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Sam W. Lee

Researcher at Harvard University

Publications -  148
Citations -  22846

Sam W. Lee is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & DNA damage. The author has an hindex of 65, co-authored 148 publications receiving 19066 citations. Previous affiliations of Sam W. Lee include University of Michigan & Broad Institute.

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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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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Journal Article

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, +168 more
- 01 Jan 2018 - 
TL;DR: An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
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Selective killing of cancer cells by a small molecule targeting the stress response to ROS

TL;DR: The ability of a small molecule to induce apoptosis selectively in cells that have a cancer genotypes is demonstrated, by targeting a non-oncogene co-dependency acquired through the expression of the cancer genotype in response to transformation-induced oxidative stress.
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Pin1 is overexpressed in breast cancer and cooperates with Ras signaling in increasing the transcriptional activity of c-Jun towards cyclin D1

TL;DR: It is reported that Pin1 is strikingly overexpressed in human breast cancers, and that its levels correlate with cyclin D1 levels in tumors, and the results suggest that overexpression of Pin1 may promote tumor growth.