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3. A Call for Discovery and Therapeutic Development for Cutaneous Neurofibromas

Author

Blakeley, Jaishri O, Le, Lu Q, Lee, Sang Y, Ly, Ina, Rhodes, Steven D, Romo, Carlos G, Sarin, Kavita Y, Staedtke, Verena, Steensma, Matthew R, Wolkenstein, Pierre, Participants, 2022 NTAP Cutaneous Neurofibroma Symposium, Largaespada, David, Serra, Eduard, Haniffa, Muzlifah, Bakker, Annette, McCormick, Frank, Cagan, Ross L, Ju, William, Stemmer-Rachamimov, Anat, Grimes, Kevin, Topilko, Piotr, Kornacki, Deanna, Kelly, Kristen M, Gottesman, Sally, York, Zachary, and Epps, Roselyn

Subjects
Humans, Neurofibroma, Neurofibromatosis 1, Skin Neoplasms, Connective Tissue Diseases, NTAP Cutaneous Neurofibroma Symposium Participants, Clinical Sciences, Oncology and Carcinogenesis, Dermatology & Venereal Diseases
Published
2023

4. Prospective phase II trial of the dual mTORC1/2 inhibitor vistusertib for progressive or symptomatic meningiomas in persons with neurofibromatosis 2.

Author

Jordan, Justin, Orr, Christina, Thalheimer, Raquel, Cambillo, Josephine, Beauchamp, Roberta, Shaikh, Ghalib, Muzikansky, Alona, Stemmer-Rachamimov, Anat, Giovannini, Marco, Kalamarides, Michel, Barker, Fred, Ramesh, Vijaya, and Plotkin, Scott

Subjects
NF2, mTOR, mTORC1, mTORC2, meningioma, neurofibromatosis 2, vistusertib
Abstract

BACKGROUND: Meningiomas occur in 80% of persons with neurofibromatosis 2 (NF2) and cause significant mortality and morbidity, yet there are no effective medical treatments. NF2-deficient tumors have constitutive activation of mammalian/mechanistic target of rapamycin (mTOR), and treatment with mTORC1 inhibitors results in growth arrest in a minority of tumors, with paradoxical activation of the mTORC2/AKT pathway. We studied the effect of vistusertib, a dual mTORC1/mTORC2 inhibitor, in NF2 patients with progressive or symptomatic meningiomas. METHODS: Vistusertib was administered orally at 125 mg twice daily for 2 consecutive days each week. The primary endpoint was the imaging response in the target meningioma, defined as a volume decrease of 20% compared with the baseline. Secondary endpoints included toxicity, imaging response of nontarget tumors, quality of life, and genetic biomarkers. RESULTS: Eighteen participants (13 female), median age of 41 (range, 18-61) years, were enrolled. In target meningiomas, the best response was partial response (PR) in 1/18 tumors (6%) and stable disease (SD) in 17/18 tumors (94%). For all measured intracranial meningiomas and vestibular schwannomas, the best imaging response was PR in 6/59 tumors (10%) and SD in 53 (90%). Treatment-related grade 3/4 adverse events occurred in 14 (78%) participants, and 9 participants discontinued treatment due to side effects. CONCLUSIONS: Although the study did not meet the primary endpoint, vistusertib treatment was associated with high rates of SD in progressive NF2-related tumors. However, this dosing regimen for vistusertib was poorly tolerated. Future studies of dual mTORC inhibitors for NF2 should focus on optimizing tolerability and evaluating the relevance of tumor stability in participants.

Published
2023

6. Gene replacement therapy in a schwannoma mouse model of neurofibromatosis type 2

Author

Prabhakar, Shilpa, Beauchamp, Roberta L, Cheah, Pike See, Yoshinaga, Akiko, Haidar, Edwina Abou, Lule, Sevda, Mani, Gayathri, Maalouf, Katia, Stemmer-Rachamimov, Anat, Jung, David H, Welling, D Bradley, Giovannini, Marco, Plotkin, Scott R, Maguire, Casey A, Ramesh, Vijaya, and Breakefield, Xandra O

Subjects
Medical Biotechnology, Biomedical and Clinical Sciences, Biotechnology, Genetics, Orphan Drug, Gene Therapy, Pediatric, Neurosciences, Cancer, Rare Diseases, Neurofibromatosis, Development of treatments and therapeutic interventions, 5.2 Cellular and gene therapies, Schwann cells, adeno-associated viral vector, gene therapy, neurofibromatosis type 2, schwannoma, Medical biotechnology
Abstract

Loss of function of the neurofibromatosis type 2 (NF2) tumor suppressor gene leads to the formation of schwannomas, meningiomas, and ependymomas, comprising ∼50% of all sporadic cases of primary nervous system tumors. NF2 syndrome is an autosomal dominant condition, with bi-allelic inactivation of germline and somatic alleles resulting in loss of function of the encoded protein merlin and activation of mammalian target of rapamycin (mTOR) pathway signaling in NF2-deficient cells. Here we describe a gene replacement approach through direct intratumoral injection of an adeno-associated virus vector expressing merlin in a novel human schwannoma model in nude mice. In culture, the introduction of an AAV1 vector encoding merlin into CRISPR-modified human NF2-null arachnoidal cells (ACs) or Schwann cells (SCs) was associated with decreased size and mTORC1 pathway activation consistent with restored merlin activity. In vivo, a single injection of AAV1-merlin directly into human NF2-null SC-derived tumors growing in the sciatic nerve of nude mice led to regression of tumors over a 10-week period, associated with a decrease in dividing cells and an increase in apoptosis, in comparison with vehicle. These studies establish that merlin re-expression via gene replacement in NF2-null schwannomas is sufficient to cause tumor regression, thereby potentially providing an effective treatment for NF2.

Published
2022

7. Revised diagnostic criteria for neurofibromatosis type 1 and Legius syndrome: an international consensus recommendation

Author

Legius, Eric, Messiaen, Ludwine, Wolkenstein, Pierre, Pancza, Patrice, Avery, Robert A, Berman, Yemima, Blakeley, Jaishri, Babovic-Vuksanovic, Dusica, Cunha, Karin Soares, Ferner, Rosalie, Fisher, Michael J, Friedman, Jan M, Gutmann, David H, Kehrer-Sawatzki, Hildegard, Korf, Bruce R, Mautner, Victor-Felix, Peltonen, Sirkku, Rauen, Katherine A, Riccardi, Vincent, Schorry, Elizabeth, Stemmer-Rachamimov, Anat, Stevenson, David A, Tadini, Gianluca, Ullrich, Nicole J, Viskochil, David, Wimmer, Katharina, Yohay, Kaleb, Huson, Susan M, Evans, D Gareth, and Plotkin, Scott R

Subjects
Biological Sciences, Genetics, Neurosciences, Rare Diseases, Clinical Research, Neurofibromatosis, Cafe-au-Lait Spots, Consensus, Genetic Testing, Humans, Neurofibromatosis 1, International Consensus Group on Neurofibromatosis Diagnostic Criteria, Clinical Sciences, Genetics & Heredity
Abstract

PurposeBy incorporating major developments in genetics, ophthalmology, dermatology, and neuroimaging, to revise the diagnostic criteria for neurofibromatosis type 1 (NF1) and to establish diagnostic criteria for Legius syndrome (LGSS).MethodsWe used a multistep process, beginning with a Delphi method involving global experts and subsequently involving non-NF experts, patients, and foundations/patient advocacy groups.ResultsWe reached consensus on the minimal clinical and genetic criteria for diagnosing and differentiating NF1 and LGSS, which have phenotypic overlap in young patients with pigmentary findings. Criteria for the mosaic forms of these conditions are also recommended.ConclusionThe revised criteria for NF1 incorporate new clinical features and genetic testing, whereas the criteria for LGSS were created to differentiate the two conditions. It is likely that continued refinement of these new criteria will be necessary as investigators (1) study the diagnostic properties of the revised criteria, (2) reconsider criteria not included in this process, and (3) identify new clinical and other features of these conditions. For this reason, we propose an initiative to update periodically the diagnostic criteria for NF1 and LGSS.

Published
2021

9. Gene therapy with apoptosis-associated speck-like protein, a newly described schwannoma tumor suppressor, inhibits schwannoma growth in vivo

Author

Ahmed, Sherif G, Abdelnabi, Ahmed, Maguire, Casey A, Doha, Mohamed, Sagers, Jessica E, Lewis, Rebecca M, Muzikansky, Alona, Giovannini, Marco, Stemmer-Rachamimov, Anat, Stankovic, Konstantina M, Fulci, Giulia, and Brenner, Gary J

Subjects
Medical Biotechnology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Genetics, Orphan Drug, Neurofibromatosis, Gene Therapy, Cancer, Neurosciences, Biotechnology, Development of treatments and therapeutic interventions, 5.2 Cellular and gene therapies, Aetiology, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Animals, Apoptosis, Biomarkers, Tumor, CARD Signaling Adaptor Proteins, Cancer Pain, Cell Proliferation, DNA Methylation, Dependovirus, Genetic Therapy, Humans, Male, Mice, Neurilemmoma, Prognosis, Promoter Regions, Genetic, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, ASC, AAV1, gene therapy, methylation, schwannoma, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundWe evaluated apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) as a schwannoma tumor suppressor and explored its utilization in a schwannoma gene therapy strategy that may be translated to clinical use.MethodsASC protein expression and mRNA level were assessed in human schwannoma by immunohistochemistry and quantitative PCR, respectively. Methylation- specific PCR was used to assess ASC promoter methylation. The effect of ASC overexpression in schwannoma cells was evaluated through ATP-based viability, lactate dehydrogenase release, and apoptosis staining. Western blotting and colorimetric assay were used to test the effect of ASC overexpression on endogenous pro-apoptotic pathways. Bioluminescence imaging, behavioral testing, and immunohistochemistry in human xenograft and murine allograft schwannoma models were used to examine the efficacy and toxicity of intratumoral injection of adeno-associated virus (AAV) vector encoding ASC.ResultsASC expression was suppressed via promoter methylation in over 80% of the human schwannomas tested. ASC overexpression in schwannoma cells results in cell death and is associated with activation of endogenous caspase-9, caspase-3, and upregulation of BH3 interacting-domain death agonist. In a human xenograft schwannoma model, AAV1-mediated ASC delivery reduced tumor growth and resolved tumor-associated pain without detectable toxicity, and tumor control was associated with reduced Ki67 mitotic index and increased tumor-cell apoptosis. Efficacy of this schwannoma gene therapy strategy was confirmed in a murine schwannoma model.ConclusionWe have identified ASC as a putative schwannoma tumor suppressor with high potential clinical utility for schwannoma gene therapy and generated a vector that treats schwannomas via a novel mechanism that does not overlap with current treatments.

Published
2019

10. Updated diagnostic criteria and nomenclature for neurofibromatosis type 2 and schwannomatosis: An international consensus recommendation

Author

Anten, Monique, Aylsworth, Arthur, Baralle, Diana, Barbarot, Sebastien, Barker, Fred, II, Ben-Shachar, Shay, Bergner, Amanda, Bessis, Didier, Blanco, Ignacio, Cassiman, Catherine, Ciavarelli, Patricia, Clementi, Maurizio, Frébourg, Thierry, Gomes, Alicia, Halliday, Dorothy, Helen Hanson Arvid Heiberg, Chris Hammond, Joly, Pascal, Jordan, Justin T., Karajannis, Matthias, Kroshinsky, Daniela, Larralde, Margarita, Lázaro, Conxi, Le, Lu, Link, Michael, Listernick, Robert, Mallucci, Conor, Merker, Vanessa L., Moertel, Christopher, Mueller, Amy, Ngeow, Joanne, Oostenbrink, Rianne, Packer, Roger, Parry, Allyson, Peltonen, Juha, Pichard, Dominique, Poppe, Bruce, Rezende, Nilton, Rodrigues, Luiz Oswaldo, Rosser, Tena, Ruggieri, Martino, Serra, Eduard, Steinke-Lange, Verena, Stivaros, Stavros Michael, Taylor, Amy, Toelen, Jaan, Tonsgard, James, Trevisson, Eva, Upadhyaya, Meena, Varan, Ali, Wilson, Meredith, Wu, Hao, Zadeh, Gelareh, Plotkin, Scott R., Messiaen, Ludwine, Legius, Eric, Pancza, Patrice, Avery, Robert A., Blakeley, Jaishri O., Babovic-Vuksanovic, Dusica, Ferner, Rosalie, Fisher, Michael J., Friedman, Jan M., Giovannini, Marco, Gutmann, David H., Hanemann, Clemens Oliver, Kalamarides, Michel, Kehrer-Sawatzki, Hildegard, Korf, Bruce R., Mautner, Victor-Felix, MacCollin, Mia, Papi, Laura, Rauen, Katherine A., Riccardi, Vincent, Schorry, Elizabeth, Smith, Miriam J., Stemmer-Rachamimov, Anat, Stevenson, David A., Ullrich, Nicole J., Viskochil, David, Wimmer, Katharina, Yohay, Kaleb, Huson, Susan M., Wolkenstein, Pierre, and Evans, D. Gareth

Published
2022
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11. A Glial Signature and Wnt7 Signaling Regulate Glioma-Vascular Interactions and Tumor Microenvironment

Author

Griveau, Amelie, Seano, Giorgio, Shelton, Samuel J, Kupp, Robert, Jahangiri, Arman, Obernier, Kirsten, Krishnan, Shanmugarajan, Lindberg, Olle R, Yuen, Tracy J, Tien, An-Chi, Sabo, Jennifer K, Wang, Nancy, Chen, Ivy, Kloepper, Jonas, Larrouquere, Louis, Ghosh, Mitrajit, Tirosh, Itay, Huillard, Emmanuelle, Alvarez-Buylla, Arturo, Oldham, Michael C, Persson, Anders I, Weiss, William A, Batchelor, Tracy T, Stemmer-Rachamimov, Anat, Suvà, Mario L, Phillips, Joanna J, Aghi, Manish K, Mehta, Shwetal, Jain, Rakesh K, and Rowitch, David H

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Neurosciences, Rare Diseases, Cancer, Brain Cancer, Brain Disorders, 2.1 Biological and endogenous factors, Aetiology, Animals, Bevacizumab, Blood-Brain Barrier, Brain Neoplasms, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Glioma, Humans, Mice, Neoplasm Transplantation, Oligodendrocyte Transcription Factor 2, Oligodendroglia, Temozolomide, Tumor Cells, Cultured, Tumor Microenvironment, Wnt Proteins, Wnt Signaling Pathway, Olig2, Wnt, angiogenesis, astrocyte, blood-brain barrier, glioma, invasiveness, oligodendrocyte precursor, p53, vessel co-option, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Gliomas comprise heterogeneous malignant glial and stromal cells. While blood vessel co-option is a potential mechanism to escape anti-angiogenic therapy, the relevance of glial phenotype in this process is unclear. We show that Olig2+ oligodendrocyte precursor-like glioma cells invade by single-cell vessel co-option and preserve the blood-brain barrier (BBB). Conversely, Olig2-negative glioma cells form dense perivascular collections and promote angiogenesis and BBB breakdown, leading to innate immune cell activation. Experimentally, Olig2 promotes Wnt7b expression, a finding that correlates in human glioma profiling. Targeted Wnt7a/7b deletion or pharmacologic Wnt inhibition blocks Olig2+ glioma single-cell vessel co-option and enhances responses to temozolomide. Finally, Olig2 and Wnt7 become upregulated after anti-VEGF treatment in preclinical models and patients. Thus, glial-encoded pathways regulate distinct glioma-vascular microenvironmental interactions.

Published
2018

12. Genetically engineered minipigs model the major clinical features of human neurofibromatosis type 1

Author

Isakson, Sara H, Rizzardi, Anthony E, Coutts, Alexander W, Carlson, Daniel F, Kirstein, Mark N, Fisher, James, Vitte, Jeremie, Williams, Kyle B, Pluhar, G Elizabeth, Dahiya, Sonika, Widemann, Brigitte C, Dombi, Eva, Rizvi, Tilat, Ratner, Nancy, Messiaen, Ludwine, Stemmer-Rachamimov, Anat O, Fahrenkrug, Scott C, Gutmann, David H, Giovannini, Marco, Moertel, Christopher L, Largaespada, David A, and Watson, Adrienne L

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Neurofibromatosis, Neurosciences, Brain Disorders, Rare Diseases, Brain Cancer, Biological sciences, Biomedical and clinical sciences
Abstract

Neurofibromatosis Type 1 (NF1) is a genetic disease caused by mutations in Neurofibromin 1 (NF1). NF1 patients present with a variety of clinical manifestations and are predisposed to cancer development. Many NF1 animal models have been developed, yet none display the spectrum of disease seen in patients and the translational impact of these models has been limited. We describe a minipig model that exhibits clinical hallmarks of NF1, including café au lait macules, neurofibromas, and optic pathway glioma. Spontaneous loss of heterozygosity is observed in this model, a phenomenon also described in NF1 patients. Oral administration of a mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor suppresses Ras signaling. To our knowledge, this model provides an unprecedented opportunity to study the complex biology and natural history of NF1 and could prove indispensable for development of imaging methods, biomarkers, and evaluation of safety and efficacy of NF1-targeted therapies.

Published
2018

14. Gene replacement therapy in a schwannoma mouse model of neurofibromatosis type 2

Author

Prabhakar, Shilpa, primary, Beauchamp, Roberta L., additional, Cheah, Pike See, additional, Yoshinaga, Akiko, additional, Abou Haidar, Edwina, additional, Lule, Sevda, additional, Mani, Gayathri, additional, Maalouf, Katia, additional, Stemmer-Rachamimov, Anat, additional, Jung, David H., additional, Welling, D. Bradley, additional, Giovannini, Marco, additional, Plotkin, Scott R., additional, Maguire, Casey A., additional, Ramesh, Vijaya, additional, and Breakefield, Xandra O., additional

Published
2024
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15. Histopathologic evaluation of atypical neurofibromatous tumors and their transformation into malignant peripheral nerve sheath tumor in patients with neurofibromatosis 1—a consensus overview

Author

Miettinen, Markku M, Antonescu, Cristina R, Fletcher, Christopher DM, Kim, Aerang, Lazar, Alexander J, Quezado, Martha M, Reilly, Karlyne M, Stemmer-Rachamimov, Anat, Stewart, Douglas R, Viskochil, David, Widemann, Brigitte, and Perry, Arie

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Biotechnology, Cancer, Clinical Research, Pediatric, Neurofibromatosis, Neurosciences, Orphan Drug, Biomarkers, Tumor, Biopsy, Cell Nucleus, Consensus, Disease Progression, Humans, Immunohistochemistry, Mitosis, Neoplasm Grading, Neurilemmoma, Neurofibromatosis 1, Predictive Value of Tests, Terminology as Topic, Neurofibroma, Atypia, Malignant peripheral nerve sheath tumor, Transformation, Pathology, Clinical sciences
Abstract

Patients with neurofibromatosis 1 (NF1) develop multiple neurofibromas, with 8% to 15% of patients experiencing malignant peripheral nerve sheath tumor (MPNST) during their lifetime. Prediction of transformation, typically from plexiform neurofibroma, is clinically and histologically challenging. In this overview, after a consensus meeting in October 2016, we outline the histopathologic features and molecular mechanisms involved in the malignant transformation of neurofibromas. Nuclear atypia alone is generally insignificant. However, with atypia, loss of neurofibroma architecture, high cellularity, and/or mitotic activity >1/50 but

Published
2017

16. The path forward: 2015 International Children's Tumor Foundation conference on neurofibromatosis type 1, type 2, and schwannomatosis

Author

Blakeley, Jaishri O, Bakker, Annette, Barker, Anne, Clapp, Wade, Ferner, Rosalie, Fisher, Michael J, Giovannini, Marco, Gutmann, David H, Karajannis, Matthias A, Kissil, Joseph L, Legius, Eric, Lloyd, Alison C, Packer, Roger J, Ramesh, Vijaya, Riccardi, Vincent M, Stevenson, David A, Ullrich, Nicole J, Upadhyaya, Meena, and Stemmer‐Rachamimov, Anat

Subjects
Biomedical and Clinical Sciences, Immunology, Brain Disorders, Neurofibromatosis, Pediatric, Rare Diseases, Orphan Drug, Cancer, Pediatric Cancer, Pediatric Research Initiative, Neurosciences, Brain Cancer, Child, Humans, Neurilemmoma, Neurofibromatoses, Neurofibromatosis 1, Neurofibromatosis 2, Pediatrics, Skin Neoplasms, neurofibromatosis type 1, neurofibromatosis type 2, pediatric tumors, rare disease, schwannomatosis, therapeutic discovery, Genetics, Clinical Sciences, Clinical sciences
Abstract

The Annual Children's Tumor Foundation International Neurofibromatosis Meeting is the premier venue for connecting discovery, translational and clinical scientists who are focused on neurofibromatosis types 1 and 2 (NF1 and NF2) and schwannomatosis (SWN). The meeting also features rare tumors such as glioma, meningioma, sarcoma, and neuroblastoma that occur both within these syndromes and spontaneously; associated with somatic mutations in NF1, NF2, and SWN. The meeting addresses both state of the field for current clinical care as well as emerging preclinical models fueling discovery of new therapeutic targets and discovery science initiatives investigating mechanisms of tumorigenesis. Importantly, this conference is a forum for presenting work in progress and bringing together all stakeholders in the scientific community. A highlight of the conference was the involvement of scientists from the pharmaceutical industry who presented growing efforts for rare disease therapeutic development in general and specifically, in pediatric patients with rare tumor syndromes. Another highlight was the focus on new investigators who presented new data about biomarker discovery, tumor pathogenesis, and diagnostic tools for NF1, NF2, and SWN. This report summarizes the themes of the meeting and a synthesis of the scientific discoveries presented at the conference in order to make the larger research community aware of progress in the neurofibromatoses.

Published
2017

18. Epigenomic, genomic, and transcriptomic landscape of schwannomatosis

Author

Mansouri, Sheila, Suppiah, Suganth, Mamatjan, Yasin, Paganini, Irene, Liu, Jeffrey C., Karimi, Shirin, Patil, Vikas, Nassiri, Farshad, Singh, Olivia, Sundaravadanam, Yogi, Rath, Prisni, Sestini, Roberta, Gensini, Francesca, Agnihotri, Sameer, Blakeley, Jaishri, Ostrow, Kimberly, Largaespada, David, Plotkin, Scott R., Stemmer-Rachamimov, Anat, Ferrer, Marcela Maria, Pugh, Trevor J., Aldape, Kenneth D., Papi, Laura, and Zadeh, Gelareh

Published
2021
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19. Current status and recommendations for biomarkers and biobanking in neurofibromatosis

Author

Hanemann, C Oliver, Blakeley, Jaishri O, Nunes, Fabio P, Robertson, Kent, Stemmer-Rachamimov, Anat, Mautner, Victor, Kurtz, Andreas, Ferguson, Michael, Widemann, Brigitte C, Evans, D Gareth, Ferner, Rosalie, Carroll, Steven L, Korf, Bruce, Wolkenstein, Pierre, Knight, Pamela, and Plotkin, Scott R

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Neurofibromatosis, Pediatric, Neurosciences, Biological Specimen Banks, Biomarkers, Datasets as Topic, Humans, Neurilemmoma, Neurofibromatoses, Neurofibromatosis 1, Neurofibromatosis 2, Skin Neoplasms, REiNS International Collaboration, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveClinically validated biomarkers for neurofibromatosis 1 (NF1), neurofibromatosis 2 (NF2), and schwannomatosis (SWN) have not been identified to date. The biomarker working group's goals are to (1) define biomarker needs in NF1, NF2, and SWN; (2) summarize existing data on biomarkers in NF1, NF2, and SWN; (3) outline recommendations for sample collection and biomarker development; and (4) standardize sample collection and methodology protocols where possible to promote comparison between studies by publishing standard operating procedures (SOPs).MethodsThe biomarker group reviewed published data on biomarkers in NF1, NF2, and SWN and on biobanking efforts outside these diseases via literature search, defined the need for biomarkers in NF, and developed recommendations in a series of consensus meetings.ResultsWe describe existing biomarkers in NF and report consensus recommendations for SOP and a minimal clinical dataset to accompany samples derived from patients with NF1, NF2, and SWN in decentralized biobanks.ConclusionsThese recommendations are intended to provide clinicians and researchers with a common set of guidelines to collect and store biospecimens and for establishment of biobanks for NF1, NF2, and SWN.

Published
2016

20. Insertional Mutagenesis Identifies a STAT3/Arid1b/β-catenin Pathway Driving Neurofibroma Initiation.

Author

Wu, Jianqiang, Keng, Vincent, Patmore, Deanna, Kendall, Jed, Patel, Ami, Jousma, Edwin, Jessen, Walter, Choi, Kwangmin, Tschida, Barbara, Silverstein, Kevin, Fan, Danhua, Schwartz, Eric, Fuchs, James, Zou, Yuanshu, Kim, Mi-Ok, Dombi, Eva, Levy, David, Huang, Gang, Cancelas, Jose, Stemmer-Rachamimov, Anat, Spinner, Robert, Largaespada, David, and Ratner, Nancy

Subjects
Animals, Carcinogenesis, DNA Helicases, DNA-Binding Proteins, Disease Models, Animal, Female, Gene Expression Regulation, Neoplastic, Glycogen Synthase Kinase 3 beta, Histones, Humans, Mice, Mice, Nude, Mutagenesis, Insertional, N-Terminal Acetyltransferase A, Neoplasm Transplantation, Neural Stem Cells, Neurofibromatosis 1, Neurofibromin 1, Nuclear Proteins, Peripheral Nervous System Neoplasms, Phosphorylation, RNA, Small Interfering, STAT3 Transcription Factor, Schwann Cells, Signal Transduction, Transcription Factors, beta Catenin
Abstract

To identify genes and signaling pathways that initiate Neurofibromatosis type 1 (NF1) neurofibromas, we used unbiased insertional mutagenesis screening, mouse models, and molecular analyses. We mapped an Nf1-Stat3-Arid1b/β-catenin pathway that becomes active in the context of Nf1 loss. Genetic deletion of Stat3 in Schwann cell progenitors (SCPs) and Schwann cells (SCs) prevents neurofibroma formation, decreasing SCP self-renewal and β-catenin activity. β-catenin expression rescues effects of Stat3 loss in SCPs. Importantly, P-STAT3 and β-catenin expression correlate in human neurofibromas. Mechanistically, P-Stat3 represses Gsk3β and the SWI/SNF gene Arid1b to increase β-catenin. Knockdown of Arid1b or Gsk3β in Stat3(fl/fl);Nf1(fl/fl);DhhCre SCPs rescues neurofibroma formation after in vivo transplantation. Stat3 represses Arid1b through histone modification in a Brg1-dependent manner, indicating that epigenetic modification plays a role in early tumorigenesis. Our data map a neural tumorigenesis pathway and support testing JAK/STAT and Wnt/β-catenin pathway inhibitors in neurofibroma therapeutic trials.

Published
2016

22. Phase 2 study of bosutinib, a Src inhibitor, in adults with recurrent glioblastoma

Author

Taylor, Jennie W, Dietrich, Jorg, Gerstner, Elizabeth R, Norden, Andrew D, Rinne, Mikael L, Cahill, Daniel P, Stemmer-Rachamimov, Anat, Wen, Patrick Y, Betensky, Rebecca A, Giorgio, Diana H, Snodgrass, Kellis, Randall, Alison E, Batchelor, Tracy T, and Chi, Andrew S

Subjects
Brain Disorders, Brain Cancer, Rare Diseases, Clinical Research, Cancer, Neurosciences, Clinical Trials and Supportive Activities, 6.2 Cellular and gene therapies, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Adult, Aniline Compounds, Antineoplastic Agents, Brain Neoplasms, Disease-Free Survival, Female, Glioblastoma, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Neoplasm Recurrence, Local, Nitriles, Proportional Hazards Models, Quinolines, src-Family Kinases, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Tumor cell infiltration is a major mechanism of treatment escape in glioblastoma. Src is an intracellular tyrosine kinase that mediates tumor cell motility and invasiveness. We evaluated the efficacy and safety of bosutinib, a tyrosine kinase inhibitor that potently inhibits Src and Abl, in patients with recurrent glioblastoma. In this two-arm study, patients with histologically confirmed recurrent glioblastoma and ≤2 relapses, not previously treated with anti-vascular endothelial growth factor (VEGF) therapy, were administered oral bosutinib 400 mg daily. Arm A planned for 6 patients who were candidates for surgical resection to be given bosutinib for 7-9 days prior to resection. Arm B was a two-stage design phase 2 trial targeting 30 patients. The primary endpoint was progression-free survival at 6 months (PFS6) in Arm B. After 9 patients enrolled onto stage 1 of Arm B, 9 (100 %) patients progressed within 6 months. Therefore, the study met the pre-specified criteria for early closure and both Arms were closed. In Arm B, Median PFS was 7.71 weeks and median OS was 50 weeks. Best objective response was stable disease in one patient (11.1 %). Seven patients (77.8 %) had treatment-related AEs of any grade and 2 (22.2 %) were grade ≥3. Arm A was closed after 2 patients enrolled. Src activation was evident in all archival tumor samples. Bosutinib monotherapy does not appear to be effective in recurrent glioblastoma. However, Src remains a potential target based on its upregulation in tumor samples and role in glioma invasion.

Published
2015

24. An Integrative Model of Cellular States, Plasticity, and Genetics for Glioblastoma

Author

Neftel, Cyril, Laffy, Julie, Filbin, Mariella G., Hara, Toshiro, Shore, Marni E., Rahme, Gilbert J., Richman, Alyssa R., Silverbush, Dana, Shaw, McKenzie L., Hebert, Christine M., Dewitt, John, Gritsch, Simon, Perez, Elizabeth M., Gonzalez Castro, L. Nicolas, Lan, Xiaoyang, Druck, Nicholas, Rodman, Christopher, Dionne, Danielle, Kaplan, Alexander, Bertalan, Mia S., Small, Julia, Pelton, Kristine, Becker, Sarah, Bonal, Dennis, Nguyen, Quang-De, Servis, Rachel L., Fung, Jeremy M., Mylvaganam, Ravindra, Mayr, Lisa, Gojo, Johannes, Haberler, Christine, Geyeregger, Rene, Czech, Thomas, Slavc, Irene, Nahed, Brian V., Curry, William T., Carter, Bob S., Wakimoto, Hiroaki, Brastianos, Priscilla K., Batchelor, Tracy T., Stemmer-Rachamimov, Anat, Martinez-Lage, Maria, Frosch, Matthew P., Stamenkovic, Ivan, Riggi, Nicolo, Rheinbay, Esther, Monje, Michelle, Rozenblatt-Rosen, Orit, Cahill, Daniel P., Patel, Anoop P., Hunter, Tony, Verma, Inder M., Ligon, Keith L., Louis, David N., Regev, Aviv, Bernstein, Bradley E., Tirosh, Itay, and Suvà, Mario L.

Published
2019
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26. EPCO-03. A COMPREHENSIVE SINGLE-CELL ATLAS OF SCHWANNOMA REVEALS CONSERVED CELLULAR STATES ACROSS DIFFERENT GENETIC BACKGROUNDS AND ANATOMIC LOCATIONS

Author

Castro, Luis Nicolas Gonzalez, primary, Gavish, Avishai, additional, Bussema, Lillian, additional, Neftel, Cyril, additional, Nomura, Masashi, additional, Chiocca, E Antonio, additional, Bi, Wenya Linda, additional, Arnaout, Omar, additional, Barker, Frederick, additional, Brown, Justin, additional, Jordan, Justin T, additional, Stemmer-Rachamimov, Anat, additional, Plotkin, Scott R, additional, Tirosh, Itay, additional, and Suva, Mario, additional

Published
2023
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27. 1040-E Deciphering and targeting the schwannoma-neuron-macrophage crosstalk for the treatment of schwannomatosis and associated pain

Author

Yin, Zhenzhen, primary, Wu, Limeng, additional, Zhang, Yanling, additional, Sun, Yao, additional, Chen, John W, additional, Subudhi, Sonu, additional, Lee, Grace, additional, Wang, Athena, additional, Gao, Xing, additional, Ren, Jun, additional, Muzikansky, Alona, additional, Stemmer-Rachamimov, Anat, additional, Mao, Jianren, additional, Plotkin, Scott R, additional, and Xu, Lei, additional

Published
2023
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29. Defining T Cell States Associated with Response to Checkpoint Immunotherapy in Melanoma

Author

Sade-Feldman, Moshe, Yizhak, Keren, Bjorgaard, Stacey L., Ray, John P., de Boer, Carl G., Jenkins, Russell W., Lieb, David J., Chen, Jonathan H., Frederick, Dennie T., Barzily-Rokni, Michal, Freeman, Samuel S., Reuben, Alexandre, Hoover, Paul J., Villani, Alexandra-Chloé, Ivanova, Elena, Portell, Andrew, Lizotte, Patrick H., Aref, Amir R., Eliane, Jean-Pierre, Hammond, Marc R., Vitzthum, Hans, Blackmon, Shauna M., Li, Bo, Gopalakrishnan, Vancheswaran, Reddy, Sangeetha M., Cooper, Zachary A., Paweletz, Cloud P., Barbie, David A., Stemmer-Rachamimov, Anat, Flaherty, Keith T., Wargo, Jennifer A., Boland, Genevieve M., Sullivan, Ryan J., Getz, Gad, and Hacohen, Nir

Published
2018
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32. Increase in tumor-associated macrophages after antiangiogenic therapy is associated with poor survival among patients with recurrent glioblastoma

Author

Lu-Emerson, Christine, Snuderl, Matija, Kirkpatrick, Nathaniel D, Goveia, Jermaine, Davidson, Christian, Huang, Yuhui, Riedemann, Lars, Taylor, Jennie, Ivy, Percy, Duda, Dan G, Ancukiewicz, Marek, Plotkin, Scott R, Chi, Andrew S, Gerstner, Elizabeth R, Eichler, April F, Dietrich, Jorg, Stemmer-Rachamimov, Anat O, Batchelor, Tracy T, and Jain, Rakesh K

Subjects
Cancer, Rare Diseases, Neurosciences, Brain Disorders, Brain Cancer, Adolescent, Adult, Aged, Aged, 80 and over, Angiogenesis Inhibitors, Antigens, CD, Autopsy, Biomarkers, Tumor, Brain Neoplasms, Female, Flow Cytometry, Follow-Up Studies, Glioblastoma, Humans, Immunoenzyme Techniques, Macrophages, Male, Middle Aged, Neoplasm Grading, Neoplasm Recurrence, Local, Prognosis, Survival Rate, Tumor Microenvironment, Young Adult, antiangiogenic therapy, glioblastoma, myeloid cells, relapse, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Antiangiogenic therapy is associated with increased radiographic responses in glioblastomas, but tumors invariably recur. Because tumor-associated macrophages have been shown to mediate escape from antiangiogenic therapy in preclinical models, we examined the role of macrophages in patients with recurrent glioblastoma. We compared autopsy brain specimens from 20 patients with recurrent glioblastoma who received antiangiogenic treatment and chemoradiation with 8 patients who received chemotherapy and/or radiotherapy without antiangiogenic therapy or no treatment. Tumor-associated macrophages were morphologically and phenotypically analyzed using flow cytometry and immunohistochemistry for CD68, CD14, CD163, and CD11b expression. Flow cytometry showed an increase in macrophages in the antiangiogenic-treated patients. Immunohistochemical analysis demonstrated an increase in CD68+ macrophages in the tumor bulk (P < .01) and infiltrative areas (P = .02) in antiangiogenic-treated patients. We also observed an increase in CD11b+ cells in the tumor bulk (P < .01) and an increase in CD163+ macrophages in infiltrative tumor (P = .02). Of note, an increased number of CD11b+ cells in bulk and infiltrative tumors (P = .05 and P = .05, respectively) correlated with poor overall survival among patients who first received antiangiogenic therapy at recurrence. In summary, recurrent glioblastomas showed an increased infiltration in myeloid populations in the tumor bulk and in the infiltrative regions after antiangiogenic therapy. Higher numbers of CD11b+ cells correlated with poor survival among these patients. These data suggest that tumor-associated macrophages may participate in escape from antiangiogenic therapy and may represent a potential biomarker of resistance and a potential therapeutic target in recurrent glioblastoma.

Published
2013

35. Schwannomas

Author

Karajannis, Matthias A., Stemmer-Rachamimov, Anat, Cagle, Philip T., Series editor, Karajannis, Matthias A., editor, and Zagzag, David, editor

Published
2015
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36. DMD genomic deletions characterize a subset of progressive/higher-grade meningiomas with poor outcome

Author

Juratli, Tareq A., McCabe, Devin, Nayyar, Naema, Williams, Erik A., Silverman, Ian M., Tummala, Shilpa S., Fink, Alexandria L., Baig, Aymen, Martinez-Lage, Maria, Selig, Martin K., Bihun, Ivanna V., Shankar, Ganesh M., Penson, Tristan, Lastrapes, Matthew, Daubner, Dirk, Meinhardt, Matthias, Hennig, Silke, Kaplan, Alexander B., Fujio, Shingo, Kuter, Benjamin M., Bertalan, Mia S., Miller, Julie J., Batten, Julie M., Ely, Heather A., Christiansen, Jason, Baretton, Gustavo B., Stemmer-Rachamimov, Anat O., Santagata, Sandro, Rivera, Miguel N., Barker, II, Fred G., Schackert, Gabriele, Wakimoto, Hiroaki, Iafrate, A. John, Carter, Scott L., Cahill, Daniel P., and Brastianos, Priscilla K.

Published
2018
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38. Comparison of Therapeutic Efficacy of Gene Therapy for Tuberous Sclerosis Type 2 with Standard of Care Everolimus in Preclinical Model (S14.002)

Author

Haidar, Edwina Abou, primary, Prabhakar, Shilpa, additional, Cheah, Pike See, additional, Lule, Sevda, additional, Beauchamp, Roberta L., additional, Yoshinaga, Akiko, additional, Geffrey, Alexandra L., additional, Stemmer-Rachamimov, Anat, additional, Ramesh, Vijaya, additional, Maguire, Casey A., additional, and Breakefield, Xandra O., additional

Published
2023
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39. Prospective phase 2 trial of the dual mTORC1/2 inhibitor vistusertib for progressive or symptomatic meningiomas in persons with neurofibromatosis 2

Author

Jordan, Justin T, primary, Orr, Christina C, additional, Thalheimer, Raquel D, additional, Cambillo, Josephine V, additional, Beauchamp, Roberta L, additional, Shaike, Ghalib, additional, Muzikansky, Alona, additional, Stemmer-Rachamimov, Anat, additional, Giovannini, Marco, additional, Kalamarides, Michel, additional, Barker, Fred G, additional, Ramesh, Vijaya, additional, and Plotkin, Scott R, additional

Published
2023
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40. Supplementary Table S1 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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41. Data from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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42. Supplementary Methods, Figures S1 - S20 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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43. Data from Ex Vivo Profiling of PD-1 Blockade Using Organotypic Tumor Spheroids

Author

Jenkins, Russell W., primary, Aref, Amir R., primary, Lizotte, Patrick H., primary, Ivanova, Elena, primary, Stinson, Susanna, primary, Zhou, Chensheng W., primary, Bowden, Michaela, primary, Deng, Jiehui, primary, Liu, Hongye, primary, Miao, Diana, primary, He, Meng Xiao, primary, Walker, William, primary, Zhang, Gao, primary, Tian, Tian, primary, Cheng, Chaoran, primary, Wei, Zhi, primary, Palakurthi, Sangeetha, primary, Bittinger, Mark, primary, Vitzthum, Hans, primary, Kim, Jong Wook, primary, Merlino, Ashley, primary, Quinn, Max, primary, Venkataramani, Chandrasekar, primary, Kaplan, Joshua A., primary, Portell, Andrew, primary, Gokhale, Prafulla C., primary, Phillips, Bart, primary, Smart, Alicia, primary, Rotem, Asaf, primary, Jones, Robert E., primary, Keogh, Lauren, primary, Anguiano, Maria, primary, Stapleton, Lance, primary, Jia, Zhiheng, primary, Barzily-Rokni, Michal, primary, Cañadas, Israel, primary, Thai, Tran C., primary, Hammond, Marc R., primary, Vlahos, Raven, primary, Wang, Eric S., primary, Zhang, Hua, primary, Li, Shuai, primary, Hanna, Glenn J., primary, Huang, Wei, primary, Hoang, Mai P., primary, Piris, Adriano, primary, Eliane, Jean-Pierre, primary, Stemmer-Rachamimov, Anat O., primary, Cameron, Lisa, primary, Su, Mei-Ju, primary, Shah, Parin, primary, Izar, Benjamin, primary, Thakuria, Manisha, primary, LeBoeuf, Nicole R., primary, Rabinowits, Guilherme, primary, Gunda, Viswanath, primary, Parangi, Sareh, primary, Cleary, James M., primary, Miller, Brian C., primary, Kitajima, Shunsuke, primary, Thummalapalli, Rohit, primary, Miao, Benchun, primary, Barbie, Thanh U., primary, Sivathanu, Vivek, primary, Wong, Joshua, primary, Richards, William G., primary, Bueno, Raphael, primary, Yoon, Charles H., primary, Miret, Juan, primary, Herlyn, Meenhard, primary, Garraway, Levi A., primary, Van Allen, Eliezer M., primary, Freeman, Gordon J., primary, Kirschmeier, Paul T., primary, Lorch, Jochen H., primary, Ott, Patrick A., primary, Hodi, F. Stephen, primary, Flaherty, Keith T., primary, Kamm, Roger D., primary, Boland, Genevieve M., primary, Wong, Kwok-Kin, primary, Dornan, David, primary, Paweletz, Cloud Peter, primary, and Barbie, David A., primary

Published
2023
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44. Supplementary File 3 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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45. Supplementary File Legends from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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46. Supp. Movie 3 from Ex Vivo Profiling of PD-1 Blockade Using Organotypic Tumor Spheroids

Author

Jenkins, Russell W., primary, Aref, Amir R., primary, Lizotte, Patrick H., primary, Ivanova, Elena, primary, Stinson, Susanna, primary, Zhou, Chensheng W., primary, Bowden, Michaela, primary, Deng, Jiehui, primary, Liu, Hongye, primary, Miao, Diana, primary, He, Meng Xiao, primary, Walker, William, primary, Zhang, Gao, primary, Tian, Tian, primary, Cheng, Chaoran, primary, Wei, Zhi, primary, Palakurthi, Sangeetha, primary, Bittinger, Mark, primary, Vitzthum, Hans, primary, Kim, Jong Wook, primary, Merlino, Ashley, primary, Quinn, Max, primary, Venkataramani, Chandrasekar, primary, Kaplan, Joshua A., primary, Portell, Andrew, primary, Gokhale, Prafulla C., primary, Phillips, Bart, primary, Smart, Alicia, primary, Rotem, Asaf, primary, Jones, Robert E., primary, Keogh, Lauren, primary, Anguiano, Maria, primary, Stapleton, Lance, primary, Jia, Zhiheng, primary, Barzily-Rokni, Michal, primary, Cañadas, Israel, primary, Thai, Tran C., primary, Hammond, Marc R., primary, Vlahos, Raven, primary, Wang, Eric S., primary, Zhang, Hua, primary, Li, Shuai, primary, Hanna, Glenn J., primary, Huang, Wei, primary, Hoang, Mai P., primary, Piris, Adriano, primary, Eliane, Jean-Pierre, primary, Stemmer-Rachamimov, Anat O., primary, Cameron, Lisa, primary, Su, Mei-Ju, primary, Shah, Parin, primary, Izar, Benjamin, primary, Thakuria, Manisha, primary, LeBoeuf, Nicole R., primary, Rabinowits, Guilherme, primary, Gunda, Viswanath, primary, Parangi, Sareh, primary, Cleary, James M., primary, Miller, Brian C., primary, Kitajima, Shunsuke, primary, Thummalapalli, Rohit, primary, Miao, Benchun, primary, Barbie, Thanh U., primary, Sivathanu, Vivek, primary, Wong, Joshua, primary, Richards, William G., primary, Bueno, Raphael, primary, Yoon, Charles H., primary, Miret, Juan, primary, Herlyn, Meenhard, primary, Garraway, Levi A., primary, Van Allen, Eliezer M., primary, Freeman, Gordon J., primary, Kirschmeier, Paul T., primary, Lorch, Jochen H., primary, Ott, Patrick A., primary, Hodi, F. Stephen, primary, Flaherty, Keith T., primary, Kamm, Roger D., primary, Boland, Genevieve M., primary, Wong, Kwok-Kin, primary, Dornan, David, primary, Paweletz, Cloud Peter, primary, and Barbie, David A., primary

Published
2023
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48. Supp. Movie 1 from Ex Vivo Profiling of PD-1 Blockade Using Organotypic Tumor Spheroids

Author

Jenkins, Russell W., primary, Aref, Amir R., primary, Lizotte, Patrick H., primary, Ivanova, Elena, primary, Stinson, Susanna, primary, Zhou, Chensheng W., primary, Bowden, Michaela, primary, Deng, Jiehui, primary, Liu, Hongye, primary, Miao, Diana, primary, He, Meng Xiao, primary, Walker, William, primary, Zhang, Gao, primary, Tian, Tian, primary, Cheng, Chaoran, primary, Wei, Zhi, primary, Palakurthi, Sangeetha, primary, Bittinger, Mark, primary, Vitzthum, Hans, primary, Kim, Jong Wook, primary, Merlino, Ashley, primary, Quinn, Max, primary, Venkataramani, Chandrasekar, primary, Kaplan, Joshua A., primary, Portell, Andrew, primary, Gokhale, Prafulla C., primary, Phillips, Bart, primary, Smart, Alicia, primary, Rotem, Asaf, primary, Jones, Robert E., primary, Keogh, Lauren, primary, Anguiano, Maria, primary, Stapleton, Lance, primary, Jia, Zhiheng, primary, Barzily-Rokni, Michal, primary, Cañadas, Israel, primary, Thai, Tran C., primary, Hammond, Marc R., primary, Vlahos, Raven, primary, Wang, Eric S., primary, Zhang, Hua, primary, Li, Shuai, primary, Hanna, Glenn J., primary, Huang, Wei, primary, Hoang, Mai P., primary, Piris, Adriano, primary, Eliane, Jean-Pierre, primary, Stemmer-Rachamimov, Anat O., primary, Cameron, Lisa, primary, Su, Mei-Ju, primary, Shah, Parin, primary, Izar, Benjamin, primary, Thakuria, Manisha, primary, LeBoeuf, Nicole R., primary, Rabinowits, Guilherme, primary, Gunda, Viswanath, primary, Parangi, Sareh, primary, Cleary, James M., primary, Miller, Brian C., primary, Kitajima, Shunsuke, primary, Thummalapalli, Rohit, primary, Miao, Benchun, primary, Barbie, Thanh U., primary, Sivathanu, Vivek, primary, Wong, Joshua, primary, Richards, William G., primary, Bueno, Raphael, primary, Yoon, Charles H., primary, Miret, Juan, primary, Herlyn, Meenhard, primary, Garraway, Levi A., primary, Van Allen, Eliezer M., primary, Freeman, Gordon J., primary, Kirschmeier, Paul T., primary, Lorch, Jochen H., primary, Ott, Patrick A., primary, Hodi, F. Stephen, primary, Flaherty, Keith T., primary, Kamm, Roger D., primary, Boland, Genevieve M., primary, Wong, Kwok-Kin, primary, Dornan, David, primary, Paweletz, Cloud Peter, primary, and Barbie, David A., primary

Published
2023
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49. Table S3 from Ex Vivo Profiling of PD-1 Blockade Using Organotypic Tumor Spheroids

Author

Jenkins, Russell W., primary, Aref, Amir R., primary, Lizotte, Patrick H., primary, Ivanova, Elena, primary, Stinson, Susanna, primary, Zhou, Chensheng W., primary, Bowden, Michaela, primary, Deng, Jiehui, primary, Liu, Hongye, primary, Miao, Diana, primary, He, Meng Xiao, primary, Walker, William, primary, Zhang, Gao, primary, Tian, Tian, primary, Cheng, Chaoran, primary, Wei, Zhi, primary, Palakurthi, Sangeetha, primary, Bittinger, Mark, primary, Vitzthum, Hans, primary, Kim, Jong Wook, primary, Merlino, Ashley, primary, Quinn, Max, primary, Venkataramani, Chandrasekar, primary, Kaplan, Joshua A., primary, Portell, Andrew, primary, Gokhale, Prafulla C., primary, Phillips, Bart, primary, Smart, Alicia, primary, Rotem, Asaf, primary, Jones, Robert E., primary, Keogh, Lauren, primary, Anguiano, Maria, primary, Stapleton, Lance, primary, Jia, Zhiheng, primary, Barzily-Rokni, Michal, primary, Cañadas, Israel, primary, Thai, Tran C., primary, Hammond, Marc R., primary, Vlahos, Raven, primary, Wang, Eric S., primary, Zhang, Hua, primary, Li, Shuai, primary, Hanna, Glenn J., primary, Huang, Wei, primary, Hoang, Mai P., primary, Piris, Adriano, primary, Eliane, Jean-Pierre, primary, Stemmer-Rachamimov, Anat O., primary, Cameron, Lisa, primary, Su, Mei-Ju, primary, Shah, Parin, primary, Izar, Benjamin, primary, Thakuria, Manisha, primary, LeBoeuf, Nicole R., primary, Rabinowits, Guilherme, primary, Gunda, Viswanath, primary, Parangi, Sareh, primary, Cleary, James M., primary, Miller, Brian C., primary, Kitajima, Shunsuke, primary, Thummalapalli, Rohit, primary, Miao, Benchun, primary, Barbie, Thanh U., primary, Sivathanu, Vivek, primary, Wong, Joshua, primary, Richards, William G., primary, Bueno, Raphael, primary, Yoon, Charles H., primary, Miret, Juan, primary, Herlyn, Meenhard, primary, Garraway, Levi A., primary, Van Allen, Eliezer M., primary, Freeman, Gordon J., primary, Kirschmeier, Paul T., primary, Lorch, Jochen H., primary, Ott, Patrick A., primary, Hodi, F. Stephen, primary, Flaherty, Keith T., primary, Kamm, Roger D., primary, Boland, Genevieve M., primary, Wong, Kwok-Kin, primary, Dornan, David, primary, Paweletz, Cloud Peter, primary, and Barbie, David A., primary

Published
2023
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50. Supplementary File 2 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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