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  1. Article ; Online: The efficacy of an unrestricted cycling ketogenic diet in preclinical models of IDH wild-type and IDH mutant glioma

    Rodrigo Javier / Wenxia Wang / Michael Drumm / Kathleen McCortney / Jann N. Sarkaria / Craig Horbinski

    PLoS ONE, Vol 17, Iss

    2022  Volume 2

    Abstract: Infiltrative gliomas are the most common neoplasms arising in the brain, and remain largely incurable despite decades of research. A subset of these gliomas contains mutations in isocitrate dehydrogenase 1 (IDH1mut) or, less commonly, IDH2 (together ... ...

    Abstract Infiltrative gliomas are the most common neoplasms arising in the brain, and remain largely incurable despite decades of research. A subset of these gliomas contains mutations in isocitrate dehydrogenase 1 (IDH1mut) or, less commonly, IDH2 (together called “IDHmut”). These mutations alter cellular biochemistry, and IDHmut gliomas are generally less aggressive than IDH wild-type (IDHwt) gliomas. Some preclinical studies and clinical trials have suggested that various forms of a ketogenic diet (KD), characterized by low-carbohydrate and high-fat content, may be beneficial in slowing glioma progression. However, adherence to a strict KD is difficult, and not all studies have shown promising results. Furthermore, no study has yet addressed whether IDHmut gliomas might be more sensitive to KD. The aim of the current study was to compare the effects of a unrestricted, cycling KD (weekly alternating between KD and standard diet) in preclinical models of IDHwt versus IDHmut gliomas. In vitro, simulating KD by treatment with the ketone body β-hydroxybutyrate had no effect on the proliferation of patient-derived IDHwt or IDHmut glioma cells, either in low or normal glucose conditions. Likewise, an unrestricted, cycling KD had no effect on the in vivo growth of patient-derived IDHwt or IDHmut gliomas, even though the cycling KD did result in persistently elevated circulating ketones. Furthermore, this KD conferred no survival benefit in mice engrafted with Sleeping-Beauty transposase-engineered IDHmut or IDHwt glioma. These data suggest that neither IDHwt nor IDHmut gliomas are particularly responsive to an unrestricted, cycling form of KD.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: The efficacy of an unrestricted cycling ketogenic diet in preclinical models of IDH wild-type and IDH mutant glioma.

    Rodrigo Javier / Wenxia Wang / Michael Drumm / Kathleen McCortney / Jann N Sarkaria / Craig Horbinski

    PLoS ONE, Vol 17, Iss 2, p e

    2022  Volume 0257725

    Abstract: Infiltrative gliomas are the most common neoplasms arising in the brain, and remain largely incurable despite decades of research. A subset of these gliomas contains mutations in isocitrate dehydrogenase 1 (IDH1mut) or, less commonly, IDH2 (together ... ...

    Abstract Infiltrative gliomas are the most common neoplasms arising in the brain, and remain largely incurable despite decades of research. A subset of these gliomas contains mutations in isocitrate dehydrogenase 1 (IDH1mut) or, less commonly, IDH2 (together called "IDHmut"). These mutations alter cellular biochemistry, and IDHmut gliomas are generally less aggressive than IDH wild-type (IDHwt) gliomas. Some preclinical studies and clinical trials have suggested that various forms of a ketogenic diet (KD), characterized by low-carbohydrate and high-fat content, may be beneficial in slowing glioma progression. However, adherence to a strict KD is difficult, and not all studies have shown promising results. Furthermore, no study has yet addressed whether IDHmut gliomas might be more sensitive to KD. The aim of the current study was to compare the effects of a unrestricted, cycling KD (weekly alternating between KD and standard diet) in preclinical models of IDHwt versus IDHmut gliomas. In vitro, simulating KD by treatment with the ketone body β-hydroxybutyrate had no effect on the proliferation of patient-derived IDHwt or IDHmut glioma cells, either in low or normal glucose conditions. Likewise, an unrestricted, cycling KD had no effect on the in vivo growth of patient-derived IDHwt or IDHmut gliomas, even though the cycling KD did result in persistently elevated circulating ketones. Furthermore, this KD conferred no survival benefit in mice engrafted with Sleeping-Beauty transposase-engineered IDHmut or IDHwt glioma. These data suggest that neither IDHwt nor IDHmut gliomas are particularly responsive to an unrestricted, cycling form of KD.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Methylation and transcription patterns are distinct in IDH mutant gliomas compared to other IDH mutant cancers

    Dusten Unruh / Makda Zewde / Adam Buss / Michael R. Drumm / Anh N. Tran / Denise M. Scholtens / Craig Horbinski

    Scientific Reports, Vol 9, Iss 1, Pp 1-

    2019  Volume 11

    Abstract: Abstract Mutations in isocitrate dehydrogenases 1 and 2 (IDHmut) are present in a variety of cancers, including glioma, acute myeloid leukemia (AML), melanoma, and cholangiocarcinoma. These mutations promote hypermethylation, yet it is only a favorable ... ...

    Abstract Abstract Mutations in isocitrate dehydrogenases 1 and 2 (IDHmut) are present in a variety of cancers, including glioma, acute myeloid leukemia (AML), melanoma, and cholangiocarcinoma. These mutations promote hypermethylation, yet it is only a favorable prognostic marker in glioma, for reasons that are unclear. We hypothesized that the patterns of DNA methylation, and transcriptome profiles, would vary among IDHmut cancers, especially gliomas. Using Illumina 450K and RNA-Seq data from The Cancer Genome Atlas, we show that of 365,092 analyzed CpG sites, 70,591 (19%) were hypermethylated in IDHmut gliomas compared to wild-type (IDHwt) gliomas, and only 3%, 2%, and 4% of CpG sites were hypermethylated in IDHmut AML, melanoma, and cholangiocarcinoma, relative to each of their IDHwt counterparts. Transcriptome differences showed pro-malignant genes that appear to be unique to IDHmut gliomas. However, genes involved in differentiation and immune response were suppressed in all IDHmut cancers. Additionally, IDHmut caused a greater degree of hypermethylation in undifferentiated neural progenitor cells than in mature astrocytes. These data suggest that the extent and targets of IDHmut-induced genomic hypermethylation vary greatly according to the cellular context and may help explain why IDHmut is only a favorable prognostic marker in gliomas.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2019-06-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Postoperative risk of IDH-mutant glioma–associated seizures and their potential management with IDH-mutant inhibitors

    Michael R. Drumm / Wenxia Wang / Thomas K. Sears / Kirsten Bell-Burdett / Rodrigo Javier / Kristen Y. Cotton / Brynna Webb / Kayla Byrne / Dusten Unruh / Vineeth Thirunavu / Jordain Walshon / Alicia Steffens / Kathleen McCortney / Rimas V. Lukas / Joanna J. Phillips / Esraa Mohamed / John D. Finan / Lucas Santana-Santos / Amy B. Heimberger /
    Colin K. Franz / Jonathan Kurz / Jessica W. Templer / Geoffrey T. Swanson / Craig Horbinski

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Volume 12

    Abstract: Seizures are a frequent complication of adult-type diffuse gliomas, and are often difficult to control with medications. Gliomas with mutations in isocitrate dehydrogenase 1 or 2 (IDHmut) are more likely than IDH–wild type (IDHwt) gliomas to cause ... ...

    Abstract Seizures are a frequent complication of adult-type diffuse gliomas, and are often difficult to control with medications. Gliomas with mutations in isocitrate dehydrogenase 1 or 2 (IDHmut) are more likely than IDH–wild type (IDHwt) gliomas to cause seizures as part of their initial clinical presentation. However, whether IDHmut is also associated with seizures during the remaining disease course, and whether IDHmut inhibitors can reduce seizure risk, are unclear. Clinical multivariable analyses showed that preoperative seizures, glioma location, extent of resection, and glioma molecular subtype (including IDHmut status) all contributed to postoperative seizure risk in adult-type diffuse glioma patients, and that postoperative seizures were often associated with tumor recurrence. Experimentally, the metabolic product of IDHmut, d-2-hydroxyglutarate, rapidly synchronized neuronal spike firing in a seizure-like manner, but only when non-neoplastic glial cells were present. In vitro and in vivo models recapitulated IDHmut glioma–associated seizures, and IDHmut inhibitors currently being evaluated in glioma clinical trials inhibited seizures in those models, independent of their effects on glioma growth. These data show that postoperative seizure risk in adult-type diffuse gliomas varies in large part by molecular subtype, and that IDHmut inhibitors could play a key role in mitigating such risk in IDHmut glioma patients.
    Keywords Neuroscience ; Oncology ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Central nervous system immune interactome is a function of cancer lineage, tumor microenvironment, and STAT3 expression

    Hinda Najem / Martina Ott / Cynthia Kassab / Arvind Rao / Ganesh Rao / Anantha Marisetty / Adam M. Sonabend / Craig Horbinski / Roel Verhaak / Anand Shankar / Santhoshi N. Krishnan / Frederick S. Varn / Víctor A. Arrieta / Pravesh Gupta / Sherise D. Ferguson / Jason T. Huse / Gregory N. Fuller / James P. Long / Daniel E. Winkowski /
    Ben A. Freiberg / Charles David James / Leonidas C. Platanias / Maciej S. Lesniak / Jared K. Burks / Amy B. Heimberger

    JCI Insight, Vol 7, Iss

    2022  Volume 9

    Abstract: BACKGROUND Immune cell profiling of primary and metastatic CNS tumors has been focused on the tumor, not the tumor microenvironment (TME), or has been analyzed via biopsies.METHODS En bloc resections of gliomas (n = 10) and lung metastases (n = 10) were ... ...

    Abstract BACKGROUND Immune cell profiling of primary and metastatic CNS tumors has been focused on the tumor, not the tumor microenvironment (TME), or has been analyzed via biopsies.METHODS En bloc resections of gliomas (n = 10) and lung metastases (n = 10) were analyzed via tissue segmentation and high-dimension Opal 7-color multiplex imaging. Single-cell RNA analyses were used to infer immune cell functionality.RESULTS Within gliomas, T cells were localized in the infiltrating edge and perivascular space of tumors, while residing mostly in the stroma of metastatic tumors. CD163+ macrophages were evident throughout the TME of metastatic tumors, whereas in gliomas, CD68+, CD11c+CD68+, and CD11c+CD68+CD163+ cell subtypes were commonly observed. In lung metastases, T cells interacted with CD163+ macrophages as dyads and clusters at the brain-tumor interface and within the tumor itself and as clusters within the necrotic core. In contrast, gliomas typically lacked dyad and cluster interactions, except for T cell CD68+ cell dyads within the tumor. Analysis of transcriptomic data in glioblastomas revealed that innate immune cells expressed both proinflammatory and immunosuppressive gene signatures.CONCLUSION Our results show that immunosuppressive macrophages are abundant within the TME and that the immune cell interactome between cancer lineages is distinct. Further, these data provide information for evaluating the role of different immune cell populations in brain tumor growth and therapeutic responses.FUNDING This study was supported by the NIH (NS120547), a Developmental research project award (P50CA221747), ReMission Alliance, institutional funding from Northwestern University and the Lurie Comprehensive Cancer Center, and gifts from the Mosky family and Perry McKay. Performed in the Flow Cytometry & Cellular Imaging Core Facility at MD Anderson Cancer Center, this study received support in part from the NIH (CA016672) and the National Cancer Institute (NCI) Research Specialist award 1 (R50 CA243707). Additional ...
    Keywords Immunology ; Oncology ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Lgr5 Marks Post-Mitotic, Lineage Restricted Cerebellar Granule Neurons during Postnatal Development.

    Tyler E Miller / Jun Wang / Kumar Sukhdeo / Craig Horbinski / Paul J Tesar / Robert J Wechsler-Reya / Jeremy N Rich

    PLoS ONE, Vol 9, Iss 12, p e

    2014  Volume 114433

    Abstract: Wnt signaling regulates self-renewal and fate commitment of stem and progenitor cells in development and homeostasis. Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) is a co-receptor for Wnt signaling that marks highly proliferative ... ...

    Abstract Wnt signaling regulates self-renewal and fate commitment of stem and progenitor cells in development and homeostasis. Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) is a co-receptor for Wnt signaling that marks highly proliferative stem and progenitor cells in many epithelial tissue types. Wnt signaling instructs neural developmental and homeostatic processes; however, Lgr5 expression in the developing and adult brain has not been characterized. Here we report that Lgr5 is expressed in the postnatal cerebellum during the maturation and synaptogenesis of cerebellar granule neurons (CGNs), processes controlled by Wnt signaling. Using a transgenic reporter mouse for in vivo Lgr5 expression analysis and lineage tracing, we reveal that Lgr5 specifically identified CGNs and was restricted temporally to the CGN maturation phase within the internal granule layer, but absent in the adult brain. Cells marked by Lgr5 were lineage restricted, post-mitotic and long-lived. The ligand for Lgr5, R-spondin, was secreted in a paracrine fashion that evolved during the maturation of CGNs, which coincided with the Lgr5 expression pattern. Our findings provide potential new insight into the critical regulation of Wnt signaling in the developing cerebellum and support a novel role for Lgr5 in the regulation of post-mitotic cells.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Super-enhancer hijacking drives ectopic expression of hedgehog pathway ligands in meningiomas

    Mark W. Youngblood / Zeynep Erson-Omay / Chang Li / Hinda Najem / Süleyman Coșkun / Evgeniya Tyrtova / Julio D. Montejo / Danielle F. Miyagishima / Tanyeri Barak / Sayoko Nishimura / Akdes Serin Harmancı / Victoria E. Clark / Daniel Duran / Anita Huttner / Timuçin Avşar / Yasar Bayri / Johannes Schramm / Julien Boetto / Matthieu Peyre /
    Maximilien Riche / Roland Goldbrunner / Nduka Amankulor / Angeliki Louvi / Kaya Bilgüvar / M. Necmettin Pamir / Koray Özduman / Türker Kilic / James R. Knight / Matthias Simon / Craig Horbinski / Michel Kalamarides / Marco Timmer / Amy B. Heimberger / Ketu Mishra-Gorur / Jennifer Moliterno / Katsuhito Yasuno / Murat Günel

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 16

    Abstract: Abstract Hedgehog signaling mediates embryologic development of the central nervous system and other tissues and is frequently hijacked by neoplasia to facilitate uncontrolled cellular proliferation. Meningiomas, the most common primary brain tumor, ... ...

    Abstract Abstract Hedgehog signaling mediates embryologic development of the central nervous system and other tissues and is frequently hijacked by neoplasia to facilitate uncontrolled cellular proliferation. Meningiomas, the most common primary brain tumor, exhibit Hedgehog signaling activation in 6.5% of cases, triggered by recurrent mutations in pathway mediators such as SMO. In this study, we find 35.6% of meningiomas that lack previously known drivers acquired various types of somatic structural variations affecting chromosomes 2q35 and 7q36.3. These cases exhibit ectopic expression of Hedgehog ligands, IHH and SHH, respectively, resulting in Hedgehog signaling activation. Recurrent tandem duplications involving IHH permit de novo chromatin interactions between super-enhancers within DIRC3 and a locus containing IHH. Our work expands the landscape of meningioma molecular drivers and demonstrates enhancer hijacking of Hedgehog ligands as a route to activate this pathway in neoplasia.
    Keywords Science ; Q
    Subject code 570
    Language English
    Publishing date 2023-10-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Combined PDGFR and HDAC Inhibition Overcomes PTEN Disruption in Chordoma.

    Dae-Hee Lee / Ying Zhang / Amin B Kassam / Myung-Jin Park / Paul Gardner / Daniel Prevedello / Stephanie Henry / Craig Horbinski / Jan H Beumer / Hussein Tawbi / Brian J Williams / Mark E Shaffrey / Merrill J Egorin / Roger Abounader / Deric M Park

    PLoS ONE, Vol 10, Iss 8, p e

    2015  Volume 0134426

    Abstract: The majority of chordomas show activation of the platelet-derived growth factor receptor (PDGFR). Based on in vitro intertumoral variation in response to recombinant PDGF protein and PDGFR inhibition, and variable tumor response to imatinib, we ... ...

    Abstract The majority of chordomas show activation of the platelet-derived growth factor receptor (PDGFR). Based on in vitro intertumoral variation in response to recombinant PDGF protein and PDGFR inhibition, and variable tumor response to imatinib, we hypothesized that chordomas resistant to PDGFR inhibition may possess downstream activation of the pathway.Molecular profiling was performed on 23 consecutive chordoma primary tissue specimens. Primary cultures established from 20 of the 23 specimens, and chordoma cell lines, UCH-1 and UCH-2, were used for in vitro experiments.Loss of heterozygosity (LOH) at the phosphatase and tensin homolog (PTEN) locus was observed in 6 specimens (26%). PTEN disruption statistically correlated with increased Ki-67 proliferation index, an established marker of poor outcome for chordoma. Compared to wild type, PTEN deficient chordomas displayed increased proliferative rate, and responded less favorably to PDGFR inhibition. PTEN gene restoration abrogated this growth advantage. Chordomas are characterized by intratumoral hypoxia and local invasion, and histone deacetylase (HDAC) inhibitors are capable of attenuating both hypoxic signaling and cell migration. The combination of PDGFR and HDAC inhibition effectively disrupted growth and invasion of PTEN deficient chordoma cells.Loss of heterozygosity of the PTEN gene seen in a subset of chordomas is associated with aggressive in vitro behavior and strongly correlates with increased Ki-67 proliferative index. Combined inhibition of PDGFR and HDAC attenuates proliferation and invasion in chordoma cells deficient for PTEN.
    Keywords Medicine ; R ; Science ; Q
    Subject code 572
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Cancer-Associated IDH1 Promotes Growth and Resistance to Targeted Therapies in the Absence of Mutation

    Andrea E. Calvert / Alexandra Chalastanis / Yongfei Wu / Lisa A. Hurley / Fotini M. Kouri / Yingtao Bi / Maureen Kachman / Jasmine L. May / Elizabeth Bartom / Youjia Hua / Rama K. Mishra / Gary E. Schiltz / Oleksii Dubrovskyi / Andrew P. Mazar / Marcus E. Peter / Hongwu Zheng / C. David James / Charles F. Burant / Navdeep S. Chandel /
    Ramana V. Davuluri / Craig Horbinski / Alexander H. Stegh

    Cell Reports, Vol 19, Iss 9, Pp 1858-

    2017  Volume 1873

    Abstract: Oncogenic mutations in two isocitrate dehydrogenase (IDH)-encoding genes (IDH1 and IDH2) have been identified in acute myelogenous leukemia, low-grade glioma, and secondary glioblastoma (GBM). Our in silico and wet-bench analyses indicate that non- ... ...

    Abstract Oncogenic mutations in two isocitrate dehydrogenase (IDH)-encoding genes (IDH1 and IDH2) have been identified in acute myelogenous leukemia, low-grade glioma, and secondary glioblastoma (GBM). Our in silico and wet-bench analyses indicate that non-mutated IDH1 mRNA and protein are commonly overexpressed in primary GBMs. We show that genetic and pharmacologic inactivation of IDH1 decreases GBM cell growth, promotes a more differentiated tumor cell state, increases apoptosis in response to targeted therapies, and prolongs the survival of animal subjects bearing patient-derived xenografts (PDXs). On a molecular level, diminished IDH1 activity results in reduced α-ketoglutarate (αKG) and NADPH production, paralleled by deficient carbon flux from glucose or acetate into lipids, exhaustion of reduced glutathione, increased levels of reactive oxygen species (ROS), and enhanced histone methylation and differentiation marker expression. These findings suggest that IDH1 upregulation represents a common metabolic adaptation by GBMs to support macromolecular synthesis, aggressive growth, and therapy resistance.
    Keywords wild-type IDH1 ; GBM ; metabolism ; differentiation ; NADPH ; lipids ; reactive oxygen species (ROS) ; EGFR ; targeted therapy ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2017-05-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: External validation and recalibration of an incidental meningioma prognostic model – IMPACT

    Julie Woodfield / Boris Krischek / Giles Critchley / Damian Holliman / Angelos Kolias / Thomas Santarius / Ola Rominiyi / Michael McDermott / Michael D Jenkinson / Jörg-Christian Tonn / Mohsen Javadpour / Andrea Saladino / Tiit Illimar Mathiesen / Rory Piper / Michael Vogelbaum / Chaya Brodie / Sara Venturini / Daniel M Fountain / Roland Goldbrunner /
    Elliot Tilling / Felix Sahm / Priscilla Brastianos / Rory J Piper / Antonio Santoro / Sylvia Kurz / Pierfrancesco Lapolla / Andrea Mingoli / Jennifer Brown / Debraj Mukherjee / Simon Walling / Andrew Morokoff / Patrick Wen / Ghazaleh Tabatabai / Jill Barnholtz-Sloan / Ryan K Mathew / Alexander Smedley / Helen Shih / William Taylor / Minh Nguyen / Bryony Ford / Samantha J Mills / Tamara Ali / Ruwanthi Kolamunnage-Dona / Josephine Jung / Muhammed Elhadi / Erminia Albanese / Aswin Chari / David Rowland / Melissa Gough / Michael Cearns / Simon Lammy / Yasir Chowdhury / Christian Mawrin / Mahmoud Saleh / Jens Schittenhelm / Farshad Nassiri / Raymond Huang / Pietro Familiari / Manfred Westphal / Warren Selman / Daniel Brown / Nathan McSorley / Oliver Hanemann / Richard Pullicino / Francesco Gaillard / Mirjam Renovanz / Chris Barrett / Christine Jungk / Aaron Cohen-Gadol / Javier Martín-Alonso / Gelareh Zadeh / Hytham Hamid / Abdurrahman I Islim / Christopher P Millward / Shaveta Mehta / Usama Ali / Shelli Diane Koszdin / Theo Georgious / Andrew R Brodbelt / Mohamed Abdelsadg / Suhaib Abualsaud / Amro Abuleil / Kevin Agyemang / Hanan Akbari / Likhith Alakandy / Clarissa Alfonso / Arousa Ali / Michael Amoo / Mohamed A. R. Arbab / Mutiu Asha / Kareem Austin / Khaled Badran / Jarnail Bal / Parameswaran Bhattathiri / Paul M. Brennan / Andrew R. Brodbelt / Ferran Brugada-Bellsolà / Placido Bruzzaniti / Annabel Butcher / Rory S. Cairns / Michael Canty / Sachiv Chakravarti / Rebecca Chave-Cox / Anna Craig-McQuade / Peter Crossley / Elizabeth Culpin / Alessia D'Amico / Bassam Dabbous / Pedro David Delgado-López / Mohamed Draz / Katharine J. Drummond / Rusiru T. Ekanayaka / Ibrahim Elmaadawi / Omar Elmandouh / Mazin Elsharif / Daisy Evans / Andreas Fahlström / Fleur L. Fisher / Daniel M. Fountain / Keiko Fox / Chloé Gelder / Shamayitri Ghosh / Aimee Goel / Athanasios Grivas / Andrew Gvozdanovic / Allan Hall / Liv Hartrick / Samih Hassan / Jack Henry / Abdurrahman I. Islim / Asgeir S. Jakola / Michael D. Jenkinson / Sanjeeva Jeyaretna / Adrian Jimenez / Andranik Kahramanian / Neeraj Kalra / David O. Kamson / Oliver Kennion / Adham M. Khalafallah / Sarah Kingdon / Howra Ktayen / Aditaya Kumar / Jun Yi Lau / Jing Xian Lee / Ryan Leyden / Patricia Littlechild / Sophie Liu / Darmanin Lora-Kay / Vivia Lung / Stephen T. Magill / Hani J. Marcus / Fawaz E. Marhoom / Ryan K. Mathew / Calan Mathieson / Tobias Mederer / Torstien R. Meling / Samantha J. Mills / Christopher P. Millward / Mujtaba Mohammad / Amir H. Zamanipoor Najafabadi / Olivia Näslund / Imran Noorani / Gildas Patet / Omar N. Pathmanaban / Andrea Perera / Amit Persad / See Yung Phang / Rory J. Piper / Jonathan Pollock / Benjamin Price / Martin Proescholdt / James Robins / Bobby Sachdev / Fozia Saeed / Ieva Sataite / Antony Kevin Scafa / Verena Schadewaldt / Syed Wajahat Shah / Mustafa El Sheikh / Zenab Sher / Bente Sandvei Skeie / Agbolahan Sofela / Jerome St George / Torbjørn Strømsnes / Nigel Suttner / Philip Theodosopoulos / Manjul Tripathi / Ismail Ughratdar / James Ulrich / Adithya Varma / Anil Varma / Maria Velicu / Esther Wu / Jacob Young / Giuseppa Zancana / Catherine Zhang / Karolyn Au / Felix Behling / Linda Bi / Nicholas Butowski / Ana Castro / Marta Couce / Francesco Dimeco / Katherine J. Drummond / Ian Dunn / Craig Erker / Michelle Felicella / Eva Galanis / Norbert Galldiks / Caterina Giannini / Christel Herold-Mende / Luke Hnenny / Craig Horbinski / Gerhard Jungwirth / Timothy Kaufmann / Daniel Lachance / Christian Lafougere / Katrin Lamszus / Serge Makarenko / Tathiana Malta / Jennifer Moliterno-Gunel / HK Ng / Houtan Noushmehr / Arie Perry / Laila Poisson / Bianco Pollo / Aditya Ragunathan / David Raleigh / Franz Ricklefs / Antonio Santacroce / Christian Schichor / Nils Schimdt / Andrew Sloan / Matija Snuderl / Jim Snyder / Erik Sulman / Suganth Suppiah / Marcos Tatagiba / Marco Timmer / Andreas Von Deimling / Tobias Walbert / Justin Z. Wang / Stephen Yip / Gabriel Zada / Viktor Zherebitskiy / Michael T.C. Poon

    BMJ Open, Vol 12, Iss

    protocol for an international multicentre retrospective cohort study

    2022  Volume 1

    Keywords Medicine ; R
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher BMJ Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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