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Article ; Online: On the role of bacterial metalloproteases in COVID-19 associated cytokine storm.

Földvári-Nagy, László / Schnabel, Tamás / Dörnyei, Gabriella / Korcsmáros, Tamás / Lenti, Katalin

2021 Volume 19, Issue 1, Page(s) 7

Abstract: The cytokine release syndrome or cytokine storm, which is the hyper-induction of inflammatory responses has a central role in the mortality rate of COVID-19 and some other viral infections. Interleukin-6 (IL-6) is a key player in the development of ... ...

Abstract	The cytokine release syndrome or cytokine storm, which is the hyper-induction of inflammatory responses has a central role in the mortality rate of COVID-19 and some other viral infections. Interleukin-6 (IL-6) is a key player in the development of cytokine storms. Shedding of interleukin-6 receptor (IL-6Rα) results in the accumulation of soluble interleukin-6 receptors (sIL-6R). Only relatively few cells express membrane-bound IL-6Rα. However, sIL-6R can act on potentially all cells and organs through the ubiquitously expressed gp130, the coreceptor of IL-6Rα. Through this, so-called trans-signaling, IL-6-sIL-6R is a powerful factor in the development of cytokine storms and multiorgan involvement. Some bacteria (e.g., Serratia marcescens, Staphylococcus aureus, Pseudomonas aeruginosa, Listeria monocytogenes), commonly considered to cause co-infections during viral pneumonia, can directly induce the shedding of membrane receptors, including IL-6Rα, or enhance endogenous shedding mechanisms causing the increase of sIL-6R level. Here we hypothesise that bacteria promoting shedding and increase the sIL-6R level can be an important contributing factor for the development of cytokine storms. Therefore, inhibition of IL-6Rα shedding by drastically reducing the number of relevant bacteria may be a critical element in reducing the chance of a cytokine storm. Validation of this hypothesis can support the consideration of the prophylactic use of antibiotics more widely and at an earlier stage of infection to decrease the mortality rate of COVID-19. Video abstract.
MeSH term(s)	Bacteria/enzymology ; Bacterial Proteins/metabolism ; COVID-19/complications ; COVID-19/pathology ; COVID-19/virology ; Cytokine Release Syndrome/etiology ; Cytokine Release Syndrome/microbiology ; Humans ; Interleukin-6/metabolism ; Metalloproteases/metabolism ; Receptors, Interleukin-6/metabolism ; SARS-CoV-2/isolation & purification ; Signal Transduction
Chemical Substances	Bacterial Proteins ; Interleukin-6 ; Receptors, Interleukin-6 ; Metalloproteases (EC 3.4.-)
Language	English
Publishing date	2021-01-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/s12964-020-00699-3
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Article: No Association between Gastrointestinal Rebleeding and DOAC Therapy Resumption: A Systematic Review and Meta-Analysis.

Pálinkás, Dániel / Teutsch, Brigitta / Gagyi, Endre Botond / Engh, Marie Anne / Kalló, Patrícia / Veres, Dániel S / Földvári-Nagy, László / Hosszúfalusi, Nóra / Hegyi, Péter / Erőss, Bálint

Biomedicines

2023 Volume 11, Issue 2

Abstract: Background: There are recommendations for anticoagulation resumption after gastrointestinal bleeding (GIB), although data addressing this topic by direct oral anticoagulants (DOACs)-treated patients is lacking. We aim to determine the safety and ... ...

Abstract	Background: There are recommendations for anticoagulation resumption after gastrointestinal bleeding (GIB), although data addressing this topic by direct oral anticoagulants (DOACs)-treated patients is lacking. We aim to determine the safety and efficacy of restarting DOACs after GIB. Methods: Studies that reported rebleeding, thromboembolic events, and mortality after restarting or withholding DOACs were selected. The systematic research was conducted in five databases (MEDLINE, EMBASE, CENTRAL, Web of Science, and Scopus). The random effect model was implemented to calculate the pooled odds ratio (OR). The ROBINS-I tool was used for risk of bias assessment, and the certainty of the evidence was evaluated with the GRADE approach. Results: Four retrospective cohort studies (1722 patients) were included in the meta-analysis. We did not find a significant increase in the risk of rebleeding in patients restarting DOACs after index GIB (OR = 1.12; 95% CI: 0.74-1.68). The outcomes of thromboembolic events and mortality data were not suitable for meta-analytic calculations. Single studies did not show statistically significant differences. Data quality assessment showed a serious overall risk of bias and very low quality of evidence (GRADE D). Conclusion: DOAC resumption after a GIB episode may not elevate the risk of rebleeding. However, the need for high-quality randomized clinical trials is crucial.
Language	English
Publishing date	2023-02-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11020554
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Article ; Online: Probiotic supplementation during antibiotic treatment is unjustified in maintaining the gut microbiome diversity: a systematic review and meta-analysis.

Éliás, Anna Júlia / Barna, Viktória / Patoni, Cristina / Demeter, Dóra / Veres, Dániel Sándor / Bunduc, Stefania / Erőss, Bálint / Hegyi, Péter / Földvári-Nagy, László / Lenti, Katalin

BMC medicine

2023 Volume 21, Issue 1, Page(s) 262

Abstract: Background: Probiotics are often used to prevent antibiotic-induced low-diversity dysbiosis, however their effect is not yet sufficiently summarized in this regard. We aimed to investigate the effects of concurrent probiotic supplementation on gut ... ...

Abstract	Background: Probiotics are often used to prevent antibiotic-induced low-diversity dysbiosis, however their effect is not yet sufficiently summarized in this regard. We aimed to investigate the effects of concurrent probiotic supplementation on gut microbiome composition during antibiotic therapy. Methods: We performed a systematic review and meta-analysis of randomized controlled trials reporting the differences in gut microbiome diversity between patients on antibiotic therapy with and without concomitant probiotic supplementation. The systematic search was performed in three databases (MEDLINE (via PubMed), Embase, and Cochrane Central Register of Controlled Trials (CENTRAL)) without filters on 15 October 2021. A random-effects model was used to estimate pooled mean differences (MD) with 95% confidence intervals (CI). This review was registered on PROSPERO (CRD42021282983). Results: Of 11,769 identified articles, 15 were eligible in the systematic review and 5 in the meta-analyses. Quantitative data synthesis for Shannon (MD = 0.23, 95% CI: [(-)0.06-0.51]), Chao1 (MD = 11.59 [(-)18.42-41.60]) and observed OTUs (operational taxonomic unit) (MD = 17.15 [(-)9.43-43.73]) diversity indices revealed no significant difference between probiotic supplemented and control groups. Lacking data prevented meta-analyzing other diversity indices; however, most of the included studies reported no difference in the other reported α- and ß-diversity indices between the groups. Changes in the taxonomic composition varied across the eligible studies but tended to be similar in both groups. However, they showed a potential tendency to restore baseline levels in both groups after 3-8 weeks. This is the first meta-analysis and the most comprehensive review of the topic to date using high quality methods. The limited number of studies and low sample sizes are the main limitations of our study. Moreover, there was high variability across the studies regarding the indication of antibiotic therapy and the type, dose, and duration of antimicrobials and probiotics. Conclusions: Our results showed that probiotic supplementation during antibiotic therapy was not found to be influential on gut microbiome diversity indices. Defining appropriate microbiome diversity indices, their standard ranges, and their clinical relevance would be crucial.
MeSH term(s)	Humans ; Gastrointestinal Microbiome ; Probiotics/therapeutic use ; Probiotics/adverse effects ; Dietary Supplements ; Anti-Bacterial Agents/adverse effects ; Dysbiosis
Chemical Substances	Anti-Bacterial Agents
Language	English
Publishing date	2023-07-19
Publishing country	England
Document type	Meta-Analysis ; Systematic Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2131669-7
ISSN	1741-7015 ; 1741-7015
ISSN (online)	1741-7015
ISSN	1741-7015
DOI	10.1186/s12916-023-02961-0
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Article: Microscopic colitis is a risk factor for low bone density: a systematic review and meta-analysis.

Rancz, Anett / Teutsch, Brigitta / Engh, Marie Anne / Veres, Dániel Sándor / Földvári-Nagy, László / Erőss, Bálint / Hosszúfalusi, Nóra / Juhász, Márk Félix / Hegyi, Péter / Mihály, Emese

Therapeutic advances in gastroenterology

2023 Volume 16, Page(s) 17562848231177151

Abstract: Background: Microscopic colitis (MC) is a chronic inflammatory disease of the large bowel characterized by watery diarrhea, substantially decreasing the patient's quality of life. Scarce data suggest that MC is associated with low bone density (LBD).: ...

Abstract	Background: Microscopic colitis (MC) is a chronic inflammatory disease of the large bowel characterized by watery diarrhea, substantially decreasing the patient's quality of life. Scarce data suggest that MC is associated with low bone density (LBD). Objectives: We aimed to assess whether MC is a risk factor for LBD and the proportion of patients with MC having LBD. Design: A systematic review and meta-analysis of studies reporting bone density measurements in MC patients. Data sources and methods: We systematically searched five databases from inception to October 16, 2021 (Pubmed, Embase, Cochrane, Scopus, and Web of Science). We used the random-effect model to calculate pooled odds ratios (ORs) and pooled event rates with 95% confidence intervals (CIs). To ascertain the quality of evidence of our outcomes, we followed the recommendations of the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) Working Group. Results: The systematic search yielded a total of 3046 articles. Four articles were eligible for quantitative synthesis. All of them used age- and sex-matched controls to evaluate LBD occurrence among patients with MC. The odds of having LBD were twofold increased (OR = 2.13, CI: 1.42-3.20) in the presence of MC, the odds of osteopenia occurrence were 2.4 (OR = 2.45, CI: 1.11-5.41), and of osteoporosis 1.4 (OR = 1.42, CI: 0.65-3.12). The proportion of LBD was 0.68 (CI: 0.56-0.78), osteopenia was 0.51 (CI: 0.43-0.58), and osteoporosis was 0.11 (CI: 0.07-0.16) among the MC population. Our findings' certainty of the evidence was very low following the GRADEPro guideline. Conclusion: Our data demonstrate that MC is associated with a twofold risk for LBD. Based on our findings, we suggest screening patients for bone mineral density upon diagnosis of MC. Further prospective studies with higher patient numbers and longer follow-up periods on this topic are needed. Registration: Our protocol was prospectively registered with PROSPERO (CRD42021283392).
Language	English
Publishing date	2023-06-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2440710-0
ISSN	1756-2848 ; 1756-283X
ISSN (online)	1756-2848
ISSN	1756-283X
DOI	10.1177/17562848231177151
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Article ; Online: A De Quervain-féle tendinopathia kezelése konzervatív módszerekkel.

Földvári-Nagy, László / Takács, Johanna / Hetthéssy, Judit Réka / Mayer, Ágnes Andrea / Szakács, Noémi / Szávin-Pósa, Ágnes / Lenti, Katalin

Orvosi hetilap

2020 Volume 161, Issue 11, Page(s) 419–424

Abstract: Introduction: ...

Title translation	Treatment of De Quervain's tendinopathy with conservative methods.
Abstract	Introduction:
MeSH term(s)	Conservative Treatment ; De Quervain Disease/diagnosis ; De Quervain Disease/therapy ; Humans ; Pain ; Pain Measurement ; Physical Therapy Modalities ; Tendinopathy/diagnosis ; Tendinopathy/therapy ; Treatment Outcome
Language	Hungarian
Publishing date	2020-02-21
Publishing country	Hungary
Document type	Journal Article
ZDB-ID	123879-6
ISSN	1788-6120 ; 0030-6002
ISSN (online)	1788-6120
ISSN	0030-6002
DOI	10.1556/650.2020.31672
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Article ; Online: AutophagyNet: high-resolution data source for the analysis of autophagy and its regulation.

Autophagy

2023 Volume 20, Issue 1, Page(s) 188–201

Abstract: Macroautophagy/autophagy is a highly-conserved catabolic procss eliminating dysfunctional cellular components and invading pathogens. Autophagy malfunction contributes to disorders such as cancer, neurodegenerative and inflammatory diseases. ... ...

Abstract	Macroautophagy/autophagy is a highly-conserved catabolic procss eliminating dysfunctional cellular components and invading pathogens. Autophagy malfunction contributes to disorders such as cancer, neurodegenerative and inflammatory diseases. Understanding autophagy regulation in health and disease has been the focus of the last decades. We previously provided an integrated database for autophagy research, the Autophagy Regulatory Network (ARN). For the last eight years, this resource has been used by thousands of users. Here, we present a new and upgraded resource, AutophagyNet. It builds on the previous database but contains major improvements to address user feedback and novel needs due to the advancement in omics data availability. AutophagyNet contains updated interaction curation and integration of over 280,000 experimentally verified interactions between core autophagy proteins and their protein, transcriptional and post-transcriptional regulators as well as their potential upstream pathway connections. AutophagyNet provides annotations for each core protein about their role: 1) in different types of autophagy (mitophagy, xenophagy, etc.); 2) in distinct stages of autophagy (initiation, expansion, termination, etc.); 3) with subcellular and tissue-specific localization. These annotations can be used to filter the dataset, providing customizable download options tailored to the user's needs. The resource is available in various file formats (e.g. CSV, BioPAX and PSI-MI), and data can be analyzed and visualized directly in Cytoscape. The multi-layered regulation of autophagy can be analyzed by combining AutophagyNet with tissue- or cell type-specific (multi-)omics datasets (e.g. transcriptomic or proteomic data). The resource is publicly accessible at http://autophagynet.org.
MeSH term(s)	Autophagy/physiology ; Proteomics ; Beclin-1 ; Mitophagy ; Signal Transduction/genetics ; MicroRNAs
Chemical Substances	Beclin-1 ; MicroRNAs
Language	English
Publishing date	2023-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2023.2247737
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Article ; Online: Starvation-response may not involve Atg1-dependent autophagy induction in non-unikont parasites.

Földvári-Nagy, László / Ari, Eszter / Csermely, Péter / Korcsmáros, Tamás / Vellai, Tibor

Scientific reports

2014 Volume 4, Page(s) 5829

Abstract: Autophagy, the lysosome-mediated self-degradation process, is implicated in survival during starvation in yeast, Dictyostelium and animals. In these eukaryotic taxa (collectively called Unikonts), autophagy is induced primarily through the Atg1/ULK1 ... ...

Abstract	Autophagy, the lysosome-mediated self-degradation process, is implicated in survival during starvation in yeast, Dictyostelium and animals. In these eukaryotic taxa (collectively called Unikonts), autophagy is induced primarily through the Atg1/ULK1 complex in response to nutrient depletion. Autophagy has also been well-studied in non-unikont parasites, such as Trypanosoma and Plasmodium, and found important in their life-cycle transitions. However, how autophagy is induced in non-unikonts remains largely unrevealed. Using a bioinformatics approach, we examined the presence of Atg1 and of its complex in the genomes of 40 non-unikonts. We found that these genomes do not encode typical Atg1 proteins: BLAST and HMMER queries matched only with the kinase domain of Atg1, while other segments responsible for regulation and protein-binding were missing. Non-unikonts also lacked other components of the Atg1-inducing complex. Orthologs of an alternative autophagy inducer, Atg6 were found only in the half of the species, indicating that the other half may possess other inducing mechanisms. As key autophagy genes have differential expression patterns during life-cycle, we raise the possibility that autophagy in these protists is induced mainly at the post-transcriptional level. Understanding Atg1-independent autophagy induction mechanisms in these parasites may lead to novel pharmacological interventions, not affecting human Atg1-dependent autophagy.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy ; Computational Biology ; Databases, Genetic ; Phylogeny ; Plasmodium/classification ; Plasmodium/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Protozoan Proteins/metabolism ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Starvation ; Trypanosoma/classification ; Trypanosoma/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Protozoan Proteins ; Saccharomyces cerevisiae Proteins ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2014-07-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep05829
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Article ; Online: SignaLink3: a multi-layered resource to uncover tissue-specific signaling networks.

Csabai, Luca / Fazekas, Dávid / Kadlecsik, Tamás / Szalay-Bekő, Máté / Bohár, Balázs / Madgwick, Matthew / Módos, Dezső / Ölbei, Márton / Gul, Lejla / Sudhakar, Padhmanand / Kubisch, János / Oyeyemi, Oyebode James / Liska, Orsolya / Ari, Eszter / Hotzi, Bernadette / Billes, Viktor A / Molnár, Eszter / Földvári-Nagy, László / Csályi, Kitti /

Demeter, Amanda / Pápai, Nóra / Koltai, Mihály / Varga, Máté / Lenti, Katalin / Farkas, Illés J / Türei, Dénes / Csermely, Péter / Vellai, Tibor / Korcsmáros, Tamás

Nucleic acids research

2021 Volume 50, Issue D1, Page(s) D701–D709

Abstract: Signaling networks represent the molecular mechanisms controlling a cell's response to various internal or external stimuli. Most currently available signaling databases contain only a part of the complex network of intertwining pathways, leaving out key ...

Abstract	Signaling networks represent the molecular mechanisms controlling a cell's response to various internal or external stimuli. Most currently available signaling databases contain only a part of the complex network of intertwining pathways, leaving out key interactions or processes. Hence, we have developed SignaLink3 (http://signalink.org/), a value-added knowledge-base that provides manually curated data on signaling pathways and integrated data from several types of databases (interaction, regulation, localisation, disease, etc.) for humans, and three major animal model organisms. SignaLink3 contains over 400 000 newly added human protein-protein interactions resulting in a total of 700 000 interactions for Homo sapiens, making it one of the largest integrated signaling network resources. Next to H. sapiens, SignaLink3 is the only current signaling network resource to provide regulatory information for the model species Caenorhabditis elegans and Danio rerio, and the largest resource for Drosophila melanogaster. Compared to previous versions, we have integrated gene expression data as well as subcellular localization of the interactors, therefore uniquely allowing tissue-, or compartment-specific pathway interaction analysis to create more accurate models. Data is freely available for download in widely used formats, including CSV, PSI-MI TAB or SQL.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Databases, Genetic ; Drosophila melanogaster/genetics ; Gene Regulatory Networks/genetics ; Humans ; Protein Interaction Maps/genetics ; Signal Transduction/genetics ; Zebrafish/genetics
Language	English
Publishing date	2021-10-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkab909
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Article ; Online: NRF2-ome: an integrated web resource to discover protein interaction and regulatory networks of NRF2.

Türei, Dénes / Papp, Diána / Fazekas, Dávid / Földvári-Nagy, László / Módos, Dezső / Lenti, Katalin / Csermely, Péter / Korcsmáros, Tamás

Oxidative medicine and cellular longevity

2013 Volume 2013, Page(s) 737591

Abstract: NRF2 is the master transcriptional regulator of oxidative and xenobiotic stress responses. NRF2 has important roles in carcinogenesis, inflammation, and neurodegenerative diseases. We developed an online resource, NRF2-ome, to provide an integrated and ... ...

Abstract	NRF2 is the master transcriptional regulator of oxidative and xenobiotic stress responses. NRF2 has important roles in carcinogenesis, inflammation, and neurodegenerative diseases. We developed an online resource, NRF2-ome, to provide an integrated and systems-level database for NRF2. The database contains manually curated and predicted interactions of NRF2 as well as data from external interaction databases. We integrated NRF2 interactome with NRF2 target genes, NRF2 regulating TFs, and miRNAs. We connected NRF2-ome to signaling pathways to allow mapping upstream NRF2 regulatory components that could directly or indirectly influence NRF2 activity totaling 35,967 protein-protein and signaling interactions. The user-friendly website allows researchers without computational background to search, browse, and download the database. The database can be downloaded in SQL, CSV, BioPAX, SBML, PSI-MI, and in a Cytoscape CYS file formats. We illustrated the applicability of the website by suggesting a posttranscriptional negative feedback of NRF2 by MAFG protein and raised the possibility of a connection between NRF2 and the JAK/STAT pathway through STAT1 and STAT3. NRF2-ome can also be used as an evaluation tool to help researchers and drug developers to understand the hidden regulatory mechanisms in the complex network of NRF2.
MeSH term(s)	Databases, Protein ; Gene Regulatory Networks ; Humans ; Internet ; NF-E2-Related Factor 2/metabolism ; Protein Interaction Maps ; Workflow
Chemical Substances	NF-E2-Related Factor 2
Language	English
Publishing date	2013-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2013/737591
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Article ; Online: Complex regulation of autophagy in cancer - integrated approaches to discover the networks that hold a double-edged sword.

Kubisch, János / Türei, Dénes / Földvári-Nagy, László / Dunai, Zsuzsanna A / Zsákai, Lilian / Varga, Máté / Vellai, Tibor / Csermely, Péter / Korcsmáros, Tamás

Seminars in cancer biology

2013 Volume 23, Issue 4, Page(s) 252–261

Abstract: Autophagy, a highly regulated self-degradation process of eukaryotic cells, is a context-dependent tumor-suppressing mechanism that can also promote tumor cell survival upon stress and treatment resistance. Because of this ambiguity, autophagy is ... ...

Abstract	Autophagy, a highly regulated self-degradation process of eukaryotic cells, is a context-dependent tumor-suppressing mechanism that can also promote tumor cell survival upon stress and treatment resistance. Because of this ambiguity, autophagy is considered as a double-edged sword in oncology, making anti-cancer therapeutic approaches highly challenging. In this review, we present how systems-level knowledge on autophagy regulation can help to develop new strategies and efficiently select novel anti-cancer drug targets. We focus on the protein interactors and transcriptional/post-transcriptional regulators of autophagy as the protein and regulatory networks significantly influence the activity of core autophagy proteins during tumor progression. We list several network resources to identify interactors and regulators of autophagy proteins. As in silico analysis of such networks often necessitates experimental validation, we briefly summarize tractable model organisms to examine the role of autophagy in cancer. We also discuss fluorescence techniques for high-throughput monitoring of autophagy in humans. Finally, the challenges of pharmacological modulation of autophagy are reviewed. We suggest network-based concepts to overcome these difficulties. We point out that a context-dependent modulation of autophagy would be favored in anti-cancer therapy, where autophagy is stimulated in normal cells, while inhibited only in stressed cancer cells. To achieve this goal, we introduce the concept of regulo-network drugs targeting specific transcription factors or miRNA families identified with network analysis. The effect of regulo-network drugs propagates indirectly through transcriptional or post-transcriptional regulation of autophagy proteins, and, as a multi-directional intervention tool, they can both activate and inhibit specific proteins in the same time. The future identification and validation of such regulo-network drug targets may serve as novel intervention points, where autophagy can be effectively modulated in cancer therapy.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Autophagy/drug effects ; Autophagy/genetics ; Autophagy/physiology ; Disease Models, Animal ; Humans ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Protein Interaction Maps/drug effects ; Protein Interaction Maps/genetics ; Protein Interaction Maps/physiology ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/physiology
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2013-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2013.06.009
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