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Terry H. Landowski

Researcher at University of Arizona

Publications -  53
Citations -  9638

Terry H. Landowski is an academic researcher from University of Arizona. The author has contributed to research in topics: Apoptosis & Imexon. The author has an hindex of 25, co-authored 50 publications receiving 9057 citations. Previous affiliations of Terry H. Landowski include VCU Medical Center & University of South Florida.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Bone marrow stromal-derived soluble factors and direct cell contact contribute to de novo drug resistance of myeloma cells by distinct mechanisms.

TL;DR: Data show that both cell–cell adhesion of BMSCs with myeloma cells and soluble factors induced by this cell– cell interaction are involved in the protection of myelomas cells from mitoxantrone-induced apoptosis; however, the mechanisms contributing to the drug resistance are different.
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Mutations in the Fas antigen in patients with multiple myeloma

TL;DR: It is proposed that Fas antigen mutations may contribute to the pathogenesis and progression of the neoplastic disease, multiple myeloma in some patients.
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Mitochondrial-Mediated Disregulation of Ca2+ Is a Critical Determinant of Velcade (PS-341/Bortezomib) Cytotoxicity in Myeloma Cell Lines

TL;DR: Analysis of oligonucleotide microarray analysis of the 8226 multiple myeloma cell line showed a predominant induction of gene products associated with the endoplasmic reticulum secretory pathway following short-term, high-dose exposure to bortezomib, supporting the hypothesis that intracellular Ca2+ disregulation is a critical determinant of bortzomib cytotoxicity.