<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.drupjournal.com//inpress?rss=yes"><title>Drug Resistance Updates - Articles in Press</title><description>Drug Resistance Updates RSS feed: Articles in Press. 
 Drug Resistance Updates  is a bimonthly publication that contains thought-provoking reviews and commentaries on important developments 
in drug resistance in infectious disease and cancer. 
 
It covers both basic research and clinical aspects of drug resistance, and involves 
disciplines as diverse as molecular biology, biochemistry, cell biology, pharmacology, microbiology, oncology and clinical medicine.

 
 
Articles are written by leaders in the field, in response to an invitation from the Editors, and are peer-reviewed prior to publication. 
Articles are clear, readable, and up-to-date, suitable for a multidisciplinary readership and include schematic diagrams and other illustrations 
conveying the major points of the article. The goal is to highlight recent areas of growth and put them in perspective.    
 
 • 
Reviews the best in clinical and basic drug resistance research in oncology and infectious disease  • Describes emerging technologies 
and therapies  • Highlights key references in the drug resistance literature  • Features commentaries on important 
research articles  • Emphasises common themes in microbial and cancer research 
 
Features include: 
 
 • Clear, concise 
reviews  • Interdisciplinary perspectives  • Summary tables and figures to convey key points  • Conference 
reports  • Literature analysis  
 
 
If you have a suggestion for a review article title or wish to discuss the opportunity 
to publish a manuscript of your own in  Drug Resistance Updates , please contact the the Publisher:  andrew.miller@elsevier.com .</description><link>http://www.drupjournal.com//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc.  </dc:rights><prism:publicationName>Drug Resistance Updates</prism:publicationName><prism:issn>1368-7646</prism:issn><prism:publicationDate>2010-03-18</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc.  </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.drupjournal.com/article/PIIS1368764610000051/abstract?rss=yes"/><rdf:li rdf:resource="http://www.drupjournal.com/article/PIIS136876461000004X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.drupjournal.com/article/PIIS1368764610000038/abstract?rss=yes"/><rdf:li rdf:resource="http://www.drupjournal.com/article/PIIS1368764610000026/abstract?rss=yes"/><rdf:li rdf:resource="http://www.drupjournal.com/article/PIIS1368764609000776/abstract?rss=yes"/><rdf:li rdf:resource="http://www.drupjournal.com/article/PIIS1368764609000764/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.drupjournal.com/article/PIIS1368764610000051/abstract?rss=yes"><title>Implication of microRNAs in drug resistance for designing novel cancer therapy - Corrected Proof</title><link>http://www.drupjournal.com/article/PIIS1368764610000051/abstract?rss=yes</link><description>Abstract: Recently, microRNAs (miRNAs) have received increasing attention in the field of cancer research. miRNAs play important roles in many normal biological processes; however, the aberrant miRNA expression and its correlation with the development and progression of cancers is an emerging field. Therefore, miRNAs could be used as biomarkers for diagnosis of cancer and prediction of prognosis. Importantly, some miRNAs could regulate the formation of cancer stem cells and the acquisition of epithelial–mesenchymal transition, which are critically associated with drug resistance. Moreover, some miRNAs could target genes related to drug sensitivity, resulting in the altered sensitivity of cancer cells to anti-cancer drugs. Emerging evidences have also shown that knock-down or re-expression of specific miRNAs by synthetic anti-sense oligonucleotides or pre-miRNAs could induce drug sensitivity, leading to increased inhibition of cancer cell growth, invasion, and metastasis. More importantly, recent studies have shown that natural agents including isoflavone, 3,3′-diindolylmethane, and (−)-epigallocatechin-3-gallate altered miRNA expression profiles, leading to an increased sensitivity of cancer cells to conventional therapeutics. These emerging results suggest that specific targeting of miRNAs by different approaches could open new avenues for cancer treatment through overcoming drug resistance and thereby improve the outcome of cancer therapy.</description><dc:title>Implication of microRNAs in drug resistance for designing novel cancer therapy - Corrected Proof</dc:title><dc:creator>Fazlul H. Sarkar, Yiwei Li, Zhiwei Wang, Dejuan Kong, Shadan Ali</dc:creator><dc:identifier>10.1016/j.drup.2010.02.001</dc:identifier><dc:source>Drug Resistance Updates (2010)</dc:source><dc:date>2010-03-18</dc:date><prism:publicationName>Drug Resistance Updates</prism:publicationName><prism:publicationDate>2010-03-18</prism:publicationDate></item><item rdf:about="http://www.drupjournal.com/article/PIIS136876461000004X/abstract?rss=yes"><title>The long road to colorectal cancer therapy: Searching for the right signals - Corrected Proof</title><link>http://www.drupjournal.com/article/PIIS136876461000004X/abstract?rss=yes</link><description>Abstract: During the last 25 years, improvements in our understanding of signaling processes mediating tumor initiation, growth and dissemination have opened the door towards increasingly efficient, selective, but also complex therapeutic approaches. In parallel, the better characterization of altered signaling pathways in tumor cells, as well as the relationship between these alterations and the sensitivity of tumors to given compounds, have forced us to contemplate the use of biomarkers allowing patient selection and evaluation of treatment efficacy. Such biomarkers should become a corner stone for the success of a more rational and “personalized” clinical approach to colorectal cancer. Here we give an overview of the “signaling pathway-selective” compounds that are currently in use or under clinical development in the setting of colorectal cancer (CRC) and we discuss promising targets, based on our current knowledge of colorectal tumor cell biology, such as Src family, Wnt and Hegdehog signaling.</description><dc:title>The long road to colorectal cancer therapy: Searching for the right signals - Corrected Proof</dc:title><dc:creator>Frédéric Hollande, Julie Pannequin, Dominique Joubert</dc:creator><dc:identifier>10.1016/j.drup.2009.01.002</dc:identifier><dc:source>Drug Resistance Updates (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>Drug Resistance Updates</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.drupjournal.com/article/PIIS1368764610000038/abstract?rss=yes"><title>Novel therapeutics in combination with radiotherapy to improve cancer treatment: Rationale, mechanisms of action and clinical perspective - Corrected Proof</title><link>http://www.drupjournal.com/article/PIIS1368764610000038/abstract?rss=yes</link><description>Abstract: Our increased understanding of the molecular processes underlying cellular sensitivity to ionizing radiation has led to the identification of novel targets for intervention. New agents have become available for combined use to overcome radioresistance and enhance the clinical efficacy of radiotherapy. This rational selection of potential radiosensitizers contrasts with the empirical approach that has dominated the field of chemo-radiotherapy over the last decades. It allows the identification of those patients who will benefit most from a specific combination by exploiting new predictive biomarkers of response. In this review we present several approaches of targeted radiosensitization and discuss the available in vitro and in vivo results that support their translation into clinical trials. We focus on EGFR-inhibiting, anti-angiogenic, apoptosis-modulating and PARP-interfering strategies.</description><dc:title>Novel therapeutics in combination with radiotherapy to improve cancer treatment: Rationale, mechanisms of action and clinical perspective - Corrected Proof</dc:title><dc:creator>Marcel Verheij, Conchita Vens, Baukelien van Triest</dc:creator><dc:identifier>10.1016/j.drup.2010.01.002</dc:identifier><dc:source>Drug Resistance Updates (2010)</dc:source><dc:date>2010-02-19</dc:date><prism:publicationName>Drug Resistance Updates</prism:publicationName><prism:publicationDate>2010-02-19</prism:publicationDate></item><item rdf:about="http://www.drupjournal.com/article/PIIS1368764610000026/abstract?rss=yes"><title>A message from the New Editor-in-Chief: Drug Resistance Updates—The past and the future - Corrected Proof</title><link>http://www.drupjournal.com/article/PIIS1368764610000026/abstract?rss=yes</link><description>Twelve years have passed since Drug Resistance Updates was founded. During this period the journal has maintained its original mission: to critically review and analyze chemotherapeutic resistance in infectious diseases and cancer; to integrate recent developments in both basic research and clinical medicine; and to highlight innovative strategies for current and emerging therapies. With the first issue of 2010 of Drug Resistance Updates a change of Editorship will be effectuated and a new Editor-in-Chief has taken over the tasks from Nafsika Georgopapadakou.</description><dc:title>A message from the New Editor-in-Chief: Drug Resistance Updates—The past and the future - Corrected Proof</dc:title><dc:creator>Christian G. Giske, Henk J. Broxterman</dc:creator><dc:identifier>10.1016/j.drup.2010.01.001</dc:identifier><dc:source>Drug Resistance Updates (2010)</dc:source><dc:date>2010-02-18</dc:date><prism:publicationName>Drug Resistance Updates</prism:publicationName><prism:publicationDate>2010-02-18</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.drupjournal.com/article/PIIS1368764609000776/abstract?rss=yes"><title>Evading tumor evasion: Current concepts and perspectives of anti-angiogenic cancer therapy - Corrected Proof</title><link>http://www.drupjournal.com/article/PIIS1368764609000776/abstract?rss=yes</link><description>Abstract: Within three decades, anti-angiogenic therapy has rapidly evolved into an integral component of current standard anti-cancer treatment. Anti-angiogenic therapy has fulfilled a number of its earlier proposed promises. The universality of this approach is demonstrated by the broad spectrum of malignant and benign tumor entities, as well as non-neoplastic diseases, that are currently treated with anti-angiogenic agents. In contrast to tumor cell targeting therapies, the development of acquired drug resistance (e.g., via mutations in growth factor receptor signaling genes) has not been described yet for the principal target of anti-angiogenic therapy—the tumor endothelium. Moreover, the tumor endothelium has emerged as a critical target of conventional cancer therapies, such as chemotherapy and radiotherapy. The presumption that tumor growth and metastasis are angiogenesis-dependent implies that the number of potential targets of an anti-cancer therapy could be reduced to those that stimulate the angiogenesis process. Therefore, the set of endogenous angiogenesis stimulants might constitute an “Achilles heel” of cancer. Direct targeting of tumor endothelium via, e.g., endogenous angiogenesis inhibitors poses another promising but clinically less explored therapeutic strategy. Indeed, the majority of current anti-angiogenic approaches block the activity of a single or at most a few pro-angiogenic proteins secreted by tumor cells or the tumor stroma. Based on our systems biology work on the angiogenic switch, we predicted that the redundancy of angiogenic signals might limit the efficacy of anti-angiogenic monotherapies. In support of this hypothesis, emerging experimental evidence suggests that tumors may become refractory or even evade the inhibition of a single pro-angiogenic pathway via compensatory upregulation of alternative angiogenic factors. Here, we discuss current concepts and propose novel strategies to overcome tumor evasion of anti-angiogenic therapy. We believe that early detection of tumors, prediction of tumor evasive mechanisms and rational design of anti-angiogenic combinations will direct anti-angiogenic therapy towards its ultimate goal—the conversion of cancer to a dormant, chronic, manageable disease.</description><dc:title>Evading tumor evasion: Current concepts and perspectives of anti-angiogenic cancer therapy - Corrected Proof</dc:title><dc:creator>Amir Abdollahi, Judah Folkman</dc:creator><dc:identifier>10.1016/j.drup.2009.12.001</dc:identifier><dc:source>Drug Resistance Updates (2010)</dc:source><dc:date>2010-01-11</dc:date><prism:publicationName>Drug Resistance Updates</prism:publicationName><prism:publicationDate>2010-01-11</prism:publicationDate></item><item rdf:about="http://www.drupjournal.com/article/PIIS1368764609000764/abstract?rss=yes"><title>TRAIL receptor targeting therapies for non-small cell lung cancer: Current status and perspectives - Corrected Proof</title><link>http://www.drupjournal.com/article/PIIS1368764609000764/abstract?rss=yes</link><description>Abstract: Non-small cell lung cancer (NSCLC) is a common and often fatal malignancy, diagnosed at an advanced stage in more than half of the cases. Chemo-resistance remains a major problem in the treatment of NSCLC patients with conventional chemotherapeutic agents. Therefore main research efforts are focused on the development of novel targeted agents. In this review we provide an overview on the use of TNF-related apoptosis-inducing ligand (TRAIL) receptor targeting agents in NSCLC models and in early clinical studies. Different TRAIL receptor targeting agents are available which have been tested in NSCLC models and some were tested in the clinic. The efficacy of these drugs as single agents in NSCLC models is discussed as well as different mechanisms of resistance that are found in NSCLC cell lines. In order to maximize sensitivity to TRAIL receptor targeting drugs, combined use with other drugs is of interest. The current status of tested combinations of TRAIL receptor targeting agents with other therapeutics, such as classical cytotoxics, Bcl-2 family targeting agents, proteasome inhibitors, EGFR inhibitors, histone deacetylase inhibitors and COX-2 inhibitors as well as their mechanisms in preclinical studies are discussed. Clinical studies on TRAIL targeted therapies in which NSCLC patients were included are discussed and future perspectives are considered.</description><dc:title>TRAIL receptor targeting therapies for non-small cell lung cancer: Current status and perspectives - Corrected Proof</dc:title><dc:creator>J.H. Stegehuis, L.H.A.M. de Wilt, E.G.E. de Vries, H.J. Groen, S. de Jong, F.A.E. Kruyt</dc:creator><dc:identifier>10.1016/j.drup.2009.11.001</dc:identifier><dc:source>Drug Resistance Updates (2009)</dc:source><dc:date>2009-12-28</dc:date><prism:publicationName>Drug Resistance Updates</prism:publicationName><prism:publicationDate>2009-12-28</prism:publicationDate></item></rdf:RDF>