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Article ; Online: Mutant K-Ras in Pancreatic Cancer: An Insight on the Role of Wild-Type N-Ras and K-Ras-Dependent Cell Cycle Regulation.

Ferguson, Robert / Aughton, Karen / Evans, Anthony / Shaw, Victoria / Armstrong, Jane / Ware, Adam / Bennett, Laura / Costello, Eithne / Greenhalf, William

Current issues in molecular biology

2023 Volume 45, Issue 3, Page(s) 2505–2520

Abstract: The development of K-Ras independence may explain the failure of targeted therapy for pancreatic cancer (PC). In this paper, active N as well as K-Ras was shown in all human cell lines tested. In a cell line dependent on mutant K-Ras, it was shown that ... ...

Abstract	The development of K-Ras independence may explain the failure of targeted therapy for pancreatic cancer (PC). In this paper, active N as well as K-Ras was shown in all human cell lines tested. In a cell line dependent on mutant K-Ras, it was shown that depleting K-Ras reduced total Ras activity, while cell lines described as independent had no significant decline in total Ras activity. The knockdown of N-Ras showed it had an important role in controlling the relative level of oxidative metabolism, but only K-Ras depletion caused a decrease in G2 cyclins. Proteasome inhibition reversed this, and other targets of APC/c were also decreased by K-Ras depletion. K-Ras depletion did not cause an increase in ubiquitinated G2 cyclins but instead caused exit from the G2 phase to slow relative to completion of the S-phase, suggesting that the mutant K-Ras may inhibit APC/c prior to anaphase and stabilise G2 cyclins independently of this. We propose that, during tumorigenesis, cancer cells expressing wild-type N-Ras protein are selected because the protein protects cancer cells from the deleterious effects of the cell cycle-independent induction of cyclins by mutant K-Ras. Mutation independence results when N-Ras activity becomes adequate to drive cell division, even in cells where K-Ras is inhibited.
Language	English
Publishing date	2023-03-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2000024-8
ISSN	1467-3045 ; 1467-3037
ISSN (online)	1467-3045
ISSN	1467-3037
DOI	10.3390/cimb45030164
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Zs.A 5122: Show issues

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Article ; Online: The holding temperature of blood during a delay to processing can affect serum and plasma protein measurements.

Ashworth, Milton / Small, Benjamin / Oldfield, Lucy / Evans, Anthony / Greenhalf, William / Halloran, Christopher / Costello, Eithne

Scientific reports

2021 Volume 11, Issue 1, Page(s) 6487

Abstract: Accurate blood-borne biomarkers are sought for diagnosis, prognosis and treatment stratification. Consistent handling of blood is essential for meaningful data interpretation, however, delays during processing are occasionally unavoidable. We ... ...

Abstract	Accurate blood-borne biomarkers are sought for diagnosis, prognosis and treatment stratification. Consistent handling of blood is essential for meaningful data interpretation, however, delays during processing are occasionally unavoidable. We investigated the effects of immediately placing blood samples on ice versus room temperature for 1 h (reference protocol), and holding samples on ice versus room temperature during a 3 h delay to processing. Using Luminex multi-plex assays to assess cytokines (n = 29) and diabetes-associated proteins (n = 15) in healthy subjects, we observed that placing blood samples immediately on ice decreased the serum levels of several cytokines, including PAI-1, MIP1-β, IL-9, RANTES and IL-8. During a delay to processing, some analytes, e.g. leptin and insulin, showed little change in serum or plasma values. However, for approximately half of the analytes studied, a delay, regardless of the holding temperature, altered the measured levels compared to the reference protocol. Effects differed between serum and plasma and for some analytes the direction of change in level varied across individuals. The optimal holding temperature for samples during a delay was analyte-specific. In conclusion, deviations from protocol can lead to significant changes in blood analyte levels. Where possible, protocols for blood handling should be pre-determined in an analyte-specific manner.
MeSH term(s)	Biomarkers/blood ; Blood Preservation/methods ; Blood Preservation/standards ; Blood Proteins/chemistry ; Cryopreservation/methods ; Cryopreservation/standards ; Cytokines/blood ; Humans ; Ice ; Insulin/blood ; Leptin/blood ; Protein Stability
Chemical Substances	Biomarkers ; Blood Proteins ; Cytokines ; Ice ; Insulin ; Leptin
Language	English
Publishing date	2021-03-22
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/s41598-021-85052-5
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Article ; Online: Changes in hospital mortality in patients with cancer during the COVID-19 pandemic (ISARIC-CCP-UK): a prospective, multicentre cohort study.

Turtle, Lance / Elliot, Sarah / Drake, Thomas M / Thorpe, Mathew / Khoury, Emma G / Greenhalf, William / Hardwick, Hayley E / Leeming, Gary / Law, Andy / Oosthuyzen, Wilna / Pius, Riinu / Shaw, Catherine A / Baillie, J Kenneth / Openshaw, Peter J M / Docherty, Annemarie B / Semple, Malcolm G / Harrison, Ewen M / Palmieri, Carlo

The Lancet. Oncology

2024 Volume 25, Issue 5, Page(s) 636–648

Abstract: Background: Patients with cancer are at greater risk of dying from COVID-19 than many other patient groups. However, how this risk evolved during the pandemic remains unclear. We aimed to determine, on the basis of the UK national pandemic protocol, how ...

Abstract	Background: Patients with cancer are at greater risk of dying from COVID-19 than many other patient groups. However, how this risk evolved during the pandemic remains unclear. We aimed to determine, on the basis of the UK national pandemic protocol, how factors influencing hospital mortality from COVID-19 could differentially affect patients undergoing cancer treatment. We also examined changes in hospital mortality and escalation of care in patients on cancer treatment during the first 2 years of the COVID-19 pandemic in the UK. Methods: We conducted a prospective cohort study of patients aged older than 19 years and admitted to 306 health-care facilities in the UK with confirmed SARS-CoV-2 infection, who were enrolled in the International Severe Acute Respiratory and emerging Infections Consortium (ISARIC) WHO Clinical Characterisation Protocol (CCP) across the UK from April 23, 2020, to Feb 28, 2022; this analysis included all patients in the complete dataset when the study closed. The primary outcome was 30-day in-hospital mortality, comparing patients on cancer treatment and those without cancer. The study was approved by the South Central-Oxford C Research Ethics Committee in England (Ref: 13/SC/0149) and the Scotland A Research Ethics Committee (Ref 20/SS/0028), and is registered on the ISRCTN Registry (ISRCTN66726260). Findings: 177 871 eligible adult patients either with no history of cancer (n=171 303) or on cancer treatment (n=6568) were enrolled; 93 205 (52·4%) were male, 84 418 (47·5%) were female, and in 248 (13·9%) sex or gender details were not specified or data were missing. Patients were followed up for a median of 13 (IQR 6-21) days. Of the 6568 patients receiving cancer treatment, 2080 (31·7%) died at 30 days, compared with 30 901 (18·0%) of 171 303 patients without cancer. Patients aged younger than 50 years on cancer treatment had the highest age-adjusted relative risk (hazard ratio [HR] 5·2 [95% CI 4·0-6·6], p<0·0001; vs 50-69 years 2·4 [2·2-2·6], p<0·0001; 70-79 years 1·8 [1·6-2·0], p<0·0001; and >80 years 1·5 [1·3-1·6], p<0·0001) but a lower absolute risk (51 [6·7%] of 763 patients <50 years died compared with 459 [30·2%] of 1522 patients aged >80 years). In-hospital mortality decreased for all patients during the pandemic but was higher for patients on cancer treatment than for those without cancer throughout the study period. Interpretation: People with cancer have a higher risk of mortality from COVID-19 than those without cancer. Patients younger than 50 years with cancer treatment have the highest relative risk of death. Continued action is needed to mitigate the poor outcomes in patients with cancer, such as through optimising vaccination, long-acting passive immunisation, and early access to therapeutics. These findings underscore the importance of the ISARIC-WHO pandemic preparedness initiative. Funding: National Institute for Health Research and the Medical Research Council.
MeSH term(s)	Humans ; COVID-19/mortality ; COVID-19/epidemiology ; Neoplasms/mortality ; Neoplasms/therapy ; Male ; Female ; Prospective Studies ; Aged ; Middle Aged ; Hospital Mortality ; United Kingdom/epidemiology ; SARS-CoV-2 ; Adult ; Aged, 80 and over ; Pandemics
Language	English
Publishing date	2024-04-12
Publishing country	England
Document type	Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
ZDB-ID	2049730-1
ISSN	1474-5488 ; 1470-2045
ISSN (online)	1474-5488
ISSN	1470-2045
DOI	10.1016/S1470-2045(24)00107-4
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Zs.A 5696: 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)
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Article ; Online: The Potent G-Quadruplex-Binding Compound QN-302 Downregulates S100P Gene Expression in Cells and in an In Vivo Model of Pancreatic Cancer.

Ahmed, Ahmed A / Greenhalf, William / Palmer, Daniel H / Williams, Nicole / Worthington, Jenny / Arshad, Tariq / Haider, Shozeb / Alexandrou, Effrosyni / Guneri, Dilek / Waller, Zoe A E / Neidle, Stephen

Molecules (Basel, Switzerland)

2023 Volume 28, Issue 6

Abstract: The naphthalene diimide compound QN-302, designed to bind to G-quadruplex DNA sequences within the promoter regions of cancer-related genes, has high anti-proliferative activity in pancreatic cancer cell lines and anti-tumor activity in several ... ...

Abstract	The naphthalene diimide compound QN-302, designed to bind to G-quadruplex DNA sequences within the promoter regions of cancer-related genes, has high anti-proliferative activity in pancreatic cancer cell lines and anti-tumor activity in several experimental models for the disease. We show here that QN-302 also causes downregulation of the expression of the
MeSH term(s)	Humans ; G-Quadruplexes ; Cell Line, Tumor ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Calcium-Binding Proteins/metabolism ; Gene Expression ; Neoplasm Proteins/metabolism ; Pancreatic Neoplasms
Chemical Substances	Calcium-Binding Proteins ; S100P protein, human ; Neoplasm Proteins
Language	English
Publishing date	2023-03-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules28062452
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Article ; Online: Single-Nucleotide Polymorphism to Associate Cancer Risk.

Shaw, Victoria / Bullock, Katie / Greenhalf, William

Methods in molecular biology (Clifton, N.J.)

2016 Volume 1381, Page(s) 93–110

Abstract: Genetic heterogeneity explains variation in predisposition for cancer. Whole-genome analysis allows risk to be quantified, giving better targeted screening and quantification of the personalized risk posed by environmental factors. Array-based approaches ...

Abstract	Genetic heterogeneity explains variation in predisposition for cancer. Whole-genome analysis allows risk to be quantified, giving better targeted screening and quantification of the personalized risk posed by environmental factors. Array-based approaches to whole-genome analysis are rapidly being overtaken by next-generation sequencing (NGS). In this review the different platforms currently available for NGS are compared and the opportunities and risks of this approach are discussed: including the informatics packages required and the ethical issues. Methods applicable to the personal genome machine (PGM) are given as an example of workflows.
MeSH term(s)	Genome, Human ; Genotyping Techniques/methods ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Neoplasms/genetics ; Polymerase Chain Reaction/methods ; Polymorphism, Single Nucleotide ; Single-Cell Analysis/methods
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-3204-7_6
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Article ; Online: Genomic profiling of idiopathic peri-hilar cholangiocarcinoma reveals new targets and mutational pathways.

Quinn, Leonard M / Haldenby, Sam / Antzcak, Philip / Fowler, Anna / Bullock, Katie / Kenny, John / Gilbert, Timothy / Andrews, Timothy / Diaz-Nieto, Rafael / Fenwick, Stephen / Jones, Robert / Costello-Goldring, Eithne / Poston, Graeme / Greenhalf, William / Palmer, Daniel / Malik, Hassan / Goldring, Chris

Scientific reports

2023 Volume 13, Issue 1, Page(s) 6681

Abstract: Peri-hilar cholangiocarcinoma (pCCA) is chemorefractory and limited genomic analyses have been undertaken in Western idiopathic disease. We undertook comprehensive genomic analyses of a U.K. idiopathic pCCA cohort to characterize its mutational profile ... ...

Abstract	Peri-hilar cholangiocarcinoma (pCCA) is chemorefractory and limited genomic analyses have been undertaken in Western idiopathic disease. We undertook comprehensive genomic analyses of a U.K. idiopathic pCCA cohort to characterize its mutational profile and identify new targets. Whole exome and targeted DNA sequencing was performed on forty-two resected pCCA tumors and normal bile ducts, with Gene Set Enrichment Analysis (GSEA) using one-tailed testing to generate false discovery rates (FDR). 60% of patients harbored one cancer-associated mutation, with two mutations in 20%. High frequency somatic mutations in genes not typically associated with cholangiocarcinoma included mTOR, ABL1 and NOTCH1. We identified non-synonymous mutation (p.Glu38del) in MAP3K9 in ten tumors, associated with increased peri-vascular invasion (Fisher's exact, p < 0.018). Mutation-enriched pathways were primarily immunological, including innate Dectin-2 (FDR 0.001) and adaptive T-cell receptor pathways including PD-1 (FDR 0.007), CD4 phosphorylation (FDR 0.009) and ZAP70 translocation (FDR 0.009), with overlapping HLA genes. We observed cancer-associated mutations in over half of our patients. Many of these mutations are not typically associated with cholangiocarcinoma yet may increase eligibility for contemporary targeted trials. We also identified a targetable MAP3K9 mutation, in addition to oncogenic and immunological pathways hitherto not described in any cholangiocarcinoma subtype.
MeSH term(s)	Humans ; Klatskin Tumor/pathology ; Bile Ducts, Intrahepatic/pathology ; Bile Duct Neoplasms/pathology ; Mutation ; Cholangiocarcinoma/pathology ; Genomics ; DNA Mutational Analysis ; MAP Kinase Kinase Kinases/genetics
Chemical Substances	MAP3K9 protein, human (EC 2.7.11.25) ; MAP Kinase Kinase Kinases (EC 2.7.11.25)
Language	English
Publishing date	2023-04-24
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/s41598-023-33096-0
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Article ; Online: Genetic and functional analysis of chymotrypsin-like protease (CTRL) in chronic pancreatitis.

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.

2023 Volume 23, Issue 8, Page(s) 957–963

Abstract: Background: Genetic predisposition is crucial in the pathogenesis of early-onset chronic pancreatitis (CP). So far, several genetic alterations have been identified as risk factors, predominantly in genes encoding digestive enzymes. However, many early- ... ...

Abstract	Background: Genetic predisposition is crucial in the pathogenesis of early-onset chronic pancreatitis (CP). So far, several genetic alterations have been identified as risk factors, predominantly in genes encoding digestive enzymes. However, many early-onset CP cases have no identified underlying cause. Chymotrypsins are a family of serine proteases that can cleave trypsinogen and lead to its degradation. Because genetic alterations in the chymotrypsins CTRC, CTRB1, and CTRB2 are associated with CP, we genetically and functionally investigated chymotrypsin-like protease (CTRL) as a potential risk factor. Methods: We screened 1005 non-alcoholic CP patients and 1594 controls for CTRL variants by exome sequencing. We performed Western blots and activity assays to analyse secretion and proteolytic activity. We measured BiP mRNA expression to investigate the potential impact of identified alterations on endoplasmic reticulum (ER) stress. Results: We identified 13 heterozygous non-synonymous CTRL variants: five exclusively in patients and three only in controls. Functionality was unchanged in 6/13 variants. Four alterations showed normal secretion but reduced (p.G20S, p.G56S, p.G61S) or abolished (p.S208F) activity. Another three variants (p.C201Y, p.G215R and p.C220G) were not secreted and already showed reduced or no activity intracellularly. However, intracellular retention did not lead to ER stress. Conclusion: We identified several CTRL variants, some showing potent effects on protease function and secretion. We observed these effects in variants found in patients and controls, and CTRL loss-of-function variants were not significantly more common in patients than controls. Therefore, CTRL is unlikely to play a relevant role in the development of CP.
MeSH term(s)	Humans ; Chymases/genetics ; Genetic Predisposition to Disease ; Mutation ; Pancreatitis, Chronic/genetics ; Pancreatitis, Chronic/metabolism ; Risk Factors
Chemical Substances	Chymases (EC 3.4.21.39)
Language	English
Publishing date	2023-11-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2056680-3
ISSN	1424-3911 ; 1424-3903
ISSN (online)	1424-3911
ISSN	1424-3903
DOI	10.1016/j.pan.2023.11.002
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Article ; Online: Serum biomarker-based early detection of pancreatic ductal adenocarcinomas with ensemble learning.

Nené, Nuno R / Ney, Alexander / Nazarenko, Tatiana / Blyuss, Oleg / Johnston, Harvey E / Whitwell, Harry J / Sedlak, Eva / Gentry-Maharaj, Aleksandra / Apostolidou, Sophia / Costello, Eithne / Greenhalf, William / Jacobs, Ian / Menon, Usha / Hsuan, Justin / Pereira, Stephen P / Zaikin, Alexey / Timms, John F

Communications medicine

2023 Volume 3, Issue 1, Page(s) 10

Abstract: Background: Earlier detection of pancreatic ductal adenocarcinoma (PDAC) is key to improving patient outcomes, as it is mostly detected at advanced stages which are associated with poor survival. Developing non-invasive blood tests for early detection ... ...

Abstract	Background: Earlier detection of pancreatic ductal adenocarcinoma (PDAC) is key to improving patient outcomes, as it is mostly detected at advanced stages which are associated with poor survival. Developing non-invasive blood tests for early detection would be an important breakthrough. Methods: The primary objective of the work presented here is to use a dataset that is prospectively collected, to quantify a set of cancer-associated proteins and construct multi-marker models with the capacity to predict PDAC years before diagnosis. The data used is part of a nested case-control study within the UK Collaborative Trial of Ovarian Cancer Screening and is comprised of 218 samples, collected from a total of 143 post-menopausal women who were diagnosed with pancreatic cancer within 70 months after sample collection, and 249 matched non-cancer controls. We develop a stacked ensemble modelling technique to achieve robustness in predictions and, therefore, improve performance in newly collected datasets. Results: Here we show that with ensemble learning we can predict PDAC status with an AUC of 0.91 (95% CI 0.75-1.0), sensitivity of 92% (95% CI 0.54-1.0) at 90% specificity, up to 1 year prior to diagnosis, and at an AUC of 0.85 (95% CI 0.74-0.93) up to 2 years prior to diagnosis (sensitivity of 61%, 95% CI 0.17-0.83, at 90% specificity). Conclusions: The ensemble modelling strategy explored here outperforms considerably biomarker combinations cited in the literature. Further developments in the selection of classifiers balancing performance and heterogeneity should further enhance the predictive capacity of the method.
Language	English
Publishing date	2023-01-20
Publishing country	England
Document type	Journal Article
ISSN	2730-664X
ISSN (online)	2730-664X
DOI	10.1038/s43856-023-00237-5
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Article ; Online: Blood levels of adiponectin and IL-1Ra distinguish type 3c from type 2 diabetes: Implications for earlier pancreatic cancer detection in new-onset diabetes.

Oldfield, Lucy / Evans, Anthony / Rao, Rohith Gopala / Jenkinson, Claire / Purewal, Tejpal / Psarelli, Eftychia E / Menon, Usha / Timms, John F / Pereira, Stephen P / Ghaneh, Paula / Greenhalf, William / Halloran, Christopher / Costello, Eithne

EBioMedicine

2022 Volume 75, Page(s) 103802

Abstract: Background: Screening for pancreatic ductal adenocarcinoma (PDAC) in populations at high risk is recommended. Individuals with new-onset type 2 diabetes mellitus (NOD) are the largest high-risk group for PDAC. To facilitate screening, we sought ... ...

Abstract	Background: Screening for pancreatic ductal adenocarcinoma (PDAC) in populations at high risk is recommended. Individuals with new-onset type 2 diabetes mellitus (NOD) are the largest high-risk group for PDAC. To facilitate screening, we sought biomarkers capable of stratifying NOD subjects into those with type 2 diabetes mellitus (T2DM) and those with the less prevalent PDAC-related diabetes (PDAC-DM), a form of type 3c DM commonly misdiagnosed as T2DM. Methods: Using mass spectrometry- and immunoassay-based methodologies in a multi-stage analysis of independent sample sets (n=443 samples), blood levels of 264 proteins were considered using Ingenuity Pathway Analysis, literature review and targeted training and validation. Findings: Of 30 candidate biomarkers evaluated in up to four independent patient sets, 12 showed statistically significant differences in levels between PDAC-DM and T2DM. The combination of adiponectin and interleukin-1 receptor antagonist (IL-1Ra) showed strong diagnostic potential, (AUC of 0.91; 95% CI: 0.84-0.99) for the distinction of T3cDM from T2DM. Interpretation: Adiponectin and IL-1Ra warrant further consideration for use in screening for PDAC in individuals newly-diagnosed with T2DM. Funding: North West Cancer Research, UK, Cancer Research UK, Pancreatic Cancer Action, UK.
MeSH term(s)	Adiponectin/blood ; Biomarkers ; Carcinoma, Pancreatic Ductal/diagnosis ; Diabetes Mellitus, Type 2/diagnosis ; Humans ; Interleukin 1 Receptor Antagonist Protein/blood ; Pancreatic Neoplasms/diagnosis
Chemical Substances	Adiponectin ; Biomarkers ; Interleukin 1 Receptor Antagonist Protein
Language	English
Publishing date	2022-01-03
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2021.103802
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Article ; Online: Combination therapy for the treatment of pancreatic cancer.

Greenhalf, William / Thomas, Amy

Anti-cancer agents in medicinal chemistry

2011 Volume 11, Issue 5, Page(s) 418–426

Abstract: Treatment of pancreatic cancer should be a relatively simple clinical problem, all that is needed is to find the features of pancreatic cancer cells that distinguish them from normal cells and target these differences. This is the basis of current ... ...

Abstract	Treatment of pancreatic cancer should be a relatively simple clinical problem, all that is needed is to find the features of pancreatic cancer cells that distinguish them from normal cells and target these differences. This is the basis of current therapies including gemcitabine and 5-FU which target DNA synthesis. Unfortunately, cancer cells become resistant to these therapies: By exclusion of drugs from cancer cells; by changes in enzymes metabolising the drugs; or by becoming more resistant to stress and apoptosis. Increasing levels of the drugs is limited by their somatic toxicity so numerous alternative therapies have been proposed. Testing these alternatives in clinical trials will be difficult unless they work with the standard treatments (e.g. gemcitabine). To date most work has concentrated on combining different S-phase targeting agents. Further incremental increase in survival benefit should be possible by targeting resistance to apoptosis, targeting stroma or even targeting multiple pathways in combination with gemcitabine.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Drug Resistance, Neoplasm ; Humans ; Molecular Targeted Therapy ; Pancreatic Neoplasms/drug therapy
Language	English
Publishing date	2011-03-21
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2217610-X
ISSN	1875-5992 ; 1871-5206
ISSN (online)	1875-5992
ISSN	1871-5206
DOI	10.2174/187152011795677391
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