Special Issue "Advances in Cancer Chemoprevention"

Guest Editor
Prof. Dr. Ross McKinnon
Flinders Centre for Innovation in Cancer, School of Medicine Flinders University, Sturt Road, Bedford Park, Australia
Website: http://www.unisanet.unisa.edu.au/staff/homepage.asp?Name=Ross.McKinnon
E-Mail: ross.mckinnon@flinders.edu.au

Submission

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 the Instructions for Authors page. Cancers is an international peer-reviewed Open Access quarterly 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 500 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.

Type of the Paper: Review
Title: Chemoprevention for Breast Cancer - Advocacy Inaction!
Author: Rakhshanda Layeequr Rahman
Affiliation: Amarillo Breast Center of Excellence, Texas tech University health sciences Center, 1400 S Coulter St, Amarillo, Texas, USA; E-Mail: rakhshanda.rahman@ttuhsc.edu
Abstract: According to National Health Interview Survey Cancer Control module survey of 2000, 16% of all women residing in United States were eligible for tamoxifen prevention by FDA criteria. This accounted for over 10 million women. Five percent of these had a positive risk benefit index according to Gail's risk-benefit calculation. This number would be 2.5 million women. Amongst all women that had a net benefit with tamoxifen, approximately 58,148 invasive breast cancers would develop over next five years and if these women took preventive tamoxifen, 28,492 of these cancers would be prevented. These figures demonstrate a dire need for a serious conversation regarding prevention of breast cancer.  However, despite class I evidence in favor of endocrine manipulation to prevent breast cancer, there has been a complete lack of advocacy. Breast cancer chemo prevention did not receive the same level of advocacy as lipid lowering drugs for prevention of a heart attack. Now that these drugs are generic, there is a lack of incentive for pharmaceuticals to lobby in favor of chemoprevention. It is incumbent upon medical societies and providers to re-ignite the fight against breast cancer in terms of prevention.

Type of Paper: Review
Title: Preclinical Cancer Chemoprevention Study Using Animal Models of Inflammation-associated Colorectal Carcinogenesis
Author: Takuji Tanaka^1,2
Affiliations: ¹ Department of Oncologic Pathology, Kanazawa Medical University, 1-1 daigaku, Uchinada, Ishikawa 920-0293, Japan
² Visiting Lecturer, Department of Tumor Pathology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu City, Gifu 501-1194, Japan; E-Mail: takutt@toukaisaibou.co.jp
Abstract: Chronic inflammation is a well-recognized risk factor for cancer development in several tissues, including colorectum. Inflammatory bowel disease, such as ulcerative colitis (UC) and Crohn's disease (CD) is a longstanding inflammatory disease (IBD) of intestine with increased risk for colorectal cancer (CRC). Several molecular events involving in chronic inflammatory process are reported to contribute to multi-step carcinogenesis of CRC in the inflamed colon. They include over-production of reactive oxygen and nitrogen species, over-production and up-regulation of productions and enzymes of arachidonic acid biosynthesis pathway and cytokines, and intestinal immune system dysfunction. In this short review, I would like to introduce our experimental methods to induce colorectal neoplasm in the inflamed colon. First, I will introduce a protocol of a novel inflammation-associated colon carcinogenesis in mice. Also, chemoprevention of inflammation-associated colon carcinogenesis by several candidate compounds (pitavastatin, morin, bezafibrate, and valproic acid) will be mentioned.