Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib

10.1371/journal.pone.0195956

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Main Authors:	Ladds M.J.G.W., Pastor-Fernández A., Popova G., van Leeuwen I.M.M., Eng K.E., Drummond C.J., Johansson L., Svensson R., Westwood N.J., McCarthy A.R., Tholander F., Popa M., Lane D.P., McCormack E., McInerney G.M., Bhatia R., Laín S.
Other Authors:	MEDICINE
Format:	Article
Published:	2019
Subjects:	antineoplastic agent B Raf kinase chloroquine protein p53 sirtuin 1 tenovin tenovin 1 tenovin 33 tenovin 39 tenovin 39 oh tenovin 50 tenovin 50 oh tenovin 6 tenovin D1 tenovin D3 tertiary amine unclassified drug vemurafenib benzamide derivative BRAF protein, human indole derivative sirtuin sulfonamide tenovin-6 TP53 protein, human Article autophagy cell death cell survival drug mechanism G1 phase cell cycle checkpoint human human cell melanoma cell cell proliferation chemical structure chemistry drug effect drug potentiation drug resistance gene expression regulation genetics melanoma mutation tumor cell line Antineoplastic Agents Autophagy Benzamides Cell Line, Tumor Cell Proliferation Cell Survival Drug Resistance, Neoplasm Drug Synergism Gene Expression Regulation, Neoplastic Humans Indoles Melanoma Molecular Structure Mutation Proto-Oncogene Proteins B-raf Sirtuins Sulfonamides Tumor Suppressor Protein p53
Online Access:	https://scholarbank.nus.edu.sg/handle/10635/161233
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Institution:	National University of Singapore

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spelling	sg-nus-scholar.10635-1612332024-04-24T05:53:59Z Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib Ladds M.J.G.W. Pastor-Fernández A. Popova G. van Leeuwen I.M.M. Eng K.E. Drummond C.J. Johansson L. Svensson R. Westwood N.J. McCarthy A.R. Tholander F. Popa M. Lane D.P. McCormack E. McInerney G.M. Bhatia R. Laín S. MEDICINE antineoplastic agent B Raf kinase chloroquine protein p53 sirtuin 1 tenovin tenovin 1 tenovin 33 tenovin 39 tenovin 39 oh tenovin 50 tenovin 50 oh tenovin 6 tenovin D1 tenovin D3 tertiary amine unclassified drug vemurafenib antineoplastic agent B Raf kinase benzamide derivative BRAF protein, human indole derivative protein p53 sirtuin sulfonamide tenovin-6 TP53 protein, human vemurafenib Article autophagy cell death cell survival drug mechanism G1 phase cell cycle checkpoint human human cell melanoma cell autophagy cell proliferation chemical structure chemistry drug effect drug potentiation drug resistance gene expression regulation genetics melanoma mutation tumor cell line Antineoplastic Agents Autophagy Benzamides Cell Line, Tumor Cell Proliferation Cell Survival Drug Resistance, Neoplasm Drug Synergism Gene Expression Regulation, Neoplastic Humans Indoles Melanoma Molecular Structure Mutation Proto-Oncogene Proteins B-raf Sirtuins Sulfonamides Tumor Suppressor Protein p53 10.1371/journal.pone.0195956 PLoS ONE 13 4 e0195956 2019-11-01T08:16:15Z 2019-11-01T08:16:15Z 2018 Article Ladds M.J.G.W., Pastor-Fernández A., Popova G., van Leeuwen I.M.M., Eng K.E., Drummond C.J., Johansson L., Svensson R., Westwood N.J., McCarthy A.R., Tholander F., Popa M., Lane D.P., McCormack E., McInerney G.M., Bhatia R., Laín S. (2018). Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib. PLoS ONE 13 (4) : e0195956. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0195956 19326203 https://scholarbank.nus.edu.sg/handle/10635/161233 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Unpaywall 20191101
institution	National University of Singapore
building	NUS Library
continent	Asia
country	Singapore Singapore
content_provider	NUS Library
collection	ScholarBank@NUS
topic	antineoplastic agent B Raf kinase chloroquine protein p53 sirtuin 1 tenovin tenovin 1 tenovin 33 tenovin 39 tenovin 39 oh tenovin 50 tenovin 50 oh tenovin 6 tenovin D1 tenovin D3 tertiary amine unclassified drug vemurafenib antineoplastic agent B Raf kinase benzamide derivative BRAF protein, human indole derivative protein p53 sirtuin sulfonamide tenovin-6 TP53 protein, human vemurafenib Article autophagy cell death cell survival drug mechanism G1 phase cell cycle checkpoint human human cell melanoma cell autophagy cell proliferation chemical structure chemistry drug effect drug potentiation drug resistance gene expression regulation genetics melanoma mutation tumor cell line Antineoplastic Agents Autophagy Benzamides Cell Line, Tumor Cell Proliferation Cell Survival Drug Resistance, Neoplasm Drug Synergism Gene Expression Regulation, Neoplastic Humans Indoles Melanoma Molecular Structure Mutation Proto-Oncogene Proteins B-raf Sirtuins Sulfonamides Tumor Suppressor Protein p53
spellingShingle	antineoplastic agent B Raf kinase chloroquine protein p53 sirtuin 1 tenovin tenovin 1 tenovin 33 tenovin 39 tenovin 39 oh tenovin 50 tenovin 50 oh tenovin 6 tenovin D1 tenovin D3 tertiary amine unclassified drug vemurafenib antineoplastic agent B Raf kinase benzamide derivative BRAF protein, human indole derivative protein p53 sirtuin sulfonamide tenovin-6 TP53 protein, human vemurafenib Article autophagy cell death cell survival drug mechanism G1 phase cell cycle checkpoint human human cell melanoma cell autophagy cell proliferation chemical structure chemistry drug effect drug potentiation drug resistance gene expression regulation genetics melanoma mutation tumor cell line Antineoplastic Agents Autophagy Benzamides Cell Line, Tumor Cell Proliferation Cell Survival Drug Resistance, Neoplasm Drug Synergism Gene Expression Regulation, Neoplastic Humans Indoles Melanoma Molecular Structure Mutation Proto-Oncogene Proteins B-raf Sirtuins Sulfonamides Tumor Suppressor Protein p53 Ladds M.J.G.W. Pastor-Fernández A. Popova G. van Leeuwen I.M.M. Eng K.E. Drummond C.J. Johansson L. Svensson R. Westwood N.J. McCarthy A.R. Tholander F. Popa M. Lane D.P. McCormack E. McInerney G.M. Bhatia R. Laín S. Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib
description	10.1371/journal.pone.0195956
author2	MEDICINE
author_facet	MEDICINE Ladds M.J.G.W. Pastor-Fernández A. Popova G. van Leeuwen I.M.M. Eng K.E. Drummond C.J. Johansson L. Svensson R. Westwood N.J. McCarthy A.R. Tholander F. Popa M. Lane D.P. McCormack E. McInerney G.M. Bhatia R. Laín S.
format	Article
author	Ladds M.J.G.W. Pastor-Fernández A. Popova G. van Leeuwen I.M.M. Eng K.E. Drummond C.J. Johansson L. Svensson R. Westwood N.J. McCarthy A.R. Tholander F. Popa M. Lane D.P. McCormack E. McInerney G.M. Bhatia R. Laín S.
author_sort	Ladds M.J.G.W.
title	Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib
title_short	Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib
title_full	Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib
title_fullStr	Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib
title_full_unstemmed	Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib
title_sort	autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of b-raf mutant tumour cells that survive vemurafenib
publishDate	2019
url	https://scholarbank.nus.edu.sg/handle/10635/161233
_version_	1800913784570642432

Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib

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