T
Thomas Enzler
Researcher at Columbia University Medical Center
Publications - 34
Citations - 1752
Thomas Enzler is an academic researcher from Columbia University Medical Center. The author has contributed to research in topics: Cancer & B-cell activating factor. The author has an hindex of 14, co-authored 27 publications receiving 1290 citations. Previous affiliations of Thomas Enzler include University of Arizona & Columbia University.
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Journal ArticleDOI
Gastric Cancer, Version 2.2022, NCCN Clinical Practice Guidelines in Oncology.
Jaffer A. Ajani,Thomas A. D'Amico,David J. Bentrem,Joseph Chao,David Cooke,Carlos U. Corvera,Prajnan Das,Peter C. Enzinger,Thomas Enzler,Paul T. Fanta,Farhood Farjah,Hans Gerdes,C. Michael Gibson,Steven N. Hochwald,Wayne L. Hofstetter,David H. Ilson,Rajesh N. Keswani,Sunnie Kim,Lawrence Kleinberg,Samuel J. Klempner,Jill Lacy,Quan P. Ly,Kristina A. Matkowskyj,Michael McNamara,Mary F. Mulcahy,Darryl Alan Outlaw,Haeseong Park,Kyle A. Perry,Jose M. Pimiento,George A. Poultsides,Scott I. Reznik,Robert Ross,Vivian E. Strong,Stacey Su,Hanlin L. Wang,Georgia L. Wiesner,Christopher G. Willett,Danny Yakoub,Harry H. Yoon,Nicole R. McMillian,Lenora A. Pluchino +40 more
TL;DR: Palliative management, which may include systemic therapy, chemoradiation, and/or best supportive care, is recommended for all patients with unresectable or metastatic cancer.
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Complete primary structure of human and rabbit lactase-phlorizin hydrolase: implications for biosynthesis, membrane anchoring and evolution of the enzyme.
Ned Mantei,M Villa,Thomas Enzler,H Wacker,Werner Boll,P James,Walter Hunziker,Giorgio Semenza +7 more
TL;DR: The primary structures of human and rabbit brush border membrane beta‐glycosidase complexes (pre‐pro‐lactase‐phlorizin hydrolase, or pre‐ pro‐LPH, EC 3.2.1.23‐62) are reported, suggesting that they evolved by two cycles of partial gene duplication and have implications for the decline of LPH after weaning and for human adult‐type alactasia, and for the evolutionary history of L PH.
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BAFF and APRIL support chronic lymphocytic leukemia B-cell survival through activation of the canonical NF-κB pathway
Tomoyuki Endo,Mitsufumi Nishio,Thomas Enzler,Howard B. Cottam,Tetsuya Fukuda,Danelle F. James,Michael Karin,Thomas J. Kipps +7 more
TL;DR: It is found that signaling through BR3, but not BCMA or TACI, activated the alternative nuclear factor of kappa B (NF-kappaB) pathway in CLL cells, whereas signaling through BCMA/TACI induced activation of the canonical NF- kappaB pathway.
Journal ArticleDOI
Deficiencies of GM-CSF and Interferon γ Link Inflammation and Cancer
Thomas Enzler,Silke Gillessen,John P. Manis,David O. Ferguson,James Fleming,Frederick W. Alt,Martin C. Mihm,Glenn Dranoff +7 more
TL;DR: It is reported that aged granulocyte-macrophage colony stimulating factor-deficient mice develop a systemic lupus erythematosis (SLE)-like disorder associated with the impaired phagocytosis of apoptotic cells, demonstrating that the interplay of infectious agents with cytokine-mediated regulation of immune homeostasis is a critical determinant of cancer susceptibility.
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Alternative and Classical NF-κB Signaling Retain Autoreactive B Cells in the Splenic Marginal Zone and Result in Lupus-like Disease
Thomas Enzler,Giuseppina Bonizzi,Gregg J. Silverman,Dennis C. Otero,George F. Widhopf,Amy Anzelon-Mills,Robert C. Rickert,Michael Karin +7 more
TL;DR: Both classical and alternative NF-kappaB signaling are important for development of lupus-like disease associated with BAFF overproduction, and the same mechanisms may be involved in the pathogenesis of human SLE.