Special Issue "Hormones and Carcinogenesis"

Guest Editor
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
E-Mail: fuchs-young@medicine.tamhsc.edu

Submission

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Title: Therapeutic Targeting of Desmoplasia for Pancreatic Cancer
Authors: Divya Chakravarthy¹, Robert L Reddick² and Addanki P Kumar^1,3,4,5,*
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: kumara3@uthscsa.edu.
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: smatsuda@cc.nara-wu.ac.jp
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.