomi W, Greenall, Sameer A, Longano, Anthony B, Gottardo, Nicholas G, Wang, Rong, Tabar, Viviane, Adams, Timothy E, Mischel, Paul S, and Johns, Terrance G

Subjects
EGFR, ERBB4, GBM, prognosis, therapy, Oncology and Carcinogenesis
Abstract

Glioblastoma (GBM) is often resistant to conventional and targeted therapeutics. ErbB2 Receptor Tyrosine Kinase 4 (ERBB4) is expressed throughout normal brain and is an oncogene in several pediatric brain cancers; therefore, we investigated ERBB4 as a prognostic marker and therapeutic target in GBM. Using RT-qPCR, we quantified mRNA encoding total ERBB4 and known ERBB4 variants in GBM and non-neoplastic normal brain (NNB) samples. Using immunohistochemistry, we characterized the localization of total and phosphorylated ERBB4 (p-ERBB4) and EGFR protein in archived GBM samples and assessed their association with patient survival. Furthermore, we evaluated the effect of ERBB4 phosphorylation on angiogenesis and tumorigenicity in GBM xenograft models. Total ERBB4 mRNA was significantly lower in GBM than NNB samples, with the juxtamembrane JM-a and cytoplasmic CYT-2 variants predominating. ERBB4 protein was ubiquitously expressed in GBM but was not associated with patient survival. However, high p-ERBB4 in 11% of archived GBM samples, independent of p-EGFR, was associated with shorter patient survival (12.0 ± 3.2 months) than was no p-ERBB4 (22.5 ± 9.5 months). Increased ERBB4 activation was also associated with increased proliferation, angiogenesis, tumorigenicity and reduced sensitivity to anti-EGFR treatment in xenograft models. Despite low ERBB4 mRNA in GBM, the functional effects of increased ERBB4 activation identify ERBB4 as a potential prognostic and therapeutic target.

Published
2018

4. Impact of Parental Time-Restricted Feeding on Offspring Metabolic Phenotypic Traits

Author

Fan, Yibo, primary, Peng, Xiangyuan, additional, Tabassum, Nishat I, additional, Cheng, Xiangru, additional, Selvaraji, Sharmelee, additional, Tran, Vivian, additional, Hughes, Tayla Hughes Gibson, additional, Wickramasinghe, Buddhila, additional, Jamal, Abdulsatar, additional, Dinh, Quynh Nhu, additional, Gelderblom, Mathias, additional, Drummond, Grant R, additional, Sobey, Christopher G, additional, Penman, Jim, additional, Johns, Terrance G, additional, Vemuganti, Raghu, additional, Gunaratne, Jayantha, additional, Mattson, Mark P, additional, Jo, Dong-Gyu, additional, Jelinic, Maria, additional, and Arumugam, Thiruma V, additional

Published
2024
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5. Lemming and Vole Cycles: A New Intrinsic Model.

Author

Levay, Elizabeth A., Nasser, Helen, Zelko, Matthew D., Penman, Jim, and Johns, Terrance G.

Subjects
ANIMAL populations, PHENOTYPIC plasticity, FIELD research, POPULATION density, LAGOMORPHA
Abstract

It is 100 years since the first paper described the multiannual cycles in Arctic rodents and lagomorphs. The mechanisms driving population cycles in animals like lemmings and voles are complex, often attributed to extrinsic factors, such as food availability and quality, pathogens, parasites and/or predators. While extrinsic factors provide insights into population cycles, none fully explain the phenomenon. We propose an underlying innate, intrinsic mechanism, based on epigenetic regulation, that drives population cycles under harsh arctic conditions. We propose that epigenetically driven phenotypic changes associated with sexual development, growth and behaviour accumulate over time in offspring, eventually producing a phase change from rising population density to eventual population collapse. Under this hypothesis, and unlike previous hypotheses, extrinsic factors modify population cycles but would not be primary drivers. The interaction between our intrinsic cycle and extrinsic factors explains established phenomena like delayed‐density dependence, whereby population growth is controlled by time‐dependent negative feedback. We advocate integrating a century of field research with the latest epigenetic analysis to better understand the drivers of population cycles. [ABSTRACT FROM AUTHOR]

Published
2024
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13. The dystroglycan receptor maintains glioma stem cells in the vascular niche

Author

Day, Bryan W., Lathia, Justin D., Bruce, Zara C., D’Souza, Rochelle C. J., Baumgartner, Ulrich, Ensbey, Kathleen S., Lim, Yi Chieh, Stringer, Brett W., Akgül, Seçkin, Offenhäuser, Carolin, Li, Yuchen, Jamieson, Paul R., Smith, Fiona M., Jurd, Courtney L. R., Robertson, Thomas, Inglis, Po-Ling, Lwin, Zarnie, Jeffree, Rosalind L., Johns, Terrance G., Bhat, Krishna P. L., Rich, Jeremy N., Campbell, Kevin P., and Boyd, Andrew W.

Published
2019
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16. An Anti-VEGF-B Antibody Reduces Abnormal Tumor Vasculature and Enhances the Effects of Chemotherapy.

Author

Janes, Peter W., Parslow, Adam C., Cao, Diana, Rigopoulos, Angela, Lee, Fook-Thean, Gong, Sylvia J., Cartwright, Glenn A., Burvenich, Ingrid J. G., Eriksson, Ulf, Johns, Terrance G., Scott, Fiona E., and Scott, Andrew M.

Subjects
VASCULAR endothelial growth factors, BIOLOGICAL models, RESEARCH funding, TRANSPLANTATION of organs, tissues, etc., LIGANDS (Chemistry), OXYGEN, BEVACIZUMAB, COLORECTAL cancer, NUTRITIONAL requirements, DESCRIPTIVE statistics, CANCER chemotherapy, MICE, ANIMAL experimentation, GROWTH factors, COMPARATIVE studies
Abstract

Simple Summary: In order to grow, tumors need nutrients and oxygen, which are supplied by new blood vessels that are often abnormal and leaky. The development of these blood vessels is driven by proteins called growth factors, which bind to receptor proteins on other cells. We show for the first time that an antibody against a vascular growth factor called VEGF-B, when used to treat mice with tumors, reduces the amount of abnormal tumor blood vessels, and inhibits tumor growth, as well as improving the response to chemotherapy. These results suggest that targeting VEGF-B could be a potential approach for anti-cancer therapy, particularly in combination with chemotherapy. The vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are key regulators of blood vessel formation, including in tumors, where their deregulated function can promote the production of aberrant, leaky blood vessels, supporting tumor development. Here we investigated the VEGFR1 ligand VEGF-B, which we demonstrate to be expressed in tumor cells and in tumor stroma and vasculature across a range of tumor types. We examined the anti-VEGF-B-specific monoclonal antibody 2H10 in preclinical xenograft models of breast and colorectal cancer, in comparison with the anti-VEGF-A antibody bevacizumab. Similar to bevacizumab, 2H10 therapy was associated with changes in tumor blood vessels and intra-tumoral diffusion consistent with normalization of the tumor vasculature. Accordingly, treatment resulted in partial inhibition of tumor growth, and significantly improved the response to chemotherapy. Our studies indicate the importance of VEGF-B in tumor growth, and the potential of specific anti-VEGF-B treatment to inhibit tumor development, alone or in combination with established chemotherapies. [ABSTRACT FROM AUTHOR]

Published
2024
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17. A surgically optimized intraoperative poly(I:C)-releasing hydrogel prevents cancer recurrence

Author

Rwandamuriye, Francois Xavier, primary, Evans, Cameron W., additional, Wylie, Ben, additional, Norret, Marck, additional, Vitali, Breana, additional, Ho, Diwei, additional, Nguyen, Dat, additional, Roper, Ellise A., additional, Wang, Tao, additional, Hepburn, Matt S., additional, Sanderson, Rowan W., additional, Pfirrmann, Maren, additional, Fear, Vanessa S., additional, Forbes, Catherine A., additional, Wyatt, Ken, additional, Ryan, Anne L., additional, Johns, Terrance G., additional, Phillips, Marianne B., additional, Hodder, Rupert, additional, Leslie, Connull, additional, Kennedy, Brendan F., additional, Zemek, Rachael M., additional, Iyer, Killugudi Swaminathan, additional, and Lesterhuis, Willem Joost, additional

Published
2023
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18. Publisher Correction: A reference collection of patient-derived cell line and xenograft models of proneural, classical and mesenchymal glioblastoma

Author

Stringer, Brett W., Day, Bryan W., D’Souza, Rochelle C. J., Jamieson, Paul R., Ensbey, Kathleen S., Bruce, Zara C., Lim, Yi Chieh, Goasdoué, Kate, Offenhäuser, Carolin, Akgül, Seçkin, Allan, Suzanne, Robertson, Thomas, Lucas, Peter, Tollesson, Gert, Campbell, Scott, Winter, Craig, Do, Hongdo, Dobrovic, Alexander, Inglis, Po-Ling, Jeffree, Rosalind L., Johns, Terrance G., and Boyd, Andrew W.

Published
2020
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19. A reference collection of patient-derived cell line and xenograft models of proneural, classical and mesenchymal glioblastoma

Author

Stringer, Brett W., Day, Bryan W., D’Souza, Rochelle C. J., Jamieson, Paul R., Ensbey, Kathleen S., Bruce, Zara C., Lim, Yi Chieh, Goasdoué, Kate, Offenhäuser, Carolin, Akgül, Seçkin, Allan, Suzanne, Robertson, Thomas, Lucas, Peter, Tollesson, Gert, Campbell, Scott, Winter, Craig, Do, Hongdo, Dobrovic, Alexander, Inglis, Po-Ling, Jeffree, Rosalind L., Johns, Terrance G., and Boyd, Andrew W.

Published
2019
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21. Supplementary Methods and Materials from Fyn and Src Are Effectors of Oncogenic Epidermal Growth Factor Receptor Signaling in Glioblastoma Patients

Author

Lu, Kan V., primary, Zhu, Shaojun, primary, Cvrljevic, Anna, primary, Huang, Tiffany T., primary, Sarkaria, Shawn, primary, Ahkavan, David, primary, Dang, Julie, primary, Dinca, Eduard B., primary, Plaisier, Seema B., primary, Oderberg, Isaac, primary, Lee, Yohan, primary, Chen, Zugen, primary, Caldwell, Jeremy S., primary, Xie, Yongmin, primary, Loo, Joseph A., primary, Seligson, David, primary, Chakravari, Arnab, primary, Lee, Francis Y., primary, Weinmann, Roberto, primary, Cloughesy, Timothy F., primary, Nelson, Stanley F., primary, Bergers, Gabriele, primary, Graeber, Thomas, primary, Furnari, Frank B., primary, James, C. David, primary, Cavenee, Webster K., primary, Johns, Terrance G., primary, and Mischel, Paul S., primary

Published
2023
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22. Data from Fyn and Src Are Effectors of Oncogenic Epidermal Growth Factor Receptor Signaling in Glioblastoma Patients

Author

Lu, Kan V., primary, Zhu, Shaojun, primary, Cvrljevic, Anna, primary, Huang, Tiffany T., primary, Sarkaria, Shawn, primary, Ahkavan, David, primary, Dang, Julie, primary, Dinca, Eduard B., primary, Plaisier, Seema B., primary, Oderberg, Isaac, primary, Lee, Yohan, primary, Chen, Zugen, primary, Caldwell, Jeremy S., primary, Xie, Yongmin, primary, Loo, Joseph A., primary, Seligson, David, primary, Chakravari, Arnab, primary, Lee, Francis Y., primary, Weinmann, Roberto, primary, Cloughesy, Timothy F., primary, Nelson, Stanley F., primary, Bergers, Gabriele, primary, Graeber, Thomas, primary, Furnari, Frank B., primary, James, C. David, primary, Cavenee, Webster K., primary, Johns, Terrance G., primary, and Mischel, Paul S., primary

Published
2023
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23. Supplementary Figures 1-6 from Fyn and Src Are Effectors of Oncogenic Epidermal Growth Factor Receptor Signaling in Glioblastoma Patients

Author

Lu, Kan V., primary, Zhu, Shaojun, primary, Cvrljevic, Anna, primary, Huang, Tiffany T., primary, Sarkaria, Shawn, primary, Ahkavan, David, primary, Dang, Julie, primary, Dinca, Eduard B., primary, Plaisier, Seema B., primary, Oderberg, Isaac, primary, Lee, Yohan, primary, Chen, Zugen, primary, Caldwell, Jeremy S., primary, Xie, Yongmin, primary, Loo, Joseph A., primary, Seligson, David, primary, Chakravari, Arnab, primary, Lee, Francis Y., primary, Weinmann, Roberto, primary, Cloughesy, Timothy F., primary, Nelson, Stanley F., primary, Bergers, Gabriele, primary, Graeber, Thomas, primary, Furnari, Frank B., primary, James, C. David, primary, Cavenee, Webster K., primary, Johns, Terrance G., primary, and Mischel, Paul S., primary

Published
2023
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31. Antibodies Specifically Targeting a Locally Misfolded Region of Tumor Associated EGFR

Author

Garrett, Thomas P. J., Burgess, Antony W., Gan, Hui K., Luwor, Rod B., Cartwright, Glenn, Walker, Francesca, Orchard, Suzanne G., Clayton, Andrew H. A., Nice, Edouard C., Rothacker, Julie, Catimel, Bruno, Cavenee, Webster K., Old, Lloyd J., Stockert, Elisabeth, Ritter, Gerd, Adams, Timothy E., Hoyne, Peter A., Wittrup, Dane, Chao, Ginger, Cochran, Jennifer R., Luo, Cindy, Lou, Mezhen, Huyton, Trevor, Xu, Yibin, Fairlie, W. Douglas, Yao, Shenggen, Scott, Andrew M., Johns, Terrance G., and Adams, Jerry M.

Published
2009
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32. A Phase I Clinical Trial with Monoclonal Antibody ch806 Targeting Transitional State and Mutant Epidermal Growth Factor Receptors

Author

Scott, Andrew M., Lee, Fook-Thean, Tebbutt, Niall, Herbertson, Rebecca, Gill, Sanjeev S., Liu, Zhanqi, Skrinos, Effie, Murone, Carmel, Saunder, Timothy H., Chappell, Bridget, Papenfuss, Anthony T., Poon, Aurora M. T., Hopkins, Wendie, Smyth, Fiona E., MacGregor, Duncan, Cher, Lawrence M., Jungbluth, Achim A., Ritter, Gerd, Brechbiel, Martin W., Murphy, Roger, Burgess, Antony W., Hoffman, Eric W., Johns, Terrance G., and Old, Lloyd J.

Published
2007
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34. Targeting OLIG2 increases therapeutic responses in SHH medulloblastoma mouse models and patient-derived medulloblastoma organoids

Author

Li, Yuchen, primary, Dismuke, Taylor, additional, Lim, Chaemin, additional, Bruce, Zara C., additional, Offenhäuser, Carolin, additional, Baumgartner, Ulrich, additional, Maybury, Mellissa, additional, D’Souza, Rochelle C. J., additional, Hassall, Timothy, additional, Wainwright, Brandon, additional, Stein, Gregory, additional, Piper, Michael, additional, Johns, Terrance G., additional, Sokolsky-Papkov, Marina, additional, Gershon, Timothy R., additional, and Day, Bryan W., additional

Published
2022
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39. Unligated epidermal growth factor receptor forms higher order oligomers within microclusters on A431 cells that are sensitive to tyrosine kinase inhibitor binding

Author

Clayton, Andrew H.A., Tavarnesi, Maria L., and Johns, Terrance G.

Subjects
Tyrosine -- Research, Oligomers -- Structure, Oligomers -- Research, Biological sciences, Chemistry
Abstract

The association states of unligated, immunotagged epidermal growth factor receptor (EGFR) on the surface of intact epidermoid carcinoma A431 cells are analyzed using AlexaFluor488 and Alexafluor546 anti-EGFR antibody, mAb528, as probes. The study results are consistent with a higher order nanoscale receptor organization of the unligated receptor population that is partially controlled by the kinase domains.

Published
2007

42. Functional effects of glycosylation at Asn-579 of epidermal growth factor receptor

Author

Whitson, Kristin B., Whitson, Stefanie R., Red-Brewer, Monica L., McCoy, Austin J., Vitali, Angela A., Walker, Francessca, Johns, Terrance G., Beth, Albert H., and Staros, James V.

Subjects
Epidermal growth factor -- Chemical properties, Glycosylation -- Research, Proteins -- Chemical properties, Biological sciences, Chemistry
Abstract

An investigation of functional effects of glycosylation at N(super 579) of the epidermal growth factor (EGFR) is presented. It is revealed that EGF-stimulated phosphorylation in cells expressing N579Q-EGFRs results in notable differences in the pattern of tyrosine phosphorylated proteins compared with that obtained in cells expressing (wild type) WT-EGFRs.

Published
2005

46. MK2 Inhibition Induces p53-Dependent Senescence in Glioblastoma Cells

Author

Phoa, Athena F., primary, Recasens, Ariadna, additional, Gurgis, Fadi M. S., additional, Betts, Tara A., additional, Menezes, Sharleen V., additional, Chau, Diep, additional, Nordfors, Kristiina, additional, Haapasalo, Joonas, additional, Haapasalo, Hannu, additional, Johns, Terrance G., additional, Stringer, Brett W., additional, Day, Bryan W., additional, Buckland, Michael E., additional, Lalaoui, Najoua, additional, and Munoz, Lenka, additional

Published
2020
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47. Simultaneous targeting of DNA replication and homologous recombination in glioblastoma with a polyether ionophore

Author

Lim, Yi Chieh, Ensbey, Kathleen S., Offenhäuser, Carolin, D'souza, Rochelle C.J., Cullen, Jason K., Stringer, Brett W., Quek, Hazel, Bruce, Zara C., Kijas, Amanda, Cianfanelli, Valentina, Mahboubi, Bijan, Smith, Fiona, Jeffree, Rosalind L., Wiesmüeller, Lisa, Wiegmans, Adrian P., Bain, Amanda, Lombard, Fanny J., Roberts, Tara L., Khanna, Kum Kum, Lavin, Martin F., Kim, Baek, Hamerlik, Petra, Johns, Terrance G., Coster, Mark J., Boyd, Andrew W., Day, Bryan W., Lim, Yi Chieh, Ensbey, Kathleen S., Offenhäuser, Carolin, D'souza, Rochelle C.J., Cullen, Jason K., Stringer, Brett W., Quek, Hazel, Bruce, Zara C., Kijas, Amanda, Cianfanelli, Valentina, Mahboubi, Bijan, Smith, Fiona, Jeffree, Rosalind L., Wiesmüeller, Lisa, Wiegmans, Adrian P., Bain, Amanda, Lombard, Fanny J., Roberts, Tara L., Khanna, Kum Kum, Lavin, Martin F., Kim, Baek, Hamerlik, Petra, Johns, Terrance G., Coster, Mark J., Boyd, Andrew W., and Day, Bryan W.

Abstract

Background: Despite significant endeavor having been applied to identify effective therapies to treat glioblastoma (GBM), survival outcomes remain intractable. The greatest nonsurgical benefit arises from radiotherapy, though tumors typically recur due to robust DNA repair. Patients could therefore benefit from therapies with the potential to prevent DNA repair and synergize with radiotherapy. In this work, we investigated the potential of salinomycin to enhance radiotherapy and further uncover novel dual functions of this ionophore to induce DNA damage and prevent repair. Methods: In vitro primary GBM models and ex vivo GBM patient explants were used to determine the mechanism of action of salinomycin by immunoblot, flow cytometry, immunofluorescence, immunohistochemistry, and mass spectrometry. In vivo efficacy studies were performed using orthotopic GBM animal xenograft models. Salinomycin derivatives were synthesized to increase drug efficacy and explore structure-activity relationships. Results: Here we report novel dual functions of salinomycin. Salinomycin induces toxic DNA lesions and prevents subsequent recovery by targeting homologous recombination (HR) repair. Salinomycin appears to target the more radioresistant GBM stem cell-like population and synergizes with radiotherapy to significantly delay tumor formation in vivo. We further developed salinomycin derivatives which display greater efficacy in vivo while retaining the same beneficial mechanisms of action. Conclusion: Our findings highlight the potential of salinomycin to induce DNA lesions and inhibit HR to greatly enhance the effect of radiotherapy. Importantly, first-generation salinomycin derivatives display greater efficacy and may pave the way for clinical testing of these agents.

Published
2020

48. Q-Cell Glioblastoma Resource: Proteomics Analysis Reveals Unique Cell-States are Maintained in 3D Culture

Author

D'Souza, Rochelle C.J., Offenhäuser, Carolin, Straube, Jasmin, Baumgartner, Ulrich, Kordowski, Anja, Li, Yuchen, Stringer, Brett W., Alexander, Hamish, Lwin, Zarnie, Inglis, Po Ling, Jeffree, Rosalind L., Johns, Terrance G., Boyd, Andrew W., Day, Bryan W., D'Souza, Rochelle C.J., Offenhäuser, Carolin, Straube, Jasmin, Baumgartner, Ulrich, Kordowski, Anja, Li, Yuchen, Stringer, Brett W., Alexander, Hamish, Lwin, Zarnie, Inglis, Po Ling, Jeffree, Rosalind L., Johns, Terrance G., Boyd, Andrew W., and Day, Bryan W.

Abstract

Glioblastoma (GBM) is a treatment-refractory central nervous system (CNS) tumour, and better therapies to treat this aggressive disease are urgently needed. Primary GBM models that represent the true disease state are essential to better understand disease biology and for accurate preclinical therapy assessment. We have previously presented a comprehensive transcriptome characterisation of a panel (n = 12) of primary GBM models (Q-Cell). We have now generated a systematic, quantitative, and deep proteome abundance atlas of the Q-Cell models grown in 3D culture, representing 6167 human proteins. A recent study has highlighted the degree of functional heterogeneity that coexists within individual GBM tumours, describing four cellular states (MES-like, NPC-like, OPC-like and AC-like). We performed comparative proteomic analysis, confirming a good representation of each of the four cell-states across the 13 models examined. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis identified upregulation of a number of GBM-associated cancer pathway proteins. Bioinformatics analysis, using the OncoKB database, identified a number of functional actionable targets that were either uniquely or ubiquitously expressed across the panel. This study provides an in-depth proteomic analysis of the GBM Q-Cell resource, which should prove a valuable functional dataset for future biological and preclinical investigations.

Published
2020

49. Identification of the Epitope for the Epidermal Growth Factor Receptor-specific Monoclonal Antibody 806 Reveals That It Preferentially Recognizes an Untethered Form of the Receptor

Author

Johns, Terrance G., Adams, Timothy E., Cochran, Jennifer R., Hall, Nathan E, Hoyne, Peter A., Olsen, Mark J., Kim, Yong-Sung, Rothacker, Julie, Nice, Edouard C., Walker, Francesca, Ritter, Gerd, Jungbluth, Achim A., Old, Lloyd J., Ward, Colin W., Burgess, Antony W., Wittrup, K. Dane, and Scott, Andrew M.

Published
2004
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