﻿<?xml version="1.0" encoding="utf-8"?><rss version="2.0"><channel><title>Journal of Cancer Epidemiology</title><link>http://www.hindawi.com</link><description>The latest articles from Hindawi Publishing Corporation</description><copyright>&amp;#169; 2008, Hindawi Publishing Corporation. All rights reserved.</copyright><item><title>Single Nucleotide Polymorphisms in Selected  Apoptotic Genes and BPDE-Induced Apoptotic Capacity  in Apparently Normal Primary Lymphocytes:  A Genotype-Phenotype Correlation Analysis</title><link>http://www.hindawi.com/GetArticle.aspx?doi=10.1155/2008/147905</link><description>Apoptotic capacity (AC) in primary lymphocytes may be a marker for cancer susceptibility, and functional single nucleotide polymorphisms (SNPs) in genes involved in apoptotic pathways may modulate cellular AC in response to DNA damage. To further examine the correlation between apoptotic genotypes and phenotype, we genotyped 14 published SNPs in 11 apoptosis-related genes (i.e., p53, Bcl-2, BAX, CASP9, DR4, Fas, FasL, CASP8, CASP10, CASP3, and CASP7) and assessed the AC in response to benzo[a]pyrene-7,8-9,10-diol epoxide (BPDE) in cultured primary lymphocytes from 172 cancer-free subjects. We found that among these 14 SNPs, R72P, intron 3 16-bp del/ins, and intron 6 G&amp;#62;A in p53, &amp;#x02212;938C&amp;#62;A in Bcl-2, and I522L in CASP10 were significant predictors of the BPDE-induced lymphocytic AC in single-locus analysis. In the combined analysis of the three p53 variants, we found that the individuals with the diplotypes carrying 0-1 copy of the common p53 R-del-G haplotype had higher AC values compared to other genotypes. Although the study size may not have the statistical power to detect the role of other SNPs in AC, our findings suggest that some SNPs in genes involved in the intrinsic apoptotic pathway may modulate lymphocytic AC in response to BPDE exposure in the general population. Larger studies are needed to validate these findings for further studying individual susceptibility to cancer and other apoptosis-related diseases.</description><Author>Zhibin Hu, Chunying Li, Kexin Chen, Li-E Wang, Erich M. Sturgis, Margaret R. Spitz, and Qingyi Wei</Author><copyright>&amp;#169; 2008, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Correlation of DNA Ploidy with Progression of Cervical Cancer</title><link>http://www.hindawi.com/GetArticle.aspx?doi=10.1155/2008/298495</link><description>The majority of squamous cell carcinomas of cervix are preceded by visible changes in the cervix, most often detected by cervical smear. As cervical cancer is preceded by long precancerous stages, identification of the high-risk population through detection of DNA ploidy may be of importance in effective management of this disease. Here we attempted to correlate aneuploid DNA patterns and their influence on biological behavior of flow-cytometry analysis of DNA ploidy which was carried out in cytologically diagnosed cases of mild (79), moderate (36), and severe (12) dysplasia, as well as &amp;#8220;atypical squamous cells of unknown significance (ASCUS)&amp;#8221; (57) along with controls (69), in order to understand its importance in malignant progression of disease. Cytologically diagnosed dysplasias, which were employed for DNA ploidy studies, 39 mild, 28 moderate, and 11 severe dysplasia cases were found to be aneuploid. Out of the 69 control subjects, 6 cases showed aneuploidy pattern and the rest 63 subjects were diploid. An aneuploidy pattern was observed in 8 out of 57 cases of cytologically evaluated ASCUS. The results of the followup studies showed that aberrant DNA content reliably predicts the occurrence of squamous cell carcinoma in cervical smear. Flow cytometric analysis of DNA ploidy may provide a strategic diagnostic tool for early detection of carcinoma cervix. Therefore, it is a concept of an HPV screening with reflex cytology in combination with DNA flow cytometry to detect progressive lesions with the greatest possible sensitivity and specificity.</description><Author>M. Singh, S. Mehrotra, N. Kalra, U. Singh, and Y. Shukla</Author><copyright>&amp;#169; 2008, Hindawi Publishing Corporation. All rights reserved.</copyright></item></channel></rss>