Special Issue "Toxins and Carcinogenesis"
A special issue of Toxins (ISSN 2072-6651).
Deadline for manuscript submissions: 30 June 2013
Dr. Teresa Frisan
Department Cell and Molecular Biology (CMB), Berzelius väg 35, Box 285, S-171 77 Stockholm, Sweden
Phone: +46 8 524 863 85
The role of several environmental and chemical agents in carcinogenesis has been well documented by combining molecular and epidemiological studies. The use of tobacco is a clear example of a carcinogen linked to a specific life style. An emerging feature in the field of toxin and carcinogenesis is the role of bacterial infections. Several bacteria produce toxins that directly or indirectly alter key signaling pathways that regulate the delicate balance between cell proliferation and cell death, or can directly cause DNA damage.
An interesting development in the field of toxins and cancer is the conjugation of toxins (e.g. bacterial toxins) for targeted delivery to tumor cells. Indeed, the immunotoxin Denileukin diftitox (ONTAK) has been approved for treatment of cutaneous T cell lymphoma. Although the development of such drugs has been slow, the exponential development of new technologies will surely contribute to the deployment of toxins in cancer therapy.
This special issue aims to provide the state of the art of the molecular mechanisms by which toxins promote carcinogenesis as well as the development of toxin-based therapeutic protocols for cancer treatment.
Identification of the molecular mechanisms of the toxins mode of action and their contribution to carcinogenesis is extreme valuable for the definition of efficient preventive measures and the design of novel therapeutic protocols.
Dr. Teresa Frisan
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on theInstructions for Authors page. Toxins is an international peer-reviewed Open Access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- environmental and bacterial toxins
- chronic inflammation
- genomic instability
- cell survival
- cell proliferation
- cancer risk
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of paper: Review
Title: The Cytotoxic Necrotizing Factor 1 from E. coli: A Janus Toxin Playing with Cancer Regulators
Authors: Alessia Fabbri, Sara Travaglione, Giulia Ballan and Carla Fiorentini
Affiliation: Department of Therapeutic Research and Medicines Evaluation, Istituto Superiore di Sanità, viale Regina Elena 299, 00161 Rome, Italy; E-Mail: firstname.lastname@example.org (C.F.)
Abstract: Certain Escherichia coli strains have been indicated as a risk factor for colon cancer. E. coli, a normal inhabitant of the human intestine, becomes pathogenic following the acquisition of virulence factors, including the protein toxin CNF1. This Rho GTPases-activating toxin induces dysfunctions in epithelial cells, such as apoptosis counteraction, pro-inflammatory cytokines’ release, COX2 expression, NF-kB activation and boosted cellular motility. As cancer may arise when the same regulatory pathways are affected, the contribution of CNF1-producing E. coli infections to cancer development is conceivable. This review focuses on those aspects of CNF1 linked to transformation, with the aim of contributing to the identification of a new possible carcinogenic agent from the microbial world.
Last update: 18 February 2013