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Bartlomiej P Przychodzen
Researcher at Cleveland Clinic
Publications - 164
Citations - 5061
Bartlomiej P Przychodzen is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Myeloid & Myeloid leukemia. The author has an hindex of 29, co-authored 160 publications receiving 3964 citations. Previous affiliations of Bartlomiej P Przychodzen include Cleveland Clinic Lerner Research Institute.
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Journal ArticleDOI
Mutations in the spliceosome machinery, a novel and ubiquitous pathway in leukemogenesis.
Hideki Makishima,Valeria Visconte,Hirotoshi Sakaguchi,Anna M. Jankowska,Sarah Abu Kar,Andres Jerez,Bartlomiej P Przychodzen,Manoj Bupathi,Kathryn M Guinta,Manuel G. Afable,Mikkael A. Sekeres,Richard A. Padgett,Ramon V. Tiu,Jaroslaw P. Maciejewski +13 more
TL;DR: Mutations affecting spliceosomal genes that result in defective splicing are a new leukemogenic pathway and may constitute diagnostic biomarkers that could potentially serve as therapeutic targets in myelodysplastic syndromes.
Journal ArticleDOI
STAT3 mutations unify the pathogenesis of chronic lymphoproliferative disorders of NK cells and T-cell large granular lymphocyte leukemia
Andres Jerez,Michael J. Clemente,Hideki Makishima,Hanna Koskela,Francis R LeBlanc,Kwok Peng Ng,Thomas L. Olson,Bartlomiej P Przychodzen,Manuel G. Afable,Inés Gómez-Seguí,Kathryn M Guinta,Lisa Durkin,Eric D. Hsi,Kathy L. McGraw,Dan Zhang,Marcin W. Wlodarski,Kimmo Porkka,Mikkael A. Sekeres,Alan F. List,Satu Mustjoki,Thomas P. Loughran,Jaroslaw P. Maciejewski +21 more
TL;DR: STAT3 mutations are frequent in large granular lymphocytes suggesting a similar molecular dysregulation in malignant chronic expansions of NK and CTL origin, and may distinguish truly malignant lymphoproliferations involving T and NK cells from reactive expansions.
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Inherited and Somatic Defects in DDX41 in Myeloid Neoplasms.
Chantana Polprasert,Isabell Schulze,Mikkael A. Sekeres,Hideki Makishima,Bartlomiej P Przychodzen,Naoko Hosono,Jarnail Singh,Richard A. Padgett,Xiaorong Gu,James G. Phillips,Michael J. Clemente,Yvonne Parker,Daniel J. Lindner,Brittney Dienes,Eckhard Jankowsky,Yogen Saunthararajah,Yang Du,Kevin Oakley,Nhu Nguyen,Sudipto Mukherjee,Caroline Pabst,Lucy A. Godley,Jane E. Churpek,Daniel A. Pollyea,Utz Krug,Wolfgang E. Berdel,Hans-Ulrich Klein,Martin Dugas,Yuichi Shiraishi,Kenichi Chiba,Hiroko Tanaka,Satoru Miyano,Kenichi Yoshida,Seishi Ogawa,Carsten Müller-Tidow,Carsten Müller-Tidow,Jaroslaw P. Maciejewski +36 more
TL;DR: An adult familial acute myeloid leukemia (AML) syndrome caused by germline mutations in the DEAD/H-box helicase gene DDX41 is described, suggesting that they constitute a family of tumor suppressor genes.
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Genetic abnormalities in myelodysplasia and secondary acute myeloid leukemia: impact on outcome of stem cell transplantation.
Tetsuichi Yoshizato,Yasuhito Nannya,Yoshiko Atsuta,Yusuke Shiozawa,Yusuke Shiozawa,Yuka Iijima-Yamashita,Kenichi Yoshida,Yuichi Shiraishi,Hiromichi Suzuki,Yasunobu Nagata,Yusuke Sato,Nobuyuki Kakiuchi,Keitaro Matsuo,Makoto Onizuka,Keisuke Kataoka,Kenichi Chiba,Hiroko Tanaka,Hiroo Ueno,Masahiro Nakagawa,Bartlomiej P Przychodzen,Claudia Haferlach,Wolfgang Kern,Kosuke Aoki,Hidehiro Itonaga,Yoshinobu Kanda,Mikkael A. Sekeres,Jaroslaw P. Maciejewski,Torsten Haferlach,Yasushi Miyazaki,Keizo Horibe,Masashi Sanada,Satoru Miyano,Hideki Makishima,Seishi Ogawa +33 more
TL;DR: The results suggest that TP53 and RAS-pathway mutations predicted a dismal prognosis, when associated with CK and MDS/MPNs, respectively, however, for patients with mutated TP53 or CK alone, long-term survival could be obtained with transplantation.
Journal ArticleDOI
Somatic SETBP1 mutations in myeloid malignancies
Hideki Makishima,Kenichi Yoshida,Nhu Nguyen,Bartlomiej P Przychodzen,Masashi Sanada,Masashi Sanada,Yusuke Okuno,Yusuke Okuno,Kwok Peng Ng,Kristbjorn O. Gudmundsson,Bandana A. Vishwakarma,Andres Jerez,Inés Gómez-Seguí,Mariko Takahashi,Yuichi Shiraishi,Yasunobu Nagata,Kathryn M Guinta,Hiraku Mori,Mikkael A. Sekeres,Kenichi Chiba,Hiroko Tanaka,Hideki Muramatsu,Hirotoshi Sakaguchi,Ronald Paquette,Michael A. McDevitt,Seiji Kojima,Yogen Saunthararajah,Satoru Miyano,Lee-Yung Shih,Yang Du,Seishi Ogawa,Seishi Ogawa,Jaroslaw P. Maciejewski +32 more
TL;DR: Somatic mutations of SETBP1 seem to cause gain of function, are associated with myeloid leukemic transformation and convey poor prognosis in myelodysplastic syndromes (MDS) and CMML.