554 results match your criteria Drug Resistance Updates[Journal]


Optimizing dosing of nitrofurantoin from a PK/PD point of view: What do we need to know?

Drug Resist Updat 2019 Mar 20;43:1-9. Epub 2019 Mar 20.

Department of Medical Microbiology and Infectious Diseases, Erasmus University Medical Center, Rotterdam, the Netherlands. Electronic address:

Nitrofurantoin is an old antibiotic and an important first-line oral antibiotic for the treatment of uncomplicated urinary tract infections. However despite its long term use for over 60 years, little information is available with respect to its dose justification and this may be the reason of highly variable recommended doses and dosing schedules. Furthermore, nitrofurantoin is not a uniform product -crystal sizes of nitrofurantoin, and therefore pharmacokinetic properties, differ significantly by product. Read More

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http://dx.doi.org/10.1016/j.drup.2019.03.001DOI Listing

Glioblastoma cancer stem cell biology: Potential theranostic targets.

Drug Resist Updat 2019 01 8;42:35-45. Epub 2019 Mar 8.

Pediatric Stem Cell Transplant Department, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. Electronic address:

Glioblastoma multiforme (GBM) is among the most incurable cancers. GBMs survival rate has not markedly improved, despite new radical surgery protocols, the introduction of new anticancer drugs, new treatment protocols, and advances in radiation techniques. The low efficacy of therapy, and short interval between remission and recurrence, could be attributed to the resistance of a small fraction of tumorigenic cells to treatment. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S13687646193000
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http://dx.doi.org/10.1016/j.drup.2018.03.003DOI Listing
January 2019
7 Reads
9.121 Impact Factor

Can Saccharomyces cerevisiae keep up as a model system in fungal azole susceptibility research?

Drug Resist Updat 2019 01 15;42:22-34. Epub 2019 Feb 15.

VIB-KU Leuven Center for Microbiology, Flanders, Belgium; Laboratory of Molecular Cell Biology, Institute of Botany and Microbiology, KU Leuven, Leuven, Belgium. Electronic address:

The difficulty of manipulation and limited availability of genetic tools for use in many pathogenic fungi hamper fast and adequate investigation of cellular metabolism and consequent possibilities for antifungal therapies. S. cerevisiae is a model organism that is used to study many eukaryotic systems. Read More

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http://dx.doi.org/10.1016/j.drup.2019.02.002DOI Listing
January 2019

KiSS1 in regulation of metastasis and response to antitumor drugs.

Drug Resist Updat 2019 01 11;42:12-21. Epub 2019 Feb 11.

Molecular Pharmacology Unit, Department of Applied Research and Technological Development, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42/via Venezian 1, 20133 Milan, Italy. Electronic address:

Metastatic dissemination of tumor cells represents a major obstacle towards cancer cure. Tumor cells with metastatic capacity are often resistant to chemotherapy. Experimental efforts revealed that the metastatic cascade is a complex process that involves multiple positive and negative regulators. Read More

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http://dx.doi.org/10.1016/j.drup.2019.02.001DOI Listing
January 2019

MicroRNAs as a drug resistance mechanism to targeted therapies in EGFR-mutated NSCLC: Current implications and future directions.

Drug Resist Updat 2019 01 28;42:1-11. Epub 2018 Nov 28.

Department of Medical Oncology, Amsterdam University Medical Center, VU University, 1081 HV Amsterdam, the Netherlands; Cancer Pharmacology Lab, AIRC Start-Up Unit, University of Pisa and Fondazione Pisana per la Scienza, 56100 Pisa, Italy. Electronic address:

The introduction of EGFR-tyrosine kinase inhibitors (TKIs) has revolutionized the treatment and prognosis of non-small cell lung cancer (NSCLC) patients harboring epidermal growth factor receptor (EGFR) mutations. However, these patients display disease progression driven by the onset of acquired mechanisms of drug resistance that limit the efficacy of EGFR-TKI to no longer than one year. Moreover, a small fraction of EGFR-mutated NSCLC patients does not benefit from this targeted treatment due to primary (i. Read More

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http://dx.doi.org/10.1016/j.drup.2018.11.002DOI Listing
January 2019
3 Reads

The AbaR antibiotic resistance islands found in Acinetobacter baumannii global clone 1 - Structure, origin and evolution.

Drug Resist Updat 2018 11 2;41:26-39. Epub 2018 Nov 2.

School of Molecular and Microbial Biosciences, The University of Sydney, NSW 2006, Australia. Electronic address:

In multiply resistant Acinetobacter baumannii, complex transposons located in the chromosomal comM gene carry antibiotic and heavy metal resistance determinants. For one type, known collectively as AbaR, the ancestral form, AbaR0, entered a member of global clone 1 (GC1) in the mid 1970s and continued to evolve in situ forming many variants. In AbaR0, antibiotic and mercuric ion resistance genes are located between copies of a cadmium-zinc resistance transposon, Tn6018, and this composite transposon is in a class III transposon, Tn6019, carrying arsenate/arsenite resistance genes and five tni transposition genes. Read More

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http://dx.doi.org/10.1016/j.drup.2018.10.003DOI Listing
November 2018
2 Reads

Modulating ROS to overcome multidrug resistance in cancer.

Drug Resist Updat 2018 11 14;41:1-25. Epub 2018 Nov 14.

Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, 11439, USA. Electronic address:

The successful treatment of cancer has significantly improved as a result of targeted therapy and immunotherapy. However, during chemotherapy, cancer cells evolve and can acquire "multidrug resistance" (MDR), which significantly limits the efficacy of cancer treatment and impacts patient survival and quality of life. Among the approaches to reverse MDR, modulating reactive oxidative species (ROS) may represent a strategy to kill MDR cancer cells that are mechanistically diverse. Read More

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http://dx.doi.org/10.1016/j.drup.2018.11.001DOI Listing
November 2018
35 Reads

Precision medicine in head and neck cancer.

Drug Resist Updat 2018 09 25;40:13-16. Epub 2018 Sep 25.

The Oncology Institute, Radiation Oncology Unit, Israel; Head and Neck Center, Israel.

Head and Neck cancer is among the most common cancers worldwide, with a high prevalence in south East Asia, Brazil and central Europe. Head and Neck Squamous cell carcinoma (HNSCC) is associated with elevated mutational load but lacks specific genetic mutations. Exposure to carcinogens including tobacco and alcohol are the most dominant etiologic factors of HNSCC, while Epstein-Barr (HBV) and Human Papilloma Viruses (HPV) are associated with nasopharyngeal and oropharyngeal carcinoma, respectively. Read More

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http://dx.doi.org/10.1016/j.drup.2018.09.001DOI Listing
September 2018
19 Reads

A close look onto structural models and primary ligands of metallo-β-lactamases.

Drug Resist Updat 2018 09 25;40:1-12. Epub 2018 Aug 25.

Center for Biocrystallographic Research, Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznan, Poland; Department of Crystallography, Faculty of Chemistry, A. Mickiewicz University, Poznan, Poland. Electronic address:

β-Lactamases are hydrolytic enzymes capable of opening the β-lactam ring of antibiotics such as penicillin, thus endowing the bacteria that produce them with antibiotic resistance. Of particular medical concern are metallo-β-lactamases (MBLs), with an active site built around coordinated Zn cations. MBLs are pan-reactive enzymes that can break down almost all classes of β-lactams, including such last-resort antibiotics as carbapenems. Read More

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http://dx.doi.org/10.1016/j.drup.2018.08.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6260963PMC
September 2018
6 Reads

Update on prevalence and mechanisms of resistance to linezolid, tigecycline and daptomycin in enterococci in Europe: Towards a common nomenclature.

Drug Resist Updat 2018 09 2;40:25-39. Epub 2018 Nov 2.

Department of Infectious Diseases, Division of Nosocomial Pathogens and Antibiotic Resistances, Robert Koch Institute, Wernigerode, Germany. Electronic address:

Vancomycin-resistant enterococci (VRE) are important nosocomial pathogens. Invasive VRE infections are difficult to treat since common therapeutic options including ampicillin and glycopeptides often fail. In vitro, most VRE remain susceptible to last-resort antibiotics such as linezolid, tigecycline and daptomycin. Read More

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http://dx.doi.org/10.1016/j.drup.2018.10.002DOI Listing
September 2018
21 Reads

WINDOW consortium: A path towards increased therapy efficacy against glioblastoma.

Drug Resist Updat 2018 09 30;40:17-24. Epub 2018 Oct 30.

Department of Neurosurgery, Brain Tumor Center Amsterdam, Amsterdam University Medical Center, Cancer Center Amsterdam, De Boelelaan 1117, 1081 HZ, Amsterdam, Netherlands. Electronic address:

Glioblastoma is the most common and malignant form of brain cancer, for which the standard treatment is maximal surgical resection, radiotherapy and chemotherapy. Despite these interventions, mean overall survival remains less than 15 months, during which extensive tumor infiltration throughout the brain occurs. The resulting metastasized cells in the brain are characterized by chemotherapy resistance and extensive intratumoral heterogeneity. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S13687646183004
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http://dx.doi.org/10.1016/j.drup.2018.10.001DOI Listing
September 2018
18 Reads

Host genetic profiling to increase drug safety in colorectal cancer from discovery to implementation.

Drug Resist Updat 2018 07 10;39:18-40. Epub 2018 Jul 10.

Experimental and Clinical Pharmacology Unit, Centro di Riferimento Oncologico - National Cancer Institute, 33081 Aviano, Italy. Electronic address:

Adverse events affect the pharmacological treatment of approximately 90% of colorectal cancer (CRC) patients at any stage of the disease. Chemotherapy including fluoropyrimidines, irinotecan, and oxaliplatin is the cornerstone of the pharmacological treatment of CRC. The introduction of novel targeted agents, as anti-EGFR (i. Read More

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http://dx.doi.org/10.1016/j.drup.2018.07.001DOI Listing
July 2018
21 Reads

Targeting invadopodia for blocking breast cancer metastasis.

Drug Resist Updat 2018 07 17;39:1-17. Epub 2018 May 17.

Laboratory of Cell Migration and Invasion, The Azrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel. Electronic address:

Dissemination of cancer cells from the primary tumor and their spread to distant sites of the body is the leading cause of mortality in metastatic cancer patients. Metastatic cancer cells invade surrounding tissues and blood vessels by forming F-actin-rich protrusions known as invadopodia, which degrade the extracellular matrix and enable invasion of tumor cells through it. Invadopodia have now been observed in vivo, and recent evidence demonstrates direct molecular links between assembly of invadopodia and cancer metastasis in both mouse models and in human patients. Read More

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http://dx.doi.org/10.1016/j.drup.2018.05.002DOI Listing
July 2018
2 Reads

How mutations shape p53 interactions with the genome to promote tumorigenesis and drug resistance.

Drug Resist Updat 2018 05 9;38:27-43. Epub 2018 May 9.

Department of Biology, Technion-Israel Institute of Technology, Technion City, Haifa 32000, Israel. Electronic address:

The tumor suppressive transcription factor p53 regulates a wide array of cellular processes that confer upon cells an essential protection against cancer development. Wild-type p53 regulates gene expression by directly binding to DNA in a sequence-specific manner. p53 missense mutations are the most common mutations in malignant cells and can be regarded as synonymous with anticancer drug resistance and poor prognosis. Read More

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http://dx.doi.org/10.1016/j.drup.2018.05.001DOI Listing
May 2018
2 Reads

Fighting bacterial persistence: Current and emerging anti-persister strategies and therapeutics.

Drug Resist Updat 2018 05 10;38:12-26. Epub 2018 Apr 10.

Centre of Microbial and Plant Genetics, KU Leuven, Kasteelpark Arenberg 20, Box 2460, 3001 Leuven, Belgium; Center for Microbiology, Vlaams Instituut voor Biotechnologie, Leuven, Belgium. Electronic address:

In addition to the well-known strategies of antibiotic resistance and biofilm formation, bacterial populations possess an additional survival strategy to endure hostile environments or antibiotic exposure. A small fraction of transiently antibiotic-tolerant phenotypical variants, called persister cells, is capable of surviving treatment with high doses of antibiotics. When antibiotic pressure drops, persisters that switch back to a normal phenotype can resume growth, ensuring survival of the bacterial population. Read More

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http://dx.doi.org/10.1016/j.drup.2018.03.002DOI Listing
May 2018
5 Reads

How the Warburg effect supports aggressiveness and drug resistance of cancer cells?

Drug Resist Updat 2018 05 20;38:1-11. Epub 2018 Mar 20.

Inserm U1052, CNRS UMR5286, Centre de Recherche en Cancérologie de Lyon (CRCL), France; Université Lyon Claude Bernard 1, Lyon, France; ISPB, Faculté de Pharmacie, Lyon, France. Electronic address:

Cancer cells employ both conventional oxidative metabolism and glycolytic anaerobic metabolism. However, their proliferation is marked by a shift towards increasing glycolytic metabolism even in the presence of O (Warburg effect). HIF1, a major hypoxia induced transcription factor, promotes a dissociation between glycolysis and the tricarboxylic acid cycle, a process limiting the efficient production of ATP and citrate which otherwise would arrest glycolysis. Read More

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http://dx.doi.org/10.1016/j.drup.2018.03.001DOI Listing
May 2018
2 Reads

Thymidine kinase and protein kinase in drug-resistant herpesviruses: Heads of a Lernaean Hydra.

Drug Resist Updat 2018 03 31;37:1-16. Epub 2018 Jan 31.

Rega Institute for Medical Research, KU Leuven, Herestraat 49-box 1043, 3000 Leuven, Belgium. Electronic address:

Herpesviruses thymidine kinase (TK) and protein kinase (PK) allow the activation of nucleoside analogues used in anti-herpesvirus treatments. Mutations emerging in these two genes often lead to emergence of drug-resistant strains responsible for life-threatening diseases in immunocompromised populations. In this review, we analyze the binding of different nucleoside analogues to the TK active site of the three α-herpesviruses [Herpes Simplex Virus 1 and 2 (HSV-1 and HSV-2) and Varicella-Zoster Virus (VZV)] and present the impact of known mutations on the structure of the viral TKs. Read More

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http://dx.doi.org/10.1016/j.drup.2018.01.003DOI Listing
March 2018
6 Reads

Hepatitis C virus drug resistance associated substitutions and their clinical relevance: Update 2018.

Drug Resist Updat 2018 03 21;37:17-39. Epub 2018 Feb 21.

Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy. Electronic address:

Nowadays, due to the development of potent Direct-Acting Antiviral Agents (DAAs) that specifically target NS3, NS5A and NS5B viral proteins, several new and highly efficacious options to treat chronic Hepatitis C virus (HCV) infection are available. The natural presence of resistance associated substitutions (RASs), as well as their rapid emergence during incomplete drug-pressure, are intrinsic characteristics of HCV that greatly affect treatment outcome and the chances to achieve a virolgical cure. To date, a high number of RASs in NS3, NS5A, and NS5B have been associated in vivo and/or in vitro with reduced susceptibility to DAAs, but no comprehensive RASs list is available. Read More

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http://dx.doi.org/10.1016/j.drup.2018.01.004DOI Listing
March 2018
23 Reads

Redundant angiogenic signaling and tumor drug resistance.

Drug Resist Updat 2018 01 17;36:47-76. Epub 2018 Jan 17.

The Fred Wyszkowski Cancer Research Laboratory, Department of Biology, Technion-Israel Institute of Technology, Haifa, 3200000, Israel.

Angiogenesis research in the past two decades has contributed significantly towards understanding the molecular pathophysiology of cancer progression and inspired target-oriented research and pharma industry for the development of novel anti-angiogenic agents. Currently, over eleven drugs targeting angiogenesis have been approved by the FDA for the treatment of various malignancies. Of the registered anti-angiogenic clinical trials until the end of 2017 (ClinicalTrials. Read More

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http://dx.doi.org/10.1016/j.drup.2018.01.002DOI Listing
January 2018
4 Reads

New tools for old drugs: Functional genetic screens to optimize current chemotherapy.

Drug Resist Updat 2018 01 12;36:30-46. Epub 2018 Jan 12.

Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Bern, Switzerland; Division of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands. Electronic address:

Despite substantial advances in the treatment of various cancers, many patients still receive anti-cancer therapies that hardly eradicate tumor cells but inflict considerable side effects. To provide the best treatment regimen for an individual patient, a major goal in molecular oncology is to identify predictive markers for a personalized therapeutic strategy. Regarding novel targeted anti-cancer therapies, there are usually good markers available. Read More

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http://dx.doi.org/10.1016/j.drup.2018.01.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5844649PMC
January 2018
6 Reads

An update on β-lactamase inhibitor discovery and development.

Drug Resist Updat 2018 01 7;36:13-29. Epub 2017 Nov 7.

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, Via Aldo Moro 2, 53100 Siena, Italy. Electronic address:

Antibiotic resistance, and the emergence of pan-resistant clinical isolates, seriously threatens our capability to treat bacterial diseases, including potentially deadly hospital-acquired infections. This growing issue certainly requires multiple adequate responses, including the improvement of both diagnosis methods and use of antibacterial agents, and obviously the development of novel antibacterial drugs, especially active against Gram-negative pathogens, which represent an urgent medical need. Considering the clinical relevance of both β-lactam antibiotics and β-lactamase-mediated resistance, the discovery and development of combinations including a β-lactamase inhibitor seems to be particularly attractive, despite being extremely challenging due to the enormous diversity, both structurally and mechanistically, of the potential β-lactamase targets. Read More

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http://dx.doi.org/10.1016/j.drup.2017.11.002DOI Listing
January 2018
4 Reads

Targeting bacterial energetics to produce new antimicrobials.

Drug Resist Updat 2018 01 11;36:1-12. Epub 2017 Nov 11.

Department of Microbiology and Immunology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand; Maurice Wilkins Centre for Molecular Biodiscovery, The University of Auckland, Private Bag 92019, Auckland 1042, New Zealand. Electronic address:

From the war on drug resistance, through cancer biology, even to agricultural and environmental protection: there is a huge demand for rapid and effective solutions to control infections and diseases. The development of small molecule inhibitors was once an accepted "one-size fits all" approach to these varied problems, but persistence and resistance threaten to return society to a pre-antibiotic era. Only five essential cellular targets in bacteria have been developed for the majority of our clinically-relevant antibiotics. Read More

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http://dx.doi.org/10.1016/j.drup.2017.11.001DOI Listing
January 2018
6 Reads

Not only P-glycoprotein: Amplification of the ABCB1-containing chromosome region 7q21 confers multidrug resistance upon cancer cells by coordinated overexpression of an assortment of resistance-related proteins.

Drug Resist Updat 2017 05 16;32:23-46. Epub 2017 Oct 16.

Institute of Molecular Biology and Pathology, Italian National Research Council (IBPM-CNR), c/o Dept. Biochemical Sciences, Sapienza University, P.le A. Moro 5, 00185 Rome, Italy. Electronic address:

The development of drug resistance continues to be a dominant hindrance toward curative cancer treatment. Overexpression of a wide-spectrum of ATP-dependent efflux pumps, and in particular of ABCB1 (P-glycoprotein or MDR1) is a well-known resistance mechanism for a plethora of cancer chemotherapeutics including for example taxenes, anthracyclines, Vinca alkaloids, and epipodopyllotoxins, demonstrated by a large array of published papers, both in tumor cell lines and in a variety of tumors, including various solid tumors and hematological malignancies. Upon repeated or even single dose treatment of cultured tumor cells or tumors in vivo with anti-tumor agents such as paclitaxel and doxorubicin, increased ABCB1 copy number has been demonstrated, resulting from chromosomal amplification events at 7q11. Read More

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http://dx.doi.org/10.1016/j.drup.2017.10.003DOI Listing
May 2017
24 Reads

In cancer, A-to-I RNA editing can be the driver, the passenger, or the mechanic.

Drug Resist Updat 2017 05 4;32:16-22. Epub 2017 Oct 4.

Faculty of Biology, Technion - Israel Institute of Technology, Technion City, Haifa 32000, Israel. Electronic address:

In recent years, A-to-I RNA modifications performed by the Adenosine Deaminase Acting on RNA (ADAR) protein family were found to be expressed at altered levels in multiple human malignancies. A-to-I RNA editing changes adenosine to inosine on double stranded RNA, thereby changing transcript sequence and structure. Although A-to-I RNA editing have the potential to change essential mRNA transcripts, affecting their corresponding protein structures, most of the human editing sites identified to date reside in non-coding repetitive transcripts such as Alu elements. Read More

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http://dx.doi.org/10.1016/j.drup.2017.09.001DOI Listing
May 2017
11 Reads

Immunotherapy for triple-negative breast cancer: Existing challenges and exciting prospects.

Drug Resist Updat 2017 05 19;32:1-15. Epub 2017 Aug 19.

Department of Pharmacology, The Penn State Cancer Institute, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. Electronic address:

Patients with breast tumors that do not express the estrogen receptor, the progesterone receptor, nor Her-2/neu are hence termed "triple negatives", and generally have a poor prognosis, with high rates of systemic recurrence and refractoriness to conventional therapy regardless of the choice of adjuvant treatment. Thus, more effective therapeutic options are sorely needed for triple-negative breast cancer (TNBC), which occurs in approximately 20% of diagnosed breast cancers. In recent years, exploiting intrinsic mechanisms of the host immune system to eradicate cancer cells has achieved impressive success, and the advances in immunotherapy have yielded potential new therapeutic strategies for the treatment of this devastating subtype of breast cancer. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S13687646173003
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http://dx.doi.org/10.1016/j.drup.2017.07.002DOI Listing
May 2017
19 Reads

TAK-ing aim at chemoresistance: The emerging role of MAP3K7 as a target for cancer therapy.

Drug Resist Updat 2017 11 3;33-35:36-42. Epub 2017 Nov 3.

Digestive Molecular Clinical Oncology Research Unit, Department of Medicine, Università degli studi di Verona, Verona, Italy; Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address:

Cellular drug resistance remains the main obstacle to the clinical efficacy of cancer chemotherapy. Alterations in key pathways regulating cell cycle checkpoints, apoptosis and Epithelial to Mesenchymal Transition (EMT), such as the Mitogen-activated protein kinase (MAPK) pathway, appear to be closely associated to cancer chemoresistance. Transforming growth factor-β (TGF-β)- activated kinase 1 (TAK1, also known as MAP3K7) is a serine/threonine kinase in the mitogen-activated protein kinase (MAP3K) family. Read More

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http://dx.doi.org/10.1016/j.drup.2017.10.004DOI Listing
November 2017
11 Reads

Cancer Immunotherapy Getting Brainy: Visualizing the Distinctive CNS Metastatic Niche to Illuminate Therapeutic Resistance.

Drug Resist Updat 2017 11 14;33-35:23-35. Epub 2017 Oct 14.

Department of Radiology, Stanford University, Stanford, CA 94306, USA. Electronic address:

The advent of cancer immunotherapy (CIT) and its success in treating primary and metastatic cancer may offer substantially improved outcomes for patients. Despite recent advancements, many malignancies remain resistant to CIT, among which are brain metastases, a particularly virulent disease with no apparent cure. The immunologically unique niche of the brain has prompted compelling new questions in immuno-oncology such as the effects of tissue-specific differences in immune response, heterogeneity between primary tumors and distant metastases, and the role of spatiotemporal dynamics in shaping an effective anti-tumor immune response. Read More

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http://dx.doi.org/10.1016/j.drup.2017.10.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5728435PMC
November 2017
57 Reads

Antimicrobial blue light inactivation of pathogenic microbes: State of the art.

Drug Resist Updat 2017 11 13;33-35:1-22. Epub 2017 Oct 13.

Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address:

As an innovative non-antibiotic approach, antimicrobial blue light in the spectrum of 400-470nm has demonstrated its intrinsic antimicrobial properties resulting from the presence of endogenous photosensitizing chromophores in pathogenic microbes and, subsequently, its promise as a counteracter of antibiotic resistance. Since we published our last review of antimicrobial blue light in 2012, there have been a substantial number of new studies reported in this area. Here we provide an updated overview of the findings from the new studies over the past 5 years, including the efficacy of antimicrobial blue light inactivation of different microbes, its mechanism of action, synergism of antimicrobial blue light with other angents, its effect on host cells and tissues, the potential development of resistance to antimicrobial blue light by microbes, and a novel interstitial delivery approach of antimicrobial blue light. Read More

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http://dx.doi.org/10.1016/j.drup.2017.10.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5699711PMC
November 2017
11 Reads

A mechanopharmacology approach to overcome chemoresistance in pancreatic cancer.

Drug Resist Updat 2017 03 24;31:43-51. Epub 2017 Jul 24.

Department of Medical Oncology, VU University Medical Center Amsterdam, Amsterdam, The Netherlands; Cancer Pharmacology Lab, AIRC Start-Up Unit, University Hospital of Pisa, Pisa, Italy; Institute for Nanoscience and Nanotechnologies, CNR-Nano, Pisa. Electronic address:

Pancreatic ductal adenocarcinoma (PDAC) is a highly chemoresistant malignancy. This chemoresistant phenotype has been historically associated with genetic factors. Major biomedical research efforts were concentrated that resulted in the identification of subtypes characterized by specific genetic lesions and gene expression signatures that suggest important biological differences. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S13687646173002
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http://dx.doi.org/10.1016/j.drup.2017.07.001DOI Listing
March 2017
12 Reads

Can microbial cells develop resistance to oxidative stress in antimicrobial photodynamic inactivation?

Drug Resist Updat 2017 03 26;31:31-42. Epub 2017 Jul 26.

Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA, 02114, USA; Department of Dermatology, Harvard Medical School, Boston, MA, 02115, USA; Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA, 02139, USA. Electronic address:

Infections have been a major cause of disease throughout the history of humans on earth. With the introduction of antibiotics, it was thought that infections had been conquered. However, bacteria have been able to develop resistance to antibiotics at an exponentially increasing rate. Read More

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http://dx.doi.org/10.1016/j.drup.2017.07.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5673603PMC
March 2017
15 Reads

Targeted nanomedicine for cancer therapeutics: Towards precision medicine overcoming drug resistance.

Drug Resist Updat 2017 03 21;31:15-30. Epub 2017 May 21.

The Fred Wyszkowski Cancer Research Laboratory, Department of Biology, Technion - Israel Institute of Technology, Haifa, 3200000, Israel. Electronic address:

Intrinsic anticancer drug resistance appearing prior to chemotherapy as well as acquired resistance due to drug treatment, remain the dominant impediments towards curative cancer therapy. Hence, novel targeted strategies to overcome cancer drug resistance constitute a key aim of cancer research. In this respect, targeted nanomedicine offers innovative therapeutic strategies to overcome the various limitations of conventional chemotherapy, enabling enhanced selectivity, early and more precise cancer diagnosis, individualized treatment as well as overcoming of drug resistance, including multidrug resistance (MDR). Read More

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http://dx.doi.org/10.1016/j.drup.2017.05.002DOI Listing
March 2017
26 Reads

New strategies for targeting and treatment of multi-drug resistant Staphylococcus aureus.

Drug Resist Updat 2017 03 6;31:1-14. Epub 2017 Apr 6.

Brazilian National Laboratory for Biosciences (LNBio), CNPEM, Campinas, São Paulo, Brazil; Institut de Biologie Structurale (IBS), Univ Grenoble Alpes, CEA, CNRS, Bacterial Pathogenesis Group, 38044 Grenoble, France. Electronic address:

Staphylococcus aureus is a major cause of bacterial infection in humans, and has been notoriously able to acquire resistance to a variety of antibiotics. An example is methicillin-resistant S. aureus (MRSA), which despite having been initially associated with clinical settings, now is one of the key causative agents of community-acquired infections. Read More

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http://dx.doi.org/10.1016/j.drup.2017.03.001DOI Listing
March 2017
8 Reads

Active efflux in dormant bacterial cells - New insights into antibiotic persistence.

Drug Resist Updat 2017 01 29;30:7-14. Epub 2016 Nov 29.

Biodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, China, 100871. Electronic address:

Bacterial persisters are phenotypic variants of an isogenic cell population that can survive antibiotic treatment and resume growth after the antibiotics have been removed. Cell dormancy has long been considered the principle mechanism underlying persister formation. However, dormancy alone is insufficient to explain the full range of bacterial persistence. Read More

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http://dx.doi.org/10.1016/j.drup.2016.11.002DOI Listing
January 2017
12 Reads

Drug-biomarker co-development in oncology - 20 years and counting.

Drug Resist Updat 2017 01 21;30:48-62. Epub 2017 Feb 21.

Office of Biotechnology Products, Center for Drug Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, United States. Electronic address:

Predictive biomarkers for oncology are necessary to accurately identify patients who will benefit from anticancer treatment. Recently approved oncology drugs target discrete molecular aberrations or pathways in tumor cells and consequently are active on a subset of patient population, yet clinical studies have shown that not all biomarker-positive patients respond. The advancement of predictive biomarkers needs to detect novel and evolving drug resistance mechanisms, not only to guide the selection of patient subsets for specific treatments, but to identify new therapeutic targets. Read More

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http://dx.doi.org/10.1016/j.drup.2017.02.002DOI Listing
January 2017
11 Reads

Novel immune check point inhibiting antibodies in cancer therapy-Opportunities and challenges.

Drug Resist Updat 2017 01 4;30:39-47. Epub 2017 Feb 4.

Department of Molecular Microbiology and Biotechnology, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 69978, Israel. Electronic address:

Drug resistance of tumor cells to chemotherapy is limiting the therapeutic efficacy of most anticancer drugs and represents a major obstacle in medical oncology. However, treatment of various human malignancies with biologics, mostly monoclonal antibodies (mAbs), is not limited by such chemoresistance mechanisms. However, other resistance or evasion mechanisms limit the efficacy to anticancer therapeutic mAbs that engage tumor-associated antigens on the surface of the malignant cells. Read More

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http://dx.doi.org/10.1016/j.drup.2017.02.001DOI Listing
January 2017
13 Reads

Inverse correlation between the metastasis suppressor RKIP and the metastasis inducer YY1: Contrasting roles in the regulation of chemo/immuno-resistance in cancer.

Drug Resist Updat 2017 01 9;30:28-38. Epub 2017 Jan 9.

Department of Microbiology, Immunology & Molecular Genetics, David Geffen School of Medicine, UCLA, Los Angeles, CA, 90095, United States. Electronic address:

Several gene products have been postulated to mediate inherent and/or acquired anticancer drug resistance and tumor metastasis. Among these, the metastasis suppressor and chemo-immuno-sensitizing gene product, Raf Kinase Inhibitor Protein (RKIP), is poorly expressed in many cancers. In contrast, the metastasis inducer and chemo-immuno-resistant factor Yin Yang 1 (YY1) is overexpressed in many cancers. Read More

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http://dx.doi.org/10.1016/j.drup.2017.01.001DOI Listing
January 2017
11 Reads

The importance of breast cancer resistance protein to the kidneys excretory function and chemotherapeutic resistance.

Drug Resist Updat 2017 01 11;30:15-27. Epub 2017 Jan 11.

Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Universiteitsweg 99, Utrecht 3584 CG, The Netherlands. Electronic address:

The relevance of membrane transporters gained momentum in recent years and it is now widely recognized that transporters are key players in drug disposition and chemoresistance. As such, the kidneys harbor a variety of drug transporters and are one of the main routes for xenobiotic excretion. The breast cancer resistance protein (BCRP/ABCG2) is widely accepted as a key mediator of anticancer drug resistance and is a prominent renal drug transporter. Read More

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http://dx.doi.org/10.1016/j.drup.2017.01.002DOI Listing
January 2017
12 Reads

Sensitizing pathogens to antibiotics using the CRISPR-Cas system.

Drug Resist Updat 2017 01 27;30:1-6. Epub 2016 Nov 27.

Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. Electronic address:

The extensive use of antibiotics over the last century has resulted in a significant artificial selection pressure for antibiotic-resistant pathogens to evolve. Various strategies to fight these pathogens have been introduced including new antibiotics, naturally-derived enzymes/peptides that specifically target pathogens and bacteriophages that lyse these pathogens. A new tool has recently been introduced in the fight against drug-resistant pathogens-the prokaryotic defense mechanism-clustered regularly interspaced short palindromic repeats-CRISPR associated (CRISPR-Cas) system. Read More

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http://dx.doi.org/10.1016/j.drup.2016.11.001DOI Listing
January 2017
7 Reads

Corrigendum to "The reduced concentration of citrate in cancer cells: An indicator of cancer aggressiveness and a possible therapeutic target" [Drug Resistance Updates 29 (2016) 47-53].

Drug Resist Updat 2017 01 8;30:63. Epub 2017 Feb 8.

ISPB, Faculté de Pharmacie, Lyon, France; Université Lyon 1, Lyon, France; INSERM U1052, CNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, France. Electronic address:

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https://linkinghub.elsevier.com/retrieve/pii/S13687646173000
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http://dx.doi.org/10.1016/j.drup.2017.01.003DOI Listing
January 2017
10 Reads

New insights and evolving role of pegylated liposomal doxorubicin in cancer therapy.

Drug Resist Updat 2016 11 29;29:90-106. Epub 2016 Oct 29.

Department of Immunotherapeutics and Biotechnology, Texas Tech University Health Sciences Center School of Pharmacy, Abilene, TX, USA.

We herein review various pharmacological and clinical aspects of pegylated liposomal doxorubicin (PLD), the first nanomedicine to be approved for cancer therapy, and discuss the gap between its potent antitumor activity in preclinical studies and its comparatively modest achievements in clinical studies and limited use in clinical practice. PLD is a complex formulation of doxorubicin based on pharmaceutical nanotechnology with unique pharmacokinetic and pharmacodynamic properties. Its long circulation time with stable retention of the payload and its accumulation in tumors with high vascular permeability both result in important advantages over conventional chemotherapy. Read More

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http://dx.doi.org/10.1016/j.drup.2016.10.003DOI Listing
November 2016
31 Reads
6 Citations
9.121 Impact Factor

Molecular mechanisms and clinical implications of bacterial persistence.

Drug Resist Updat 2016 11 15;29:76-89. Epub 2016 Oct 15.

Centre of Microbial and Plant Genetics, KU Leuven, Leuven, Belgium. Electronic address:

Any bacterial population harbors a small number of phenotypic variants that survive exposure to high concentrations of antibiotic. Importantly, these so-called 'persister cells' compromise successful antibiotic therapy of bacterial infections and are thought to contribute to the development of antibiotic resistance. Intriguingly, drug-tolerant persisters have also been identified as a factor underlying failure of chemotherapy in tumor cell populations. Read More

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http://dx.doi.org/10.1016/j.drup.2016.10.002DOI Listing
November 2016
11 Reads

Heparanase: From basic research to therapeutic applications in cancer and inflammation.

Drug Resist Updat 2016 11 6;29:54-75. Epub 2016 Oct 6.

Cancer and Vascular Biology Research Center, Rappaport Faculty of Medicine, Technion, Haifa 31096, Israel.

Heparanase, the sole heparan sulfate degrading endoglycosidase, regulates multiple biological activities that enhance tumor growth, angiogenesis and metastasis. Heparanase expression is enhanced in almost all cancers examined including various carcinomas, sarcomas and hematological malignancies. Numerous clinical association studies have consistently demonstrated that upregulation of heparanase expression correlates with increased tumor size, tumor angiogenesis, enhanced metastasis and poor prognosis. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S13687646163004
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http://dx.doi.org/10.1016/j.drup.2016.10.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5447241PMC
November 2016
13 Reads

The reduced concentration of citrate in cancer cells: An indicator of cancer aggressiveness and a possible therapeutic target.

Drug Resist Updat 2016 11 21;29:47-53. Epub 2016 Sep 21.

Proliferating cells reduce their oxidative metabolism and rely more on glycolysis, even in the presence of O (Warburg effect). This shift in metabolism reduces citrate biosynthesis and diminishes intracellular acidity, both of which promote glycolysis sustaining tumor growth. Because citrate is the donor of acetyl-CoA, its reduced production favors a deacetylation state of proteins favoring resistance to apoptosis and epigenetic changes, both processes contributing to tumor aggressiveness. Read More

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http://dx.doi.org/10.1016/j.drup.2016.09.003DOI Listing
November 2016
10 Reads

The rapid spread of carbapenem-resistant Enterobacteriaceae.

Drug Resist Updat 2016 11 19;29:30-46. Epub 2016 Sep 19.

Center for Genome Sciences and System Biology, Washington University School of Medicine, 4515 McKinley Avenue, Campus Box 8510, St. Louis, MO 63110, USA; Department of Pathology & Immunology, Washington University School of Medicine, 660 South Euclid Ave, St. Louis, MO 63110, USA; Department of Biomedical Engineering, Washington University in Saint Louis, 1 Brookings Drive, St. Louis, MO 63130, USA; Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave, St. Louis, MO 63110, USA. Electronic address:

Carbapenems, our one-time silver bullet for multidrug resistant bacterial infections, are now threatened by widespread dissemination of carbapenem-resistant Enterobacteriaceae (CRE). Successful expansion of Enterobacteriaceae clonal groups and frequent horizontal gene transfer of carbapenemase expressing plasmids are causing increasing carbapenem resistance. Recent advances in genetic and phenotypic detection facilitate global surveillance of CRE diversity and prevalence. Read More

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http://dx.doi.org/10.1016/j.drup.2016.09.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5140036PMC
November 2016
12 Reads

Plasmid-mediated quinolone resistance: Two decades on.

Drug Resist Updat 2016 11 13;29:13-29. Epub 2016 Sep 13.

Departamento de Microbiología, Universidad de Sevilla, Sevilla, Spain; Spanish Network for the Research in Infectious Diseases (REIPI RD12/0015), Instituto de Salud Carlos III, Madrid, Spain; Unidad de Enfermedades Infecciosas y Microbiología Clínica, Hospital Universitario Virgen Macarena, Sevilla, Spain.

After two decades of the discovery of plasmid-mediated quinolone resistance (PMQR), three different mechanisms have been associated to this phenomenon: target protection (Qnr proteins, including several families with multiple alleles), active efflux pumps (mainly QepA and OqxAB pumps) and drug modification [AAC(6')-Ib-cr acetyltransferase]. PMQR genes are usually associated with mobile or transposable elements on plasmids, and, in the case of qnr genes, are often incorporated into sul1-type integrons. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. Read More

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http://dx.doi.org/10.1016/j.drup.2016.09.001DOI Listing
November 2016
8 Reads

The semaphorins and their receptors as modulators of tumor progression.

Drug Resist Updat 2016 11 28;29:1-12. Epub 2016 Aug 28.

The Cancer Research and Vascular Biology Center, The Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa 31096, Israel.

The semaphorins were initially characterized as repulsive axon guidance factors. However, they are currently also recognized as important regulators of diverse biological processes which include regulation of immune responses, angiogenesis, organogenesis, and a variety of additional physiological and developmental functions. The semaphorin family consists of more than 20 genes divided into seven subfamilies, all of which contain the sema domain signature. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S13687646163003
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http://dx.doi.org/10.1016/j.drup.2016.08.001DOI Listing
November 2016
19 Reads

Renew or die: The molecular mechanisms of peptidoglycan recycling and antibiotic resistance in Gram-negative pathogens.

Drug Resist Updat 2016 09 29;28:91-104. Epub 2016 Jul 29.

Department of Crystallography and Structural Biology, Inst. Química-Física "Rocasolano", CSIC, Serrano 119, 28006 Madrid, Spain. Electronic address:

Antimicrobial resistance is one of the most serious health threats. Cell-wall remodeling processes are tightly regulated to warrant bacterial survival and in some cases are directly linked to antibiotic resistance. Remodeling produces cell-wall fragments that are recycled but can also act as messengers for bacterial communication, as effector molecules in immune response and as signaling molecules triggering antibiotic resistance. Read More

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http://dx.doi.org/10.1016/j.drup.2016.07.002DOI Listing
September 2016
10 Reads

Antibiotic resistance in Burkholderia species.

Drug Resist Updat 2016 09 30;28:82-90. Epub 2016 Jul 30.

Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute and Institute for Therapeutic Innovation, University of Florida, Gainesville, FL, USA. Electronic address:

The genus Burkholderia comprises metabolically diverse and adaptable Gram-negative bacteria, which thrive in often adversarial environments. A few members of the genus are prominent opportunistic pathogens. These include Burkholderia mallei and Burkholderia pseudomallei of the B. Read More

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http://dx.doi.org/10.1016/j.drup.2016.07.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5022785PMC
September 2016
6 Reads

Old drugs, novel ways out: Drug resistance toward cytotoxic chemotherapeutics.

Drug Resist Updat 2016 09 16;28:65-81. Epub 2016 Jul 16.

Division of Cell Biology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands; Department of Chemical Immunology, LUMC, Leiden, The Netherlands. Electronic address:

Efficacy of chemotherapy in the treatment of distinct malignancies is often hampered by drug resistance arising in the tumor. Understanding the molecular basis of drug resistance and translating this knowledge into personalized treatment decisions can enhance therapeutic efficacy and even curative outcome. Over the years, multiple drug resistance mechanisms have been identified that enable tumors to cope with the damage instigated by a specific drug or group of anti-tumor agents. Read More

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http://dx.doi.org/10.1016/j.drup.2016.07.001DOI Listing
September 2016
11 Reads