M
Mariateresa Fulciniti
Researcher at Harvard University
Publications - 171
Citations - 8519
Mariateresa Fulciniti is an academic researcher from Harvard University. The author has contributed to research in topics: Multiple myeloma & Stromal cell. The author has an hindex of 43, co-authored 146 publications receiving 6966 citations. Previous affiliations of Mariateresa Fulciniti include United States Department of Veterans Affairs & Veterans Health Administration.
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Journal ArticleDOI
Heterogeneity of genomic evolution and mutational profiles in multiple myeloma
Niccolo Bolli,Hervé Avet-Loiseau,David C. Wedge,Peter Van Loo,Ludmil B. Alexandrov,Inigo Martincorena,Kevin J. Dawson,Francesco Iorio,Serena Nik-Zainal,Graham R. Bignell,Jonathan Hinton,Yang Li,Jose M. C. Tubio,Stuart McLaren,Sarah O' Meara,Adam Butler,Jon W. Teague,Laura Mudie,Elizabeth Anderson,Naim U. Rashid,Yu-Tzu Tai,Masood A. Shammas,Adam S. Sperling,Mariateresa Fulciniti,Paul G. Richardson,Giovanni Parmigiani,Florence Magrangeas,Stephane Minvielle,Philippe Moreau,Michel Attal,Thierry Facon,P. Andrew Futreal,Kenneth C. Anderson,Peter J. Campbell,Nikhil C. Munshi +34 more
TL;DR: The myeloma genome is heterogeneous across the cohort, and exhibits diversity in clonal admixture and in dynamics of evolution, which may impact prognostic stratification, therapeutic approaches and assessment of disease response to treatment.
Journal ArticleDOI
Anti-DKK1 mAb (BHQ880) as a potential therapeutic agent for multiple myeloma
Mariateresa Fulciniti,Pierfrancesco Tassone,Teru Hideshima,Sonia Vallet,Puru Nanjappa,Seth Ettenberg,Zhenxin Shen,Nipun Patel,Yu-Tzu Tai,Dharminder Chauhan,Constantine S. Mitsiades,Rao Prabhala,Noopur Raje,Kenneth C. Anderson,David R. Stover,Nikhil C. Munshi,Nikhil C. Munshi +16 more
TL;DR: DKK1 is confirmed as an important therapeutic target in myeloma and the rationale for clinical evaluation of BHQ880 to improve bone disease and to inhibit MM growth is provided.
Journal ArticleDOI
Blockade of XBP1 splicing by inhibition of IRE1α is a promising therapeutic option in multiple myeloma
Naoya Mimura,Mariateresa Fulciniti,Gullu Gorgun,Yu-Tzu Tai,Diana Cirstea,Loredana Santo,Yiguo Hu,Claire Fabre,Jiro Minami,Hiroto Ohguchi,Tanyel Kiziltepe,Hiroshi Ikeda,Yutaka Kawano,Maureen French,Martina Blumenthal,Victor Tam,Nathalie L. Kertesz,Uriel M. Malyankar,Mark Hokenson,Tuan Pham,Qingping Zeng,John B. Patterson,Paul G. Richardson,Nikhil C. Munshi,Nikhil C. Munshi,Kenneth C. Anderson +25 more
TL;DR: Results demonstrate that blockade of XBP1 splicing by inhibition of IRE1α endoribonuclease domain is a potential therapeutic option in MM.
Journal ArticleDOI
Identification of novel mutational drivers reveals oncogene dependencies in multiple myeloma.
Brian A Walker,Konstantinos Mavrommatis,Christopher P. Wardell,T. Cody Ashby,Michael A Bauer,Faith E. Davies,Adam Rosenthal,Hongwei Wang,Pingping Qu,Antje Hoering,Mehmet Kemal Samur,Fadi Towfic,Maria Ortiz,Erin Flynt,Zhinuan Yu,Zhihong Yang,Dan Rozelle,John C. Obenauer,Matthew Trotter,Daniel Auclair,Jonathan J Keats,Niccolo Bolli,Mariateresa Fulciniti,Raphael Szalat,Philippe Moreau,Brian G.M. Durie,A. Keith Stewart,Hartmut Goldschmidt,Marc-Steffen Raab,Hermann Einsele,Pieter Sonneveld,Jesús F. San Miguel,Sagar Lonial,Graham Jackson,Kenneth C. Anderson,Hervé Avet-Loiseau,Nikhil C. Munshi,Anjan Thakurta,Gareth J. Morgan +38 more
TL;DR: Using integrated genomics of 1273 newly diagnosed patients with MM, associations indicate that the genomic landscape of myeloma is predetermined by the primary events upon which further dependencies are built, giving rise to a nonrandom accumulation of genetic hits.
Journal ArticleDOI
HLA class I, NKG2D, and natural cytotoxicity receptors regulate multiple myeloma cell recognition by natural killer cells.
Ennio Carbone,Paola Neri,Maria Mesuraca,Mariateresa Fulciniti,Takemi Otsuki,Daniela Pende,Veronika Groh,Thomas A. Spies,Giuditta Pollio,David Cosman,Lucio Catalano,Pierfrancesco Tassone,Bruno Rotoli,Salvatore Venuta +13 more
TL;DR: The hypothesis that NK cell cytotoxicity could sculpture myeloma and represents an important immune effector mechanism in controlling its intramedullary stages is supported.