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2. GPRC5D as a novel target for the treatment of multiple myeloma: a narrative review.

Author

Rodriguez-Otero, Paula, van de Donk, Niels, Pillarisetti, Kodandaram, Cornax, Ingrid, Vishwamitra, Deeksha, Gray, Kathleen, Hilder, Brandi, Tolbert, Jaszianne, Renaud, Thomas, Masterson, Tara, Heuck, Christoph, Kane, Colleen, Verona, Raluca, Moreau, Philippe, Bahlis, Nizar, and Chari, Ajai

Subjects
Humans, Multiple Myeloma, Receptors, Chimeric Antigen, Antibodies, Bispecific, Neoplasm Recurrence, Local, Immunotherapy, Adoptive, Receptors, G-Protein-Coupled
Abstract

Multiple myeloma is a genetically complex and heterogenous malignancy with a 5-year survival rate of approximately 60%. Despite advances in therapy, patients experience cycles of remission and relapse, with each successive line of therapy associated with poorer outcomes; therefore, therapies with different mechanisms of action against new myeloma antigens are needed. G protein-coupled receptor class C group 5 member D (GPRC5D) has emerged as a novel therapeutic target for the treatment of multiple myeloma. We review the biology and target validation of GPRC5D, and clinical data from early phase trials of GPRC5D-targeting bispecific antibodies, talquetamab and forimtamig, and chimeric antigen receptor T cell (CAR-T) therapies, MCARH109, OriCAR-017, and BMS-986393. In addition to adverse events (AEs) associated with T-cell-redirection therapies irrespective of target, a consistent pattern of dermatologic and oral AEs has been reported across several trials of GPRC5D-targeting bispecific antibodies, as well as rare cerebellar events with CAR-T therapy. Additional studies are needed to understand the underlying mechanisms involved in the development of skin- and oral-related toxicities. We review the strategies that have been used to manage these GPRC5D-related toxicities. Preliminary efficacy data showed overall response rates for GPRC5D-targeting T-cell-redirecting therapies were ≥64%; most responders achieved a very good partial response or better. Pharmacokinetics/pharmacodynamics showed that these therapies led to cytokine release and T-cell activation. In conclusion, results from early phase trials of GPRC5D-targeting T-cell-redirecting agents have shown promising efficacy and manageable safety profiles, including lower infection rates compared with B-cell maturation antigen- and Fc receptor-like protein 5-targeting bispecific antibodies. Further clinical trials, including those investigating GPRC5D-targeting T-cell-redirecting agents in combination with other anti-myeloma therapies and with different treatment modalities, may help to elucidate the future optimal treatment regimen and sequence for patients with multiple myeloma and improve survival outcomes. Video Summary.

Published
2024

4. Endothelial Heparan Sulfate Mediates Hepatic Neutrophil Trafficking and Injury during Staphylococcus aureus Sepsis

Author

Golden, Gregory J, Toledo, Alejandro Gómez, Marki, Alex, Sorrentino, James T, Morris, Claire, Riley, Raquel J, Spliid, Charlotte, Chen, Qiongyu, Cornax, Ingrid, Lewis, Nathan E, Varki, Nissi, Le, Dzung, Malmström, Johan, Karlsson, Christofer, Ley, Klaus, Nizet, Victor, and Esko, Jeffrey D

Subjects
Liver Disease, Sepsis, Infectious Diseases, Hematology, Digestive Diseases, Emerging Infectious Diseases, Clinical Research, Chronic Liver Disease and Cirrhosis, 2.1 Biological and endogenous factors, Aetiology, Cardiovascular, Inflammatory and immune system, Animals, Disease Models, Animal, Endothelial Cells, Female, Glycocalyx, Heparitin Sulfate, Liver, Lung, Male, Mice, Mice, Inbred C57BL, Neutrophil Activation, Neutrophils, Staphylococcus aureus, heparan sulfate, intravital microscopy, liver, neutrophils, proteomics, sepsis, thrombosis, Microbiology
Abstract

Hepatic failure is an important risk factor for poor outcome in septic patients. Using a chemical tagging workflow and high-resolution mass spectrometry, we demonstrate that rapid proteome remodeling of the vascular surfaces precedes hepatic damage in a murine model of Staphylococcus aureus sepsis. These early changes include vascular deposition of neutrophil-derived proteins, shedding of vascular receptors, and altered levels of heparin/heparan sulfate-binding factors. Modification of endothelial heparan sulfate, a major component of the vascular glycocalyx, diminishes neutrophil trafficking to the liver and reduces hepatic coagulopathy and organ damage during the systemic inflammatory response to infection. Modifying endothelial heparan sulfate likewise reduces neutrophil trafficking in sterile hepatic injury, reflecting a more general role of heparan sulfate contribution to the modulation of leukocyte behavior during inflammation. IMPORTANCE Vascular glycocalyx remodeling is critical to sepsis pathology, but the glycocalyx components that contribute to this process remain poorly characterized. This article shows that during Staphylococcus aureus sepsis, the liver vascular glycocalyx undergoes dramatic changes in protein composition associated with neutrophilic activity and heparin/heparan sulfate binding, all before organ damage is detectable by standard circulating liver damage markers or histology. Targeted manipulation of endothelial heparan sulfate modulates S. aureus sepsis-induced hepatotoxicity by controlling the magnitude of neutrophilic infiltration into the liver in both nonsterile and sterile injury. These data identify an important vascular glycocalyx component that impacts hepatic failure during nonsterile and sterile injury.

Published
2021

5. Neoadjuvant systemic oncolytic vesicular stomatitis virus is safe and may enhance long-term survivorship in dogs with naturally occurring osteosarcoma

Author

Makielski, Kelly M., Sarver, Aaron L., Henson, Michael S., Stuebner, Kathleen M., Borgatti, Antonella, Suksanpaisan, Lukkana, Preusser, Caitlin, Tabaran, Alexandru-Flaviu, Cornax, Ingrid, O’Sullivan, M. Gerard, Chehadeh, Andrea, Groschen, Donna, Bergsrud, Kelly, Pracht, Sara, Winter, Amber, Mills, Lauren J., Schwabenlander, Marc D., Wolfe, Melissa, Farrar, Michael A., Cutter, Gary R., Koopmeiners, Joseph S., Russell, Stephen J., Modiano, Jaime F., and Naik, Shruthi

Published
2023
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6. FIGURE 5 from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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7. FIGURE 2 from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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8. Supplementary Figure S2 from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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9. FIGURE 3 from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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10. Supplementary Table S5 from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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11. FIGURE 4 from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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12. FIGURE 1 from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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13. Data from Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., primary, Sarver, Aaron L., primary, Lee, Donghee, primary, Angelos, Mathew G., primary, Frantz, Aric M., primary, Forster, Colleen L., primary, O'Brien, Timothy D., primary, Cornax, Ingrid, primary, O'Sullivan, M. Gerard, primary, Cheng, Nuojin, primary, Lewellen, Mitzi, primary, Oseth, LeAnn, primary, Kumar, Sunil, primary, Bullman, Susan, primary, Pedamallu, Chandra Sekhar, primary, Goyal, Sagar M., primary, Meyerson, Matthew, primary, Lund, Troy C., primary, Breen, Matthew, primary, Lindblad-Toh, Kerstin, primary, Dickerson, Erin B., primary, Kaufman, Dan S., primary, and Modiano, Jaime F., primary

Published
2024
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14. Surprising synergy of dual translation inhibition vs. Acinetobacter baumannii and other multidrug-resistant bacterial pathogens

Author

Dillon, Nicholas, Holland, Michelle, Tsunemoto, Hannah, Hancock, Bryan, Cornax, Ingrid, Pogliano, Joe, Sakoulas, George, and Nizet, Victor

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Clinical Sciences, Pneumonia, Infectious Diseases, Prevention, Emerging Infectious Diseases, Lung, Pneumonia & Influenza, Antimicrobial Resistance, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Infection, Good Health and Well Being, Acinetobacter Infections, Acinetobacter baumannii, Animals, Anti-Bacterial Agents, Azithromycin, Disease Models, Animal, Dose-Response Relationship, Drug, Drug Resistance, Multiple, Bacterial, Drug Synergism, Mice, Microbial Sensitivity Tests, Protein Biosynthesis, Antibiotic therapy, Minocycline, Synergy, Translation inhibition, Antibiotic resistance, Bacterial cytological profiling, Public Health and Health Services, Clinical sciences, Epidemiology
Abstract

BackgroundMultidrug-resistant (MDR) Acinetobacter baumannii infections have high mortality rates and few treatment options. Synergistic drug combinations may improve clinical outcome and reduce further emergence of resistance in MDR pathogens. Here we show an unexpected potent synergy of two translation inhibitors against the pathogen: commonly prescribed macrolide antibiotic azithromycin (AZM), widely ignored as a treatment alternative for invasive Gram-negative pathogens, and minocycline, among the current standard-of-care agents used for A. baumannii.MethodsMedia-dependent activities of AZM and MIN were evaluated in minimum inhibitory concentration assays and kinetic killing curves, alone or in combination, both in standard bacteriologic media (cation-adjusted Mueller-Hinton Broth) and more physiologic tissue culture media (RPMI), with variations of bicarbonate as a physiologic buffer. Synergy was calculated by fractional inhibitory concentration index (FICI). Therapeutic benefit of combining AZM and MIN was tested in a murine model of A. baumannii pneumonia. AZM + MIN synergism was probed mechanistically by bacterial cytological profiling (BCP), a quantitative fluorescence microscopy technique that identifies disrupted bacterial cellular pathways on a single cell level, and real-time kinetic measurement of translation inhibition via quantitative luminescence. AZM + MIN synergism was further evaluated vs. other contemporary high priority MDR bacterial pathogens.FindingsAlthough two translation inhibitors are not expected to synergize, each drug complemented kinetic deficiencies of the other, speeding the initiation and extending the duration of translation inhibition as verified by FICI, BCP and kinetic luminescence markers. In an MDR A. baumannii pneumonia model, AZM + MIN combination therapy decreased lung bacterial burden and enhanced survival rates. Synergy between AZM and MIN was also detected vs. MDR strains of Gram-negative Klebsiella pneumoniae and Pseudomonas aeruginosa, and the leading Gram-positive pathogen methicillin-resistant Staphylococcus aureus.InterpretationAs both agents are FDA approved with excellent safety profiles, clinical investigation of AZM and MIN combination regimens may immediately be contemplated for optimal treatment of A. baumannii and other MDR bacterial infections in humans. FUND: National Institutes of Health U01 AI124326 (JP, GS, VN) and U54 HD090259 (GS, VN). IC was supported by the UCSD Research Training Program for Veterinarians T32 OD017863.

Published
2019

15. A Revised Diagnostic Classification of Canine Glioma: Towards Validation of the Canine Glioma Patient as a Naturally Occurring Preclinical Model for Human Glioma.

Author

Koehler, Jennifer W, Miller, Andrew D, Miller, C Ryan, Porter, Brian, Aldape, Kenneth, Beck, Jessica, Brat, Daniel, Cornax, Ingrid, Corps, Kara, Frank, Chad, Giannini, Caterina, Horbinski, Craig, Huse, Jason T, O'Sullivan, M Gerard, Rissi, Daniel R, Mark Simpson, R, Woolard, Kevin, Shih, Joanna H, Mazcko, Christina, Gilbert, Mark R, and LeBlanc, Amy K

Subjects
Cancer, Rare Diseases, Brain Cancer, Neurosciences, Genetics, Brain Disorders, 2', 3'-Cyclic-Nucleotide Phosphodiesterases, Animals, Brain, Brain Neoplasms, Diagnosis, Differential, Dogs, Female, Glial Fibrillary Acidic Protein, Glioma, Intermediate Filaments, Ki-67 Antigen, Male, Oligodendrocyte Transcription Factor 2, Physicians, Veterinarians, Canine, Comparative, Clinical Sciences, Neurology & Neurosurgery
Abstract

The National Cancer Institute-led multidisciplinary Comparative Brain Tumor Consortium (CBTC) convened a glioma pathology board, comprising both veterinarian and physician neuropathologists, and conducted a comprehensive review of 193 cases of canine glioma. The immediate goal was to improve existing glioma classification methods through creation of a histologic atlas of features, thus yielding greater harmonization of phenotypic characterization. The long-term goal was to support future incorporation of clinical outcomes and genomic data into proposed simplified diagnostic schema, so as to further bridge the worlds of veterinary and physician neuropathology and strengthen validity of the dog as a naturally occurring, translationally relevant animal model of human glioma. All cases were morphologically reclassified according to a new schema devised by the entire board, yielding a majority opinion diagnosis of astrocytoma (43, 22.3%), 19 of which were low-grade and 24 high-grade, and oligodendroglioma (134, 69.4%), 35 of which were low-grade and 99 were high-grade. Sixteen cases (8.3%) could not be classified as oligodendroglioma or astrocytoma based on morphology alone and were designated as undefined gliomas. The simplified classification scheme proposed herein provides a tractable means for future addition of molecular data, and also serves to highlight histologic similarities and differences between human and canine glioma.

Published
2018

16. The Mla pathway is critical for Pseudomonas aeruginosa resistance to outer membrane permeabilization and host innate immune clearance

Author

Munguia, Jason, LaRock, Doris L, Tsunemoto, Hannah, Olson, Joshua, Cornax, Ingrid, Pogliano, Joseph, and Nizet, Victor

Subjects
Medicinal and Biomolecular Chemistry, Chemical Sciences, Rare Diseases, Antimicrobial Resistance, Clinical Research, Infectious Diseases, Lung, Cystic Fibrosis, Genetics, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, 2.2 Factors relating to the physical environment, Aetiology, Infection, Animals, Antimicrobial Cationic Peptides, Bacterial Outer Membrane Proteins, Cathelicidins, Female, Gene Deletion, Humans, Immunity, Innate, Mice, Inbred C57BL, Pseudomonas Infections, Pseudomonas aeruginosa, Signal Transduction, Antimicrobial peptide, Cathelicidin, Innate immunity, Mla pathway, Pneumonia, Immunology, Medicinal and biomolecular chemistry
Abstract

Pseudomonas aeruginosa is an important opportunistic pathogen that has become a serious problem due to increased rates of antibiotic resistance. Due to this along with a dearth in novel antibiotic development, especially against Gram-negative pathogens, new therapeutic strategies are needed to prevent a post-antibiotic era. Here, we describe the importance of the vacJ/Mla pathway in resisting bactericidal actions of the host innate immune response. P. aeruginosa tn5 transposon mutants in genes from the VacJ/Mla pathway showed increased susceptibility to killing by the host cathelicidin antimicrobial peptide, LL-37, when compared to the wild-type parent strain. The P. aeruginosa vacJ - mutant demonstrated increased membrane permeability upon damage as well as sensitivity to killing in the presence of the detergent sodium dodecyl sulfate and the divalent cation chelator EDTA. When exposed to human whole blood and serum complement, the vacJ - mutant was killed more rapidly when compared to the wild-type parent strain and complemented mutant. Finally, in an in vivo mouse lung infection model, infection with the vacJ - mutant resulted in reduced mortality, lower bacterial burden, and reduced lung damage when compared to the wild-type strain. This study highlights the potential in therapeutically targeting the VacJ/Mla pathway in sensitizing P. aeruginosa to killing by the host innate immune response.Key messages• The Mla pathway regulates outer membrane dynamics in human pathogen Pseudomonas aeruginosa (PA). • Disruption of Mla pathway gene vacJ sensitizes PA to host cathelicidin antimicrobial peptide LL-37. • Loss of vacJ expression renders PA more sensitive to human whole blood and serum killing. • Loss of vacJ expression reduces PA survival and virulence in a murine lung infection model. • The Mla pathway merits exploration as a pharmacologic target to sensitize PA to host innate immunity.

Published
2017

18. Incidence and management of CAR-T neurotoxicity in patients with multiple myeloma treated with ciltacabtagene autoleucel in CARTITUDE studies

Author

Cohen, Adam D., Parekh, Samir, Santomasso, Bianca D., Gállego Pérez-Larraya, Jaime, van de Donk, Niels W. C. J., Arnulf, Bertrand, Mateos, Maria-Victoria, Lendvai, Nikoletta, Jackson, Carolyn C., De Braganca, Kevin C., Schecter, Jordan M., Marquez, Loreta, Lee, Erin, Cornax, Ingrid, Zudaire, Enrique, Li, Claire, Olyslager, Yunsi, Madduri, Deepu, Varsos, Helen, Pacaud, Lida, Akram, Muhammad, Geng, Dong, Jakubowiak, Andrzej, Einsele, Hermann, and Jagannath, Sundar

Published
2022
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19. Oncolytic vesicular stomatitis virus is safe and provides a survival benefit for dogs with naturally occurring osteosarcoma

Author

Makielski, Kelly M, primary, Sarver, Aaron L, additional, Henson, Michael S, additional, Stuebner, Kathleen M, additional, Borgatti, Antonella, additional, Suksanpaisan, Lukkan, additional, Preusser, Caitlin, additional, Tabaran, Alexandru-Flaviu, additional, Cornax, Ingrid, additional, O'Sullivan, M. Gerard, additional, Chehadeh, Andrea, additional, Groschen, Donna, additional, Bergsrud, Kelly, additional, Pracht, Sara, additional, Winter, Amber, additional, Mills, Lauren J, additional, Schwabenlander, Marc D, additional, Wolfe, Melissa, additional, Farrar, Michael A, additional, Cutter, Gary R, additional, Koopmeiners, Joseph S, additional, Russell, Stephen J, additional, Modiano, Jaime F, additional, and Naik, Shruthi, additional

Published
2023
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20. Supplementary Figure S3 from Eradication of Canine Diffuse Large B-Cell Lymphoma in a Murine Xenograft Model with CD47 Blockade and Anti-CD20

Author

Weiskopf, Kipp, primary, Anderson, Katie L., primary, Ito, Daisuke, primary, Schnorr, Peter J., primary, Tomiyasu, Hirotaka, primary, Ring, Aaron M., primary, Bloink, Kristin, primary, Efe, Jem, primary, Rue, Sarah, primary, Lowery, David, primary, Barkal, Amira, primary, Prohaska, Susan, primary, McKenna, Kelly M., primary, Cornax, Ingrid, primary, O'Brien, Timothy D., primary, O'Sullivan, M. Gerard, primary, Weissman, Irving L., primary, and Modiano, Jaime F., primary

Published
2023
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21. Data from Eradication of Canine Diffuse Large B-Cell Lymphoma in a Murine Xenograft Model with CD47 Blockade and Anti-CD20

Author

Weiskopf, Kipp, primary, Anderson, Katie L., primary, Ito, Daisuke, primary, Schnorr, Peter J., primary, Tomiyasu, Hirotaka, primary, Ring, Aaron M., primary, Bloink, Kristin, primary, Efe, Jem, primary, Rue, Sarah, primary, Lowery, David, primary, Barkal, Amira, primary, Prohaska, Susan, primary, McKenna, Kelly M., primary, Cornax, Ingrid, primary, O'Brien, Timothy D., primary, O'Sullivan, M. Gerard, primary, Weissman, Irving L., primary, and Modiano, Jaime F., primary

Published
2023
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22. Supplementary Tables 1 through 3, Supplementary Figure Legends, and Supplementary Materials and Methods from Eradication of Canine Diffuse Large B-Cell Lymphoma in a Murine Xenograft Model with CD47 Blockade and Anti-CD20

Author

Weiskopf, Kipp, primary, Anderson, Katie L., primary, Ito, Daisuke, primary, Schnorr, Peter J., primary, Tomiyasu, Hirotaka, primary, Ring, Aaron M., primary, Bloink, Kristin, primary, Efe, Jem, primary, Rue, Sarah, primary, Lowery, David, primary, Barkal, Amira, primary, Prohaska, Susan, primary, McKenna, Kelly M., primary, Cornax, Ingrid, primary, O'Brien, Timothy D., primary, O'Sullivan, M. Gerard, primary, Weissman, Irving L., primary, and Modiano, Jaime F., primary

Published
2023
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23. What Is Your Diagnosis?

Author

McRee, Anna E., Tully, Thomas N., Nevarez, Javier G., and Cornax, Ingrid

Published
2015

25. Comprehensive BCMA Expression Profiling in Adult Normal Human Brain Suggests a Low Risk of On-target Neurotoxicity in BCMA-targeting Multiple Myeloma Therapy

Author

Marella, Mathieu, primary, Yao, Xiang, additional, Carreira, Vinicius, additional, Bustamante, Marta F., additional, Clark, H. Brent, additional, Jackson, Carolyn C., additional, Zudaire, Enrique, additional, Schecter, Jordan M., additional, Glover, Tynisha D., additional, Shenton, Jacintha, additional, and Cornax, Ingrid, additional

Published
2022
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29. Abstract 1747: Oncolytic Vesicular Stomatitis Virus expressing a species relevant interferon-beta is safe and provides a survival benefit when added as neoadjuvant to the standard of care for dogs with naturally occurring bone cancer

Author

Makielski, Kelly M., primary, Sarver, Aaron L., additional, Sathyanarayan, Aishwarya, additional, Henson, Michael S., additional, Stuebner, Kathleen M., additional, Tabaran, Alexandru-Flaviu, additional, Cornax, Ingrid, additional, O'Sullivan, Gerard, additional, Chehadeh, Andrea, additional, Groschen, Donna, additional, Bergsrud, Kelly, additional, Mills, Lauren J., additional, Winter, Amber L., additional, Pracht, Sara, additional, Scott, Milcah C., additional, Farrar, Michael A., additional, Cutter, Gary R., additional, Koopmeiners, Joseph S., additional, Russell, Stephen J., additional, Naik, Shruthi, additional, and Modiano, Jaime F., additional

Published
2021
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30. Hemangiosarcoma Cells Promote Conserved Host-Derived Hematopoietic Expansion

Author

Kim, Jong Hyuk, primary, Schulte, Ashley J., additional, Sarver, Aaron L., additional, Angelos, Mathew G., additional, Frantz, Aric M., additional, Forster, Colleen L., additional, O’Brien, Timothy D., additional, Cornax, Ingrid, additional, O’Sullivan, M. Gerard, additional, Cheng, Nuojin, additional, Lewellen, Mitzi, additional, Oseth, LeAnn, additional, Kumar, Sunil, additional, Bullman, Susan, additional, Pedamallu, Chandra Sekhar, additional, Goyal, Sagar M., additional, Meyerson, Matthew, additional, Lund, Troy C., additional, Alfoldi, Jessica, additional, Breen, Matthew, additional, Lindblad-Toh, Kerstin, additional, Dickerson, Erin B., additional, Kaufman, Dan S., additional, and Modiano, Jaime F., additional

Published
2021
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31. Repurposed drugs block toxin-driven platelet clearance by the hepatic Ashwell-Morell receptor to clear Staphylococcus aureus bacteremia

Author

Sun, Josh, primary, Uchiyama, Satoshi, additional, Olson, Joshua, additional, Morodomi, Yosuke, additional, Cornax, Ingrid, additional, Ando, Nao, additional, Kohno, Yohei, additional, Kyaw, May M. T., additional, Aguilar, Bernice, additional, Haste, Nina M., additional, Kanaji, Sachiko, additional, Kanaji, Taisuke, additional, Rose, Warren E., additional, Sakoulas, George, additional, Marth, Jamey D., additional, and Nizet, Victor, additional

Published
2021
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33. Repurposed Drugs Block Toxin-Driven Platelet Clearance by the Hepatic Ashwell-Morell Receptor to Clear Staphylococcus aureus Bacteremia

Author

Sun, Josh, primary, Uchiyama, Satoshi, additional, Olson, Joshua, additional, Morodomi, Yosuke, additional, Cornax, Ingrid, additional, Ando, Nao, additional, Kohno, Yohei, additional, Kyaw, May M. T., additional, Aguilar, Bernice, additional, Haste, Nina M., additional, Kanaji, Sachiko, additional, Kanaji, Taisuke, additional, Rose, Warren E., additional, Sakoulas, George, additional, Marth, Jamey D., additional, and Nizet, Victor, additional

Published
2020
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34. Abstract A19: Interactions between tobacco smoke chemicals in rodent tumor models

Author

Peterson, Lisa A., primary, Oram, Marissa K., additional, Seabloom, Donna E., additional, Smith, William E., additional, Stornetta, Alessia, additional, Vevang, Karin R., additional, Flavin, Monica, additional, Tabaran, Alexandru F., additional, Cornax, Ingrid, additional, Gerard O’Sullivan, M., additional, Upadhyaya, Pramod, additional, Zhang, Lin, additional, Hecht, Stephen S., additional, Balbo, Silvia, additional, and Wiedmann, Timothy S., additional

Published
2020
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35. Heterotypic mouse models of canine osteosarcoma recapitulate tumor heterogeneity and biological behavior

Author

Scott, Milcah C., Tomiyasu, Hirotaka, Garbe, John R., Cornax, Ingrid, Amaya, Clarissa, O'Sullivan, M. Gerard, Subramanian, Subbaya, Bryan, Brad A., and Modiano, Jaime F.

Subjects
Osteosarcoma, Gene Expression Profiling, Xenograft, lcsh:R, Mice, Nude, lcsh:Medicine, Heterotypic models, Xenograft Model Antitumor Assays, Metastasis, Gene Expression Regulation, Neoplastic, Comparative studies, Disease Models, Animal, Dogs, Cell Line, Tumor, Tumor Microenvironment, lcsh:Pathology, Animals, Female, Tumor–stromal interactions, Neoplasm Metastasis, Stromal Cells, Research Article, Cell Proliferation, lcsh:RB1-214
Abstract

Osteosarcoma (OS) is a heterogeneous and rare disease with a disproportionate impact because it mainly affects children and adolescents. Lamentably, more than half of patients with OS succumb to metastatic disease. Clarification of the etiology of the disease, development of better strategies to manage progression, and methods to guide personalized treatments are among the unmet health needs for OS patients. Progress in managing the disease has been hindered by the extreme heterogeneity of OS; thus, better models that accurately recapitulate the natural heterogeneity of the disease are needed. For this study, we used cell lines derived from two spontaneous canine OS tumors with distinctly different biological behavior (OS-1 and OS-2) for heterotypic in vivo modeling that recapitulates the heterogeneous biology and behavior of this disease. Both cell lines demonstrated stability of the transcriptome when grown as orthotopic xenografts in athymic nude mice. Consistent with the behavior of the original tumors, OS-2 xenografts grew more rapidly at the primary site and had greater propensity to disseminate to lung and establish microscopic metastasis. Moreover, OS-2 promoted formation of a different tumor-associated stromal environment than OS-1 xenografts. OS-2-derived tumors comprised a larger percentage of the xenograft tumors than OS-1-derived tumors. In addition, a robust pro-inflammatory population dominated the stromal cell infiltrates in OS-2 xenografts, whereas a mesenchymal population with a gene signature reflecting myogenic signaling dominated those in the OS-1 xenografts. Our studies show that canine OS cell lines maintain intrinsic features of the tumors from which they were derived and recapitulate the heterogeneous biology and behavior of bone cancer in mouse models. This system provides a resource to understand essential interactions between tumor cells and the stromal environment that drive the progression and metastatic propensity of OS., Editors' choice: We developed a system that recapitulates the heterogeneous biological behavior of bone cancer in mouse models and describe novel methods to study tumor–stromal interactions in these models.

Published
2016

36. Homophilic protein interactions facilitate bacterial aggregation and IgG-dependent complex formation by the Streptococcus canis M protein SCM

Author

Nerlich, Andreas, Lapschies, Antje-Maria, Kohler, Thomas P, Cornax, Ingrid, Eichhorn, Inga, Goldmann, Oliver, Krienke, Petra, Bergmann, Simone, Nizet, Victor, Hammerschmidt, Sven, Rohde, M, Fulde, Marcus, and HZI, Helmholtz Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig Germany.

Subjects
Antigens, Bacterial, protein complex formation, M protein, fungi, Fibrinogen, Streptococcus, 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::616 Krankheiten, Antibodies, Bacterial, Bacterial Adhesion, lcsh:Infectious and parasitic diseases, Streptococcus canis, Immunoglobulin G, Humans, lcsh:RC109-216, bacterial aggregation, Carrier Proteins, Bacterial Outer Membrane Proteins, Protein Binding, Research Paper
Abstract

Streptococcus canis is a zoonotic agent that causes serious invasive diseases in domestic animals and humans, but knowledge about its pathogenic potential and underlying virulence mechanisms is limited. Here, we report on the ability of certain S. canis isolates to form large bacterial aggregates when grown in liquid broth. Bacterial aggregation was attributed to the presence and the self-binding activity of SCM, the M protein of S. canis, as evaluated by bacterial sedimentation assays, immunofluorescence- and electron microscopic approaches. Using a variety of truncated recombinant SCM fragments, we demonstrated that homophilic SCM interactions occur via the N-terminal, but not the C-terminal part, of the mature M protein. Interestingly, when incubated in human plasma, SCM forms soluble protein complexes comprising its known ligands, immunoglobulin G (IgG) and plasminogen (Plg). Co-incubation studies with purified host proteins revealed that SCM-mediated complex formation is based on the interaction of SCM with itself and with IgG, but not with Plg or fibrinogen (Fbg), well-established constituents of M protein-mediated protein complexes in human-associated streptococci. Notably, these soluble, SCM-mediated plasma complexes harbored complement factor C1q, which can induce complement breakdown in the periphery and therefore represent another immune evasion mechanism of SCM.

Published
2019

44. Slit-Robo GTPase-Activating Protein 2 as a metastasis suppressor in osteosarcoma

Author

Marko, Tracy A., primary, Shamsan, Ghaidan A., additional, Edwards, Elizabeth N., additional, Hazelton, Paige E., additional, Rathe, Susan K., additional, Cornax, Ingrid, additional, Overn, Paula R., additional, Varshney, Jyotika, additional, Diessner, Brandon J., additional, Moriarity, Branden S., additional, O’Sullivan, M. Gerard, additional, Odde, David J., additional, and Largaespada, David A., additional

Published
2016
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45. Eradication of Canine Diffuse Large B-Cell Lymphoma in a Murine Xenograft Model with CD47 Blockade and Anti-CD20

Author

Weiskopf, Kipp, primary, Anderson, Katie L., additional, Ito, Daisuke, additional, Schnorr, Peter J., additional, Tomiyasu, Hirotaka, additional, Ring, Aaron M., additional, Bloink, Kristin, additional, Efe, Jem, additional, Rue, Sarah, additional, Lowery, David, additional, Barkal, Amira, additional, Prohaska, Susan, additional, McKenna, Kelly M., additional, Cornax, Ingrid, additional, O'Brien, Timothy D., additional, O'Sullivan, M. Gerard, additional, Weissman, Irving L., additional, and Modiano, Jaime F., additional

Published
2016
Full Text
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49. Homophilic protein interactions facilitate bacterial aggregation and IgG-dependent complex formation by the Streptococcus canisM protein SCM

Author

Nerlich, Andreas, Lapschies, Antje-Maria, Kohler, Thomas P., Cornax, Ingrid, Eichhorn, Inga, Goldmann, Oliver, Krienke, Petra, Bergmann, Simone, Nizet, Victor, Hammerschmidt, Sven, Rohde, Manfred, and Fulde, Marcus

Abstract

ABSTRACTStreptococcus canisis a zoonotic agent that causes serious invasive diseases in domestic animals and humans, but knowledge about its pathogenic potential and underlying virulence mechanisms is limited. Here, we report on the ability of certain S. canisisolates to form large bacterial aggregates when grown in liquid broth. Bacterial aggregation was attributed to the presence and the self-binding activity of SCM, the M protein of S. canis, as evaluated by bacterial sedimentation assays, immunofluorescence- and electron microscopic approaches. Using a variety of truncated recombinant SCM fragments, we demonstrated that homophilic SCM interactions occur via the N-terminal, but not the C-terminal part, of the mature M protein. Interestingly, when incubated in human plasma, SCM forms soluble protein complexes comprising its known ligands, immunoglobulin G (IgG) and plasminogen (Plg). Co-incubation studies with purified host proteins revealed that SCM-mediated complex formation is based on the interaction of SCM with itself and with IgG, but not with Plg or fibrinogen (Fbg), well-established constituents of M protein-mediated protein complexes in human-associated streptococci. Notably, these soluble, SCM-mediated plasma complexes harbored complement factor C1q, which can induce complement breakdown in the periphery and therefore represent another immune evasion mechanism of SCM.

Published
2019
Full Text
View/download PDF

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