Topic: Targeted cancer therapy

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A special issue of Cancer Drug Resistance.

Deadline for manuscript submissions: 30 Jun 2018

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Guest Editor(s)

  • Dr. Elisa Giovannetti, MD, PhD
    Lab Medical Oncology, VU University Medical Center (VUmc), Cancer Center Amsterdam, The Netherlands.
    Cancer Pharmacology Lab, AIRC Start-Up Unit, University of Pisa, Italy.

    Website | E-mail

  • Dr. Jose Antonio Rodriguez, PhD
    Department of Genetics, Physical Anthropology and Animal Physiology (School of Medicine and Nursing) of the University of the Basque Country (UPV/EHU), Basque Country, Spain.

    Website | E-mail

Special Issue Introduction:

Targeted therapies in cancer aim to specifically block the activity of crucial proteins or signaling pathways necessary for the growth and/or survival of tumor cells. A major breakthrough in targeted cancer therapy was the introduction nearly two decades ago of imatinib, an inhibitor of the BCR-ABL tyrosine kinase for the treatment of chronic myeloid leukemia. Over the last years, significant advances in our understanding of tumor biology have facilitated the development of many drugs targeting not only kinases, but also other protein families and cellular processes. Several of these agents are currently employed or being implemented for the treatment of different hematologic and solid malignancies, such as lung cancer.
The special issue on “Targeted cancer therapy” will include Reviews and Commentaries updating the clinical use of targeted agents in the treatment of different tumor types, and the mechanisms that underlie the action of drugs directed to different types of targets. The special issue will also include Research articles presenting novel outstanding data on all aspects of targeted cancer therapy. All submissions will undergo rigorous peer revision and will be published free of charge upon acceptance.

Keywords:

Biomarkers, personalized medicine, new approaches to cancer treatment, molecularly targeted drugs, mechanisms of targeted drugs, resistance to targeted therapies, novel targets

Submission Information:

Articles of special issue are free of charge for article processing.
For Author Instructions, please refer to http://cdrjournal.com/pages/view/author_instructions
For Online Submission, please login at http://cdrjournal.com/login
Submission Deadline: 30 Jun 2018
Contacts: Elaine Gao, Managing Editor, editorial@cdrjournal.com

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Planned Papers

The following list shows the information of planned papers to this special issue. All the papers submitted to Cancer Drug Resistance will go through a rigorous peer review. (Please note that the information below is provisional and may be subject to future change)

Type of paper: Review

Tentative Title: Molecular bases of Sorcin-dependent resistance to chemotherapeutic agents

Authors: Ilaria Genovese, Andrea Ilari, Theo Battista, Valerio Chiarini, Francesco Fazi, Annarita Fiorillo, Gianni Colotti

Affiliation: Italian National Research Council, Institute of Molecular Biology and Pathology; Sapienza University, Dept. Biochemical Sciences

Possible Abstract: Sorcin (SOluble Resistance-related Calcium binding proteIN) is a protein initially labelled “resistance-related”, since it is co-amplified with ABCB1 in multidrug (MD)-resistant cells. While for years Sorcin overproduction was believed to be a by-product of the coamplification of its gene with P-glycoprotein genes, many recent reports have demonstrated that Sorcin plays a role in multidrug resistance (MDR), and pointed at a possible role as an oncoprotein. Sorcin is one of the most highly expressed calcium-binding proteins in many tissues, is overexpressed in many human tumors and MD resistant cancers, and may represent a novel marker.

The level of Sorcin expression in leukemia patients inversely correlates with patients’ response to chemotherapies and overall prognosis. In parallel, Sorcin is highly expressed in chemoresistant cell lines and significantly up-regulated in chemotherapeutic drug-induced MD resistance cell lines over their parent cells. Sorcin overexpression by gene transfection increased drug resistance to a variety of chemotherapeutic agents in many cancer lines. On the other hand, several studies have demonstrated that inhibition of Sorcin expression by RNA interference led to reversal of drug resistance in many cell lines.

This review describes: i) the roles of Sorcin in the cell; ii) the studies showing Sorcin overexpression in tumors and cancer cells; iii) the studies showing the effects of Sorcin overexpression and silencing; iv) the molecular effects of Sorcin overexpression; v) the structural and genetic bases of Sorcin-dependent MDR.

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