M
Maria Calaminici
Researcher at Queen Mary University of London
Publications - 55
Citations - 2914
Maria Calaminici is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Diffuse large B-cell lymphoma & Lymphoma. The author has an hindex of 18, co-authored 45 publications receiving 2199 citations. Previous affiliations of Maria Calaminici include Barts Health NHS Trust.
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Journal ArticleDOI
Genetic and Functional Drivers of Diffuse Large B Cell Lymphoma.
Anupama Reddy,Jenny Zhang,Nicholas S. Davis,Andrea B. Moffitt,Cassandra Love,Alexander Waldrop,Sirpa Leppä,Annika Pasanen,Leo Meriranta,Marja-Liisa Karjalainen-Lindsberg,Peter Nørgaard,Mette Merete Pedersen,Anne O. Gang,Estrid Høgdall,Tayla Heavican,Waseem Gul Lone,Javeed Iqbal,Qiu Qin,Guojie Li,So Young Kim,Jane Healy,Kristy L. Richards,Yuri Fedoriw,Leon Bernal-Mizrachi,Jean L. Koff,Ashley D. Staton,Christopher R. Flowers,Ora Paltiel,Neta Goldschmidt,Maria Calaminici,Andrew Clear,John G. Gribben,Evelyn T. Nguyen,Magdalena Czader,Sarah L. Ondrejka,Angela M. B. Collie,Eric D. Hsi,Eric Tse,Rex Au-Yeung,Yok-Lam Kwong,Gopesh Srivastava,William W.L. Choi,Andrew M. Evens,Monika Pilichowska,Manju Sengar,Nishitha Reddy,Shaoying Li,Amy Chadburn,Leo I. Gordon,Elaine S. Jaffe,Shawn Levy,Rachel E. Rempel,Tiffany Tzeng,Lanie Happ,Tushar Dave,Deepthi Rajagopalan,Jyotishka Datta,David B. Dunson,Sandeep S. Dave +58 more
TL;DR: An integrative analysis of whole-exome sequencing and transcriptome sequencing in a cohort of DLBCL patients is performed to comprehensively define the landscape of 150 genetic drivers of the disease and their functional roles to identify new therapeutic opportunities in the disease.
Journal ArticleDOI
Integrated genomic analysis identifies recurrent mutations and evolution patterns driving the initiation and progression of follicular lymphoma
Jessica Okosun,Csaba Bödör,Jun Wang,Shamzah Araf,Cheng Yuan Yang,Chenyi Pan,Sören Boller,Davide Cittaro,Monika Bozek,Sameena Iqbal,Janet Matthews,David Wrench,Jacek Marzec,Kiran Tawana,Nikolay Popov,Ciaran O'Riain,Derville O’Shea,Emanuela Carlotti,Andrew Davies,Charles H. Lawrie,András Matolcsy,Maria Calaminici,Andrew Norton,Richard J. Byers,Charles A. Mein,Elia Stupka,T. Andrew Lister,Georg Lenz,Silvia Montoto,John G. Gribben,Yuhong Fan,Rudolf Grosschedl,Claude Chelala,Jude Fitzgibbon +33 more
TL;DR: This study provides new insights into the genetic basis of follicular lymphoma and the clonal dynamics of transformation and suggests that personalizing therapies to target key genetic alterations in the CPC represents an attractive therapeutic strategy.
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Follicular lymphoma cells induce T-cell immunologic synapse dysfunction that can be repaired with lenalidomide: implications for the tumor microenvironment and immunotherapy
Alan G. Ramsay,Andrew Clear,Gavin Kelly,Rewas Fatah,Janet Matthews,Finlay MacDougall,T. Andrew Lister,Abigail M. Lee,Maria Calaminici,John G. Gribben +9 more
TL;DR: In this article, the authors identify impaired T-cell immunologic synapse formation as an active immunosuppressive mechanism in follicular lymphoma (FL) and diffuse large B-cell lymphoma(DLBCL).
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Defining characteristics of classical Hodgkin lymphoma microenvironment T-helper cells
Paul Greaves,Andrew Clear,Andrew Owen,Sameena Iqbal,Abigail M. Lee,Janet Matthews,Andrew Wilson,Maria Calaminici,John G. Gribben +8 more
TL;DR: Molecular insights into the CHL-associated TH offer potential diagnostic, prognostic and pharmacologically modifiable therapeutic targets and do not support the established view of a TH2-enriched, senescent/exhausted, hypofunctional, hypoproliferative infiltrate.
Journal ArticleDOI
Recurrent mTORC1-activating RRAGC mutations in follicular lymphoma
Jessica Okosun,Rachel L. Wolfson,Jun Wang,Shamzah Araf,Lucy Wilkins,Brian M. Castellano,Leire Escudero-Ibarz,Ahad F. Al Seraihi,Julia Richter,Stephan H. Bernhart,Alejo Efeyan,Sameena Iqbal,Janet Matthews,Andrew Clear,José Afonso Guerra-Assunção,Csaba Bödör,Hilmar Quentmeier,Christopher Mansbridge,Peter Johnson,Andrew Davies,Jonathan C. Strefford,Graham Packham,Sharon Barrans,Andrew Jack,Ming-Qing Du,Maria Calaminici,T. Andrew Lister,Rebecca Auer,Silvia Montoto,John G. Gribben,Reiner Siebert,Claude Chelala,Roberto Zoncu,David M. Sabatini,Jude Fitzgibbon +34 more
TL;DR: The activating nature of the RRAGC mutations, their existence in the dominant clone and their stability during disease progression support their potential as an excellent candidate for therapeutic targeting.