Special Issue "Hormones and Carcinogenesis"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (1 November 2012)
Dr. Robin Fuchs-Young
Department of Molecular and Cellular Medicine, College of Medicine and the Institute for Bioscience and Technology, 208 Reynolds Medical Building, Texas A&M Health Science Center College Station, TX 77843-1114, USA
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.
Review: Endometrial Serous Carcinoma: Its Molecular Characteristics and Histology-Specific Treatment Strategies
Cancers 2012, 4(3), 799-807; doi:10.3390/cancers4030799
Received: 4 June 2012; in revised form: 28 July 2012 / Accepted: 1 August 2012 / Published: 7 August 2012| Download PDF Full-text (933 KB) | Download XML Full-text
Cancers 2012, 4(4), 969-988; doi:10.3390/cancers4040969
Received: 4 July 2012; in revised form: 9 August 2012 / Accepted: 10 September 2012 / Published: 25 September 2012| Download PDF Full-text (190 KB) | Download XML Full-text
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.
Title: Therapeutic Targeting of Desmoplasia for Pancreatic Cancer
Authors: Divya Chakravarthy1, Robert L Reddick2 and Addanki P Kumar1,3,4,5,*
Affiliations: Department of Urology1, Pathology2, Pharmacology3, Cancer Therapy and Research Center4, South Texas Veterans Health Care System5, The University of Texas Health Science Center, San Antonio, TX, USA; E-Mail: email@example.com.
Abstract: Incidence rates of cancers including pancreatic (PanCA) have been on the rise in both men and women. Deregulation of multiple signaling pathways involved in a wide variety of cellular processes including proliferation, apoptosis, invasion, and metastasis contribute not only to cancer development but also to therapeutic resistance. Unfortunately, in PanCA the incidence is almost equal to mortality rates. The unique aspect of PanCA is “desmoplasia”, a process that involves proliferation of stromal fibroblasts and collagen deposition in and around the filtrating cancer. Recent studies have identified pancreatic stellate cells (PSC’s) as a potential source of such desmoplasia implicating a role for tumor-stromal interactions in pancreatic carcinogenesis. Therefore targeting desmoplastic reaction or tumor-stromal interactions could have a tremendous potential in the clinical management of PanCA. Although PSC biology is not well understood, available evidence indicates a role for the transcription factor family GLIs. GLI is a Zn-finger transcription factor with three known members GLI1, 2 and 3 that have been shown to be involved in mediating hedgehog signaling. In this review we will discuss the current knowledge about GLI-code with special reference to PSC’s and PanCA as well as use of natural and synthetic compounds for therapeutic disruption of the GLI-code for PanCA management.
Type of the Paper: Review
Title: Function of DNA Repair Molecules and the Transition to Hormone Independence in Cancer
Authors: Emi Sakurai, Yasuko Kitagishi and Satoru Matsuda
Affiliation: Department of Environmental Health Science, Nara Women's University Kita-Uoya Nishimachi Nara 630-8506, Japan; E-Mail: firstname.lastname@example.org
Abstract: Cancer is a complicated disease which can gain a more invasive and resistant character by numerous molecular changes that bring about genetic instability. Cells possess a machinery to maintain genomic integrity in response to oxidative stresses. Under genotoxic conditions, cells do not progress into S or M phase by activating DNA damage checkpoint. The DNA damage checkpoint acts as a process to transmit information from damaged DNA lesions to cell cycle regulators, which permits cell a genomic adaptation to acquire a growth advantage. Mutations in several genes which make the effects of DNA damage less severe are known to predispose to develop a cancer. For example, mutations in ataxia telangiectasia-mutated (ATM) have been associated with increased risk of cancer. The ATM is a checkpoint kinase that phosphorylates a number of proteins in response to DNA damage, including p53, Chk2, and BRCA1. Mutations in the p53, BRCA1, and ATM genes account for a certain amount of cancer cases. Furthermore, recent studies have reported an association between DNA repair deficiency and loss of specific hormone receptors. Some cancers from hormone dependent to hormone independent disease remain a critical issue in the management of these cancers. Recent advances in a field of DNA-repair-biology have led to a better understanding of the molecular events important in the pathogenesis of hormonal cancers. In the present review, we summarize the function of DNA repair molecules at a viewpoint of carcinogenic DNA damage and cancer cell modulation.
Last update: 25 September 2012