A special issue of Cancer Drug Resistance.
ISSN 2578-532X (Online)
Submission deadline: 31 Mar 2019
Guest Editor(s)
Special Issue Introduction
The special issue on "Drug resistance mechanisms" will include Reviews and Commentaries updating the problem of drug resistance in the clinic and how attempts have/are being made to improve the situation via laboratory based research approaches. Aspects of drug resistant disease for different tumor types with a mechanistic basis e.g. breast, lung, melanoma, colon cancers will be covered in this issue alongside any advances made in the identification of biomarkers of drug responsiveness. The special issue will also include Research articles presenting novel outstanding data on all aspects of drug resistance mechanisms in cancer. All submissions will undergo rigorous peer review and will be published free of charge upon acceptance.Keywords
Drug resistant cancers, resistance modulation, multidrug resistance, chemotherapy resistance, targeted therapy resistance, biomarkers of drug responsivenessSubmission Deadline
31 Mar 2019Submission 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://www.oaemesas.com/cdr
Submission Deadline: 31 Mar 2019
Contacts: Elaine Gao, Managing Editor, editorial@cdrjournal.com
Ellie Liang, Editor, ellie.liang@oaepublish.com
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)
Planned Papers
Type: Review
Title: Acquired resistance to long term antihormone therapy of breast cancer
Authors: Ping Fan, V. Craig Jordan
Afiliations: Department of Breast Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, USA
Abstract: The translational research strategy of targeting estrogen receptor (ER) positive breast cancer and then using long term antihormone adjuvant therapy (5-10 years) have reduced recurrences and mortality. However, resistance continues to occur and improvements are required to build on the success of tamoxifen and aromatase inhibitors (AIs) established over the past 40 years. Further translational research has described the evolution of acquired resistance of breast cancer cell lines to long tern estrogen deprivation (LTED) that parallels clinical experience over years. Additionally, recent reports have identified mutations in the ER obtained from the recurrences of AI treated patients. These mutations allow the ER to activate without ligands and auto stimulate metastatic tumor growth. Additionally, the new biology of estrogen induced apoptosis has been interrogated and applied to clinical testing. In this review, we will present new treatment strategies to circumvent the development of mutations in the ER and consider the approaches to create new treatments to trigger estrogen induced apoptosis.
Type: Review
Title: Stress and drug resistance in cancer
Authors: Renee L Flaherty, Marta Falcinelli and Melanie S Flint
Afiliations: School of Pharmacy and Biomolecular Sciences, University of Brighton, Huxley Building, Lewes road, Brighton BN2 4GJ, UK
Abstract: Patients diagnosed with cancer often experience considerable psychological distress, and activation of the psychological stress response has been linked with a poor response to chemotherapy. The psychological stress response is mediated by fluctuations of the stress hormones; glucocorticoids (GC’s) such as cortisol and catecholamines such as adrenaline/noradrenaline. Binding to their respective receptors, GC’s and catecholamines are responsible for signalling a wide range of processes involved in cell survival, cell cycle and immune function. Synthetic GC’s, such as dexamethasone, are also often prescribed as co-medication alongside chemotherapy, however increasing evidence suggests that GC’s may induce chemo-resistance in multiple cancer types. In this review, we bring together evidence linking stress hormone signalling with resistance to chemo- and immune therapies, as well as mechanistic evidence regarding the effects of exogenous stress hormones on the efficacy of chemotherapies.
Type: Review
Title: Mechanisms of therapy resistance in testicular cancer
Authors: Ratnakar Singh, Zeeshan Fazal, Sarah J. Freemantle, Michael J. Spinella.
Afiliations: Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Abstract: Testicular cancer is a chemotherapy success story with a majority of patients undergoing cures even when the disease is highly advanced and metastatic. Successful treatment of testicular cancer is primarily due to the exquisite responsiveness of this solid tumor to cisplatin-based therapy. However, a significant percentage of patients are, or become, refractory to cisplatin and die from progressive disease. In this review, we outline new strategies in pre-clinical and clinical development for the treatment of cisplatin refractory testicular cancer. From a laboratory based research perspective, we discuss potential mechanisms of cisplatin resistance in testicular cancer that may relate to the exquisite sensitivity of this solid tumor to conventional chemotherapeutics. Moreover, this review will discuss potential alternative targeted therapies alone or in combination with cisplatin to overcome drug resistance.
Type: Review
Title: Resistance to drugs and cell death in cancer stem cells
Authors: Ahmad R. Safa, Krzysztof Kamocki
Afiliations: Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, USA
Abstract: Human cancers arise from cancer stem cells (CSCs). Many mechanisms including overexpression of drug transporters as well as dysregulation of the extrinsic and intrinsic apoptotic pathways play crucial roles in CSC-induced tumor initiation, progression, cell death resistance, chemo- and radiotherapy resistance, and tumor recurrence. Several signaling pathways—including the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR), maternal embryonic leucine zipper kinase (MELK), NOTCH1, and Wnt/β-catenin—and expression of the CSC markers maintain CSC properties. Studying such pathways may help to understand CSC mechanisms of resistance to chemotherapeutic agents and apoptosis, and may lead to the development of potential therapeutic interventions to render CSCs more sensitive to anticancer agents.
Type: Review
Title: Digging deeper into the dark matter of the genome: an analysis of the mechanistic influences of miRNAs in cancer chemoresistance
Authors: Duncan Ayers
Afiliations: Centre for Molecular Medicine and Biobanking, University of Malta, Malta. & Faculty of Biology, Medicine and Health, The University of Manchester, UK.
Abstract: In the past two decades, following the discovery of the RNA interference pathway by Fire and Mello, the biological and clinical roles of microRNAs (miRNAs) and other non coding RNA families of the ‘dark matter’ of the genome have evolved rapidly. Presently, miRNAs are acknowledged to have widespread implications on all physiological processes within the mammalian cell through their highly effective gene regulatory roles. Consequently, miRNAs can also - when dysregulated - allow for the pathogenesis and progression of a myriad of medical conditions, including cancer. Furthermore, on focusing on the miRNA influences in cancer, specific tumour characteristics can be exacerbated or inhibited through miRNA direction. This review aims to delve deeper into such mechanistic implications of miRNAs in the development (and regulation) of the drug resistant tumour phenotype.
Type: Review
Title: Diacylglycerol Kinases promote chemotherapy resistance and limit immune attack of solid tumors
Authors: Antonia Avila-Flores, Javier Arranz, Isabel Mérida
Afiliations: National Biotechnology Center/CSIC, Madrid, Spain
Abstract: Diacylglycerol Kinases transform diacylglycerol into phosphatidic acid, modulating the levels of two lipids with important functions as second messengers. In T lymphocytes this reaction limits effector functions, driving T lymphocytes into anergic, hypo-responsive states. On the contrary, enhanced DGK activity contributes to the acquisition of metastatic characteristics and facilitates resistance mechanisms in solid tumors. This divergent contribution of DGK functions is exploited by highly transformed cells, where the expression of specific DGK isoforms provides chemotherapy resistance, impairing at the same time immune mediated attack. In this review we will revise the latest advances on the specific contribution of DGKa and DGKz to chemotherapy resistance as well as the limitation imposed to cytotoxic function of T lymphocytes. We will also explore the latest advances on the search for inhibitors and the therapeutic potential that limiting DGK activity may offer in the fight against cancer.
Type: Review
Title: The role of functional imaging in drug resistance mechanisms
Authors: A.O. Ankrah1,2,3, I.O. Lawal2, J. Yarney3, H.C. Klein1, A.W.J.M. Glaudemans1, M. Sathekge2
Afiliations:
1Medical Imaging Center, Department of Nuclear Medicine and Molecular Imaging, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
2Department of Nuclear Medicine, Steve Biko Academic Hospital, University of Pretoria, Pretoria, South Africa.
3National Centre for Radiotherapy and Nuclear Medicine, Korle Bu Teaching Hospital, Accra, Ghana.
Abstract: Functional imaging with single photon emission computed tomography or positron emission tomography integrated with anatomic modalities, computed tomography or magnetic resonance imaging, have been used in assessing both primary and secondary drug resistance to chemotherapy. As a whole body imaging procedure, functional imaging allows non-invasive in vivo visualization of drug resistance in a 3-dimensional manner of the entire tumor and all lesions within a patient in one study. Histologic assessment may miss resistant cells due to sampling and heterogeneity within the same lesion or other lesions in the body. Currently, there is intense research going on, with the introduction of new tracers in the clinical and preclinical settings to evaluate drug resistance.
Type: Review
Title: Therapy for Drug Resistant TNBCs: Is WNT/ β-catenin signaling the answer?
Authors: Chandra Prakash Prasad1, Sandeep R. Mathur2
Afiliations:
1Department of Medical Oncology (Lab), Dr. B.R.A. IRCH, All India Institute of Medical Sciences, New Delhi, India
2Department of Pathology, All India Institute of Medical Sciences, New Delhi, India
Abstract: Breast cancer is a heterogeneous disease and have been stratified into various molecular subtypes. Among these, Triple negative breast cancer (TNBC) subtype is the most aggressive form of breast cancer due to its high metastatic potential and resistance to conventional therapies (i.e. hormone- and chemo-therapy). Hence, development of novel therapies to block TNBCs resistance is an unmet need. Emerging evidences suggest the prominent role of WNT/ β-catenin signaling in TNBCs drug resistance. Apart from chemoresistance, WNT/β-catenin signaling induces cell migration, cell invasion and stem-like features in TNBC cells. The focus of the present review will on WNT/β-catenin signaling in the development of TNBCs, its role in TNBCs chemoresistance, and why inhibitors of WNT/β-catenin signaling are attractive candidates in the combinatorial therapies for TNBCs.