LIVIVO - Search results -

Search results

Result 1 - 10 of total 23

Search options

Article ; Online: Targeting the lysosome in cancer.

Piao, Shengfu / Amaravadi, Ravi K

Annals of the New York Academy of Sciences

2015 Volume 1371, Issue 1, Page(s) 45–54

Abstract: Lysosomes are membrane-bound intracellular organelles that receive macromolecules delivered by endocytosis, phagocytosis, and autophagy for degradation and recycling. Over the last decade, advances in lysosome research have established a broad role for ... ...

Abstract	Lysosomes are membrane-bound intracellular organelles that receive macromolecules delivered by endocytosis, phagocytosis, and autophagy for degradation and recycling. Over the last decade, advances in lysosome research have established a broad role for the lysosome in the pathophysiology of disease. In this review, we highlight the recent discoveries in lysosome biology, with an emphasis on their implications for cancer therapy. We focus on targeting the lysosome in cancer by exploring lysosomal biogenesis and its role in the crosstalk between apoptosis and autophagy. We also discuss how lysosomal inhibition could emerge as a new therapeutic strategy to overcome drug resistance in cancer.
MeSH term(s)	Animals ; Cell Death ; Endosomes/metabolism ; Humans ; Intracellular Membranes/metabolism ; Lysosomes/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Permeability
Language	English
Publishing date	2015-11-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.12953
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Se 110: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: PPT1 inhibition enhances the antitumor activity of anti-PD-1 antibody in melanoma.

JCI insight

2022 Volume 7, Issue 20

MeSH term(s)	Humans ; Melanoma ; Programmed Cell Death 1 Receptor ; Membrane Proteins ; Thiolester Hydrolases
Chemical Substances	Programmed Cell Death 1 Receptor ; PPT1 protein, human (EC 3.1.2.22) ; Membrane Proteins ; Thiolester Hydrolases (EC 3.1.2.-)
Language	English
Publishing date	2022-10-24
Publishing country	United States
Document type	Journal Article ; Published Erratum
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.165688
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: PPT1 inhibition enhances the antitumor activity of anti–PD-1 antibody in melanoma

JCI Insight, Vol 7, Iss

2022 Volume 20

Keywords	Medicine ; R
Language	English
Publishing date	2022-10-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: PPT1 inhibition enhances the antitumor activity of anti–PD-1 antibody in melanoma

JCI Insight, Vol 5, Iss

2020 Volume 17

Abstract: New strategies are needed to enhance the efficacy of anti–programmed cell death protein antibody (anti–PD-1 Ab) in cancer. Here, we report that inhibiting palmitoyl-protein thioesterase 1 (PPT1), a target of chloroquine derivatives like ... ...

Abstract	New strategies are needed to enhance the efficacy of anti–programmed cell death protein antibody (anti–PD-1 Ab) in cancer. Here, we report that inhibiting palmitoyl-protein thioesterase 1 (PPT1), a target of chloroquine derivatives like hydroxychloroquine (HCQ), enhances the antitumor efficacy of anti–PD-1 Ab in melanoma. The combination resulted in tumor growth impairment and improved survival in mouse models. Genetic suppression of core autophagy genes, but not Ppt1, in cancer cells reduced priming and cytotoxic capacity of primed T cells. Exposure of antigen-primed T cells to macrophage-conditioned medium derived from macrophages treated with PPT1 inhibitors enhanced melanoma-specific killing. Genetic or chemical Ppt1 inhibition resulted in M2 to M1 phenotype switching in macrophages. The combination was associated with a reduction in myeloid-derived suppressor cells in the tumor. Ppt1 inhibition by HCQ, or DC661, induced cyclic GMP-AMP synthase/stimulator of interferon genes/TANK binding kinase 1 pathway activation and the secretion of interferon-β in macrophages, the latter being a key component for augmented T cell–mediated cytotoxicity. Genetic Ppt1 inhibition produced similar findings. These data provide the rationale for this combination in melanoma clinical trials and further investigation in other cancers.
Keywords	Oncology ; Therapeutics ; Medicine ; R
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: PPT1 inhibition enhances the antitumor activity of anti-PD-1 antibody in melanoma.

JCI insight

2020 Volume 5, Issue 17

Abstract: New strategies are needed to enhance the efficacy of anti-programmed cell death protein antibody (anti-PD-1 Ab) in cancer. Here, we report that inhibiting palmitoyl-protein thioesterase 1 (PPT1), a target of chloroquine derivatives like ... ...

Abstract	New strategies are needed to enhance the efficacy of anti-programmed cell death protein antibody (anti-PD-1 Ab) in cancer. Here, we report that inhibiting palmitoyl-protein thioesterase 1 (PPT1), a target of chloroquine derivatives like hydroxychloroquine (HCQ), enhances the antitumor efficacy of anti-PD-1 Ab in melanoma. The combination resulted in tumor growth impairment and improved survival in mouse models. Genetic suppression of core autophagy genes, but not Ppt1, in cancer cells reduced priming and cytotoxic capacity of primed T cells. Exposure of antigen-primed T cells to macrophage-conditioned medium derived from macrophages treated with PPT1 inhibitors enhanced melanoma-specific killing. Genetic or chemical Ppt1 inhibition resulted in M2 to M1 phenotype switching in macrophages. The combination was associated with a reduction in myeloid-derived suppressor cells in the tumor. Ppt1 inhibition by HCQ, or DC661, induced cyclic GMP-AMP synthase/stimulator of interferon genes/TANK binding kinase 1 pathway activation and the secretion of interferon-β in macrophages, the latter being a key component for augmented T cell-mediated cytotoxicity. Genetic Ppt1 inhibition produced similar findings. These data provide the rationale for this combination in melanoma clinical trials and further investigation in other cancers.
MeSH term(s)	Animals ; Antibodies/immunology ; Antineoplastic Combined Chemotherapy Protocols ; Enzyme Inhibitors/administration & dosage ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Hydroxychloroquine/administration & dosage ; Hydroxychloroquine/pharmacology ; Hydroxychloroquine/therapeutic use ; Immune Checkpoint Inhibitors/administration & dosage ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Interferon-beta/metabolism ; Macrophages/drug effects ; Macrophages/immunology ; Melanoma/drug therapy ; Melanoma/immunology ; Mice ; Mice, Inbred C57BL ; Nucleotidyltransferases/metabolism ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Programmed Cell Death 1 Receptor/immunology ; RAW 264.7 Cells ; T-Lymphocytes/immunology ; Thiolester Hydrolases/antagonists & inhibitors ; Thiolester Hydrolases/genetics ; Thiolester Hydrolases/metabolism ; Tumor Cells, Cultured
Chemical Substances	Antibodies ; Enzyme Inhibitors ; Immune Checkpoint Inhibitors ; Programmed Cell Death 1 Receptor ; Hydroxychloroquine (4QWG6N8QKH) ; Interferon-beta (77238-31-4) ; Nucleotidyltransferases (EC 2.7.7.-) ; cGAS protein, mouse (EC 2.7.7.-) ; Thiolester Hydrolases (EC 3.1.2.-) ; palmitoyl-protein thioesterase (EC 3.1.2.22)
Language	English
Publishing date	2020-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.133225
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: ALDH1A1 and HLTF modulate the activity of lysosomal autophagy inhibitors in cancer cells.

Piao, Shengfu / Ojha, Rani / Rebecca, Vito W / Samanta, Arabinda / Ma, Xiao-Hong / Mcafee, Quentin / Nicastri, Michael C / Buckley, Meghan / Brown, Eric / Winkler, Jeffrey D / Gimotty, Phyllis A / Amaravadi, Ravi K

Autophagy

2017 Volume 13, Issue 12, Page(s) 2056–2071

Abstract: Lysosomal autophagy inhibitors (LAI) such as hydroxychloroquine (HCQ) have significant activity in a subset of cancer cell lines. LAIs are being evaluated in cancer clinical trials, but genetic determinants of sensitivity to LAIs are unknown, making it ... ...

Abstract	Lysosomal autophagy inhibitors (LAI) such as hydroxychloroquine (HCQ) have significant activity in a subset of cancer cell lines. LAIs are being evaluated in cancer clinical trials, but genetic determinants of sensitivity to LAIs are unknown, making it difficult to predict which tumors would be most susceptible. Here we characterize differentially expressed genes in HCQ-sensitive (-S) and -resistant (-R) cancer cells. Notably, expression of canonical macroautophagy/autophagy genes was not associated with sensitivity to HCQ. Expression patterns of ALDH1A1 (aldehyde dehydrogenase 1 family member A1) and HLTF (helicase like transcription factor) identified HCQ-S (ALDH1A1
MeSH term(s)	Aldehyde Dehydrogenase/metabolism ; Animals ; Autophagy/drug effects ; Cell Line, Tumor ; Chloroquine/pharmacology ; DNA Damage ; DNA-Binding Proteins/metabolism ; Drug Resistance, Neoplasm/drug effects ; Epigenesis, Genetic/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Hydroxychloroquine/pharmacology ; Lysosomes/drug effects ; Lysosomes/metabolism ; Mice, Nude ; Reactive Oxygen Species/metabolism ; Reproducibility of Results ; Transcription Factors/metabolism
Chemical Substances	DNA-Binding Proteins ; HLTF protein, human ; Reactive Oxygen Species ; Transcription Factors ; Hydroxychloroquine (4QWG6N8QKH) ; Chloroquine (886U3H6UFF) ; ALDH1A1 protein, human (EC 1.2.1.3) ; Aldehyde Dehydrogenase (EC 1.2.1.3)
Language	English
Publishing date	2017-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2017.1377377
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 6741: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Identification of secreted proteins that reflect autophagy dynamics within tumor cells.

Kraya, Adam A / Piao, Shengfu / Xu, Xiaowei / Zhang, Gao / Herlyn, Meenhard / Gimotty, Phyllis / Levine, Beth / Amaravadi, Ravi K / Speicher, David W

Autophagy

2014 Volume 11, Issue 1, Page(s) 60–74

Abstract: Macroautophagy, a catabolic process of cellular self-digestion, is an important tumor cell survival mechanism and a potential target in antineoplastic therapies. Recent discoveries have implicated autophagy in the cellular secretory process, but ... ...

Abstract	Macroautophagy, a catabolic process of cellular self-digestion, is an important tumor cell survival mechanism and a potential target in antineoplastic therapies. Recent discoveries have implicated autophagy in the cellular secretory process, but potential roles of autophagy-mediated secretion in modifying the tumor microenvironment are poorly understood. Furthermore, efforts to inhibit autophagy in clinical trials have been hampered by suboptimal methods to quantitatively measure tumor autophagy levels. Here, we leveraged the autophagy-based involvement in cellular secretion to identify shed proteins associated with autophagy levels in melanoma. The secretome of low-autophagy WM793 melanoma cells was compared to its highly autophagic metastatic derivative, 1205Lu in physiological 3-dimensional cell culture using quantitative proteomics. These comparisons identified candidate autophagy biomarkers IL1B (interleukin 1, β), CXCL8 (chemokine (C-X-C motif) ligand 8), LIF (leukemia inhibitory factor), FAM3C (family with sequence similarity 3, member C), and DKK3 (dickkopf WNT signaling pathway inhibitor 3) with known roles in inflammation and tumorigenesis, and these proteins were subsequently shown to be elevated in supernatants of an independent panel of high-autophagy melanoma cell lines. Secretion levels of these proteins increased when low-autophagy melanoma cells were treated with the autophagy-inducing tat-BECN1 (Beclin 1) peptide and decreased when ATG7 (autophagy-related 7) was silenced in high-autophagy cells, thereby supporting a mechanistic link between these secreted proteins and autophagy. In addition, serum from metastatic melanoma patients with high tumor autophagy levels exhibited higher levels of these proteins than serum from patients with low-autophagy tumors. These results suggest that autophagy-related secretion affects the tumor microenvironment and measurement of autophagy-associated secreted proteins in plasma and possibly in tumors can serve as surrogates for intracellular autophagy dynamics in tumor cells.
MeSH term(s)	Autophagy ; Autophagy-Related Protein 7 ; Biomarkers, Tumor/blood ; Cell Line, Tumor ; Cell Proliferation ; Culture Media ; Gene Silencing ; Humans ; Melanoma/blood ; Melanoma/pathology ; Melanoma/ultrastructure ; Neoplasm Metastasis ; Neoplasm Proteins/blood ; Neoplasm Proteins/metabolism ; RNA, Small Interfering/metabolism ; Spheroids, Cellular/pathology ; Spheroids, Cellular/ultrastructure ; Ubiquitin-Activating Enzymes/metabolism
Chemical Substances	Biomarkers, Tumor ; Culture Media ; Neoplasm Proteins ; RNA, Small Interfering ; ATG7 protein, human (EC 6.2.1.45) ; Autophagy-Related Protein 7 (EC 6.2.1.45) ; Ubiquitin-Activating Enzymes (EC 6.2.1.45)
Language	English
Publishing date	2014-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/15548627.2014.984273
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 6741: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Strong regional heterogeneity in base composition evolution on the Drosophila X chromosome.

Ko, Wen-Ya / Piao, Shengfu / Akashi, Hiroshi

Genetics

2006 Volume 174, Issue 1, Page(s) 349–362

Abstract: Fluctuations in base composition appear to be prevalent in Drosophila and mammal genome evolution, but their timescale, genomic breadth, and causes remain obscure. Here, we study base composition evolution within the X chromosomes of Drosophila ... ...

Abstract	Fluctuations in base composition appear to be prevalent in Drosophila and mammal genome evolution, but their timescale, genomic breadth, and causes remain obscure. Here, we study base composition evolution within the X chromosomes of Drosophila melanogaster and five of its close relatives. Substitutions were inferred on six extant and two ancestral lineages for 14 near-telomeric and 9 nontelomeric genes. GC content evolution is highly variable both within the genome and within the phylogenetic tree. In the lineages leading to D. yakuba and D. orena, GC content at silent sites has increased rapidly near telomeres, but has decreased in more proximal (nontelomeric) regions. D. orena shows a 17-fold excess of GC-increasing vs. AT-increasing synonymous changes within a small (approximately 130-kb) region close to the telomeric end. Base composition changes within introns are consistent with changes in mutation patterns, but stronger GC elevation at synonymous sites suggests contributions of natural selection or biased gene conversion. The Drosophila yakuba lineage shows a less extreme elevation of GC content distributed over a wider genetic region (approximately 1.2 Mb). A lack of change in GC content for most introns within this region suggests a role of natural selection in localized base composition fluctuations.
MeSH term(s)	Animals ; Base Composition ; Cell Lineage/genetics ; Codon ; Drosophila/genetics ; Evolution, Molecular ; Genetic Variation ; Introns ; Molecular Sequence Data ; Open Reading Frames ; Phylogeny ; Telomere ; X Chromosome/chemistry
Chemical Substances	Codon
Language	English
Publishing date	2006-03-17
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2167-2
ISSN	1943-2631 ; 0016-6731
ISSN (online)	1943-2631
ISSN	0016-6731
DOI	10.1534/genetics.105.054346
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.B 767: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Measurements of tumor cell autophagy predict invasiveness, resistance to chemotherapy, and survival in melanoma.

Ma, Xiao-Hong / Piao, Shengfu / Wang, Dan / McAfee, Quentin W / Nathanson, Katherine L / Lum, Julian J / Li, Lin Z / Amaravadi, Ravi K

Clinical cancer research : an official journal of the American Association for Cancer Research

2011 Volume 17, Issue 10, Page(s) 3478–3489

Abstract: Purpose: Autophagy consists of lysosome-dependent degradation of cytoplasmic contents sequestered by autophagic vesicles (AV). The role of autophagy in determining tumor aggressiveness and response to therapy in melanoma was investigated in this study.!# ...

Abstract	Purpose: Autophagy consists of lysosome-dependent degradation of cytoplasmic contents sequestered by autophagic vesicles (AV). The role of autophagy in determining tumor aggressiveness and response to therapy in melanoma was investigated in this study. Experimental design: Autophagy was measured in tumor biopsies obtained from metastatic melanoma patients enrolled on a phase II trial of temozolomide and sorafenib and correlated to clinical outcome. These results were compared with autophagy measurements in aggressive and indolent melanoma cells grown in two- and three-dimensional (3D) culture and as xenograft tumors. The effects of autophagy inhibition with either hydroxychloroquine or inducible shRNA (short hairpin RNA) against the autophagy gene ATG5 were assessed in three-dimensional spheroids. Results: Patients whose tumors had a high autophagic index were less likely to respond to treatment and had a shorter survival compared with those with a low autophagic index. Differences in autophagy were less evident in aggressive and indolent melanoma cells grown in monolayer culture. In contrast, autophagy was increased in aggressive compared with indolent melanoma xenograft tumors. This difference was recapitulated when aggressive and indolent melanoma cells were grown as spheroids. Autophagy inhibition with either hydroxychloroquine or inducible shRNA against ATG5 resulted in cell death in aggressive melanoma spheroids, and significantly augmented temozolomide-induced cell death. Conclusions: Autophagy is a potential prognostic factor and therapeutic target in melanoma. Three dimensional culture mimics the tumor microenvironment better than monolayer culture and is an appropriate model for studying therapeutic combinations involving autophagy modulators. Autophagy inhibition should be tested clinically in patients with melanoma.
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Autophagy/physiology ; Benzenesulfonates/administration & dosage ; Cell Count ; Clinical Trials, Phase II as Topic ; Dacarbazine/administration & dosage ; Dacarbazine/analogs & derivatives ; Drug Resistance, Neoplasm/physiology ; Humans ; Melanoma/diagnosis ; Melanoma/drug therapy ; Melanoma/mortality ; Melanoma/pathology ; Mice ; Mice, Nude ; Neoplasm Invasiveness ; Niacinamide/analogs & derivatives ; Phenylurea Compounds ; Prognosis ; Pyridines/administration & dosage ; Skin Neoplasms/diagnosis ; Skin Neoplasms/drug therapy ; Skin Neoplasms/mortality ; Skin Neoplasms/pathology ; Sorafenib ; Survival Analysis ; Temozolomide ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Benzenesulfonates ; Phenylurea Compounds ; Pyridines ; Niacinamide (25X51I8RD4) ; Dacarbazine (7GR28W0FJI) ; Sorafenib (9ZOQ3TZI87) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2011-02-15
Publishing country	United States
Document type	Evaluation Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-10-2372
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4223: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: PPT1 Promotes Tumor Growth and Is the Molecular Target of Chloroquine Derivatives in Cancer.

Rebecca, Vito W / Nicastri, Michael C / Fennelly, Colin / Chude, Cynthia I / Barber-Rotenberg, Julie S / Ronghe, Amruta / McAfee, Quentin / McLaughlin, Noel P / Zhang, Gao / Goldman, Aaron R / Ojha, Rani / Piao, Shengfu / Noguera-Ortega, Estela / Martorella, Alessandra / Alicea, Gretchen M / Lee, Jennifer J / Schuchter, Lynn M / Xu, Xiaowei / Herlyn, Meenhard /

Marmorstein, Ronen / Gimotty, Phyllis A / Speicher, David W / Winkler, Jeffrey D / Amaravadi, Ravi K

Cancer discovery

2018 Volume 9, Issue 2, Page(s) 220–229

Abstract: Clinical trials repurposing lysosomotropic chloroquine (CQ) derivatives as autophagy inhibitors in cancer demonstrate encouraging results, but the underlying mechanism of action remains unknown. Here, we report a novel dimeric CQ (DC661) capable of ... ...

Abstract	Clinical trials repurposing lysosomotropic chloroquine (CQ) derivatives as autophagy inhibitors in cancer demonstrate encouraging results, but the underlying mechanism of action remains unknown. Here, we report a novel dimeric CQ (DC661) capable of deacidifying the lysosome and inhibiting autophagy significantly better than hydroxychloroquine (HCQ). Using an
MeSH term(s)	Aminoquinolines/pharmacology ; Antimalarials/pharmacology ; Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Proliferation ; Chloroquine/pharmacology ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Polyamines/pharmacology ; Prognosis ; Survival Rate ; Thiolester Hydrolases/genetics ; Thiolester Hydrolases/metabolism ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Aminoquinolines ; Antimalarials ; Biomarkers, Tumor ; Lys01 ; Membrane Proteins ; Polyamines ; Chloroquine (886U3H6UFF) ; Thiolester Hydrolases (EC 3.1.2.-) ; PPT1 protein, human (EC 3.1.2.22)
Language	English
Publishing date	2018-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-18-0706
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6916: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito