Topic: Targeted cancer therapy

A special issue of Cancer Drug Resistance.

ISSN 2578-532X (Online)

Submission deadline: 3 Sep 2018

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.


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

Submission Deadline

3 Sep 2018

Submission Information

Articles of special issue are free of charge for article processing.
For Author Instructions, please refer to
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Submission Deadline: 3 Sep 2018
Contacts: Elaine Gao, Managing Editor,

Planned Papers

Type: Review

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

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

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.

Type: Review

Title: Hitting a Moving Target: Inhibition Of The Nuclear Export Receptor Xpo1/Crm1 As a Therapeutic Approach In Cancer

Authors: Maria Sendino1, Miren Josu Omaetxebarria2, Jose Antonio Rodríguez1*

Afiliations: 1Department of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country (UPV/EHU), Leioa 48940, Spain.
2Department of Biochemistry and Molecular Biology, University of the Basque Country (UPV/EHU), Leioa 48940, Spain

Abstract: Cellular homeostasis crucially relies on the correct nucleocytoplasmic distribution of a vast number of proteins and RNA molecules, which are shuttled in and out of the nucleus by specialized transport receptors. The nuclear export receptor XPO1, also called CRM1, mediates the translocation of hundreds of proteins and several classes of RNA to the cytoplasm, and thus regulates critical signaling pathways and cellular functions. The normal function of XPO1 appears to be often disrupted in malignant cells due to gene mutations or, most commonly, aberrant overexpression. Due to its important physiological roles and its frequent alteration in human tumors, XPO1 is a promising target for cancer therapy. XPO1 inhibitors have undergone extensive testing as therapeutic agents in preclinical models of cancer, with promising results. One of these inhibitors, Selinexor, is currently being evaluated in multiple clinical trials of different types of solid tumors and hematological malignancies.
Here, we review several key aspects of XPO1 function, as well as the mechanisms that may lead to its alteration in cancer, and provide an update on the status of XPO1 inhibitors being developed as drugs for cancer therapy, including the definitive results of the first clinical trials with Selinexor that have been recently published.

Type: Review

Title: Glutamine metabolism in cancer therapy

Authors: Tra-Ly Nguyen, Raúl V. Durán

Afiliations: Institut Européen de Chimie et Biologie, INSERM U1218, Université de Bordeaux, 2 Rue Robert Escarpit, 33607 Pessac, France

Abstract: The amino acid glutamine plays a key role in the metabolism of highly proliferating cells. During malignant transformation, cancer cells modify the consumption and processing of glutamine to sustain cell growth and proliferation. In some extreme cases, these cancer cells become addicted to glutamine. Thus, targeting the metabolism of glutamine has been developed during last years as a potential strategy against cancer. In this review, we summarized the last advances in our knowledge about the role of glutamine metabolism in cancer therapy.

Published Articles