Increased risk of cancer among relatives of patients with lung cancer in China

BACKGROUND: Genetic factors were considered as one of the risk factors for lung cancer or other cancers. The aim of this work was to determine whether a genetic predisposition accounts for such familial aggregation of cancer among relatives of lung cancer probands. METHODS: A case-control study was conducted in 800 case families identified by lung cancer patients (probands), and in 800 control families identified by the probands'spouses. The data were analysed with logistic regression analysis model. RESULTS: The data revealed a significantly greater overall risk of cancer (OR = 1.82, P < 0.01) in the proband group. The relatives of lung cancer probands maintained an increased risk of non-lung cancer (P < 0.05) after adjusting for confounder factors. The crude odds ratio of a proband family having one family member with cancer was 1.67 compared with control families. Proband families were 2.56 times more likely to have two other family members with cancer. For three cancers and four or more cancers, the risk increased to 3.50 and 5.91, respectively. The most striking differences in cancer prevalence between proband and control families were noted for cancer risk among female relatives. The strongest effects were for not only lung cancer in any female relatives (OR 2.17, 95%CI 1.60–3.64) and mothers (OR 2.78, 95%CI 1.23–5.12) and sisters (OR 2.03, 95%CI 1.26–3.97), but also non-lung cancer in females and mothers (OR 2.00, 95%CI 1.26–3.01, and OR 2.34, 95%CI 1.28–4.40, respectively). CONCLUSION: These data support the hypothesis of a genetic susceptibility to cancer in families with lung cancer, and the female genetic susceptibility to cancer might be greater than male

Combined effects of cigarette smoking, gene polymorphisms and methylations of tumor suppressor genes on non small cell lung cancer: a hospital-based case-control study in China

<p>Abstract</p> <p>Background</p> <p>Cigarette smoking is the most established risk factor, and genetic variants and/or gene promoter methylations are also considered to play an essential role in development of lung cancer, but the pathogenesis of lung cancer is still unclear.</p> <p>Methods</p> <p>We collected the data of 150 cases and 150 age-matched and sex-matched controls on a Hospital-Based Case-Control Study in China. Face to face interviews were conducted using a standardized questionnaire. Gene polymorphism and methylation status were measured by RFLP-PCR and MSP, respectively. Logistic regressive model was used to estimate the odds ratios (OR) for different levels of exposure.</p> <p>Results</p> <p>After adjusted age and other potential confounding factors, smoking was still main risk factor and significantly increased 3.70-fold greater risk of NSCLC as compared with nonsmokers, and the ORs across increasing levels of pack years were 1, 3.54, 3.65 and 7.76, which the general dose-response trend was confirmed. Our striking findings were that the risk increased 5.16, 8.28 and 4.10-fold, respectively, for NSCLC with promoter hypermethylation of the <it>p16</it>, <it>DAPK </it>or <it>RARβ </it>gene in smokers with <it>CYP1A1 </it>variants, and the higher risk significantly increased in smokers with null <it>GSTM1 </it>and the OR was 17.84 for NSCLC with <it>p16 </it>promoter hypermethylation, 17.41 for <it>DAPK</it>, and 8.18 for <it>RARβ </it>in smokers with null <it>GSTM1 </it>compared with controls (all p < 0.01).</p> <p>Conclusion</p> <p>Our study suggests the strong combined effects of cigarette smoke, <it>CYP1A1 </it>and <it>GSTM1 </it>Polymorphisms, hypermethylations of <it>p16</it>, <it>DAPK </it>and <it>RARβ </it>promoters in NSCLC, implying complex pathogenesis of NSCLC should be given top priority in future research.</p

Measuring the complexity of directed graphs

In this paper, we define novel graph measures for directed networks. The measures are based on graph polynomials utilizing the out- and in-degrees of directed graphs. Based on these polynomial, we define another polynomial and use their positive zeros as graph measures. The measures have meaningful properties that we investigate based on analytical and numerical results. As the computational complexity to compute the measures is polynomial, our approach is efficient and can be applied to large networks. We emphasize that our approach clearly complements the literature in this field as, to the best of our knowledge, existing complexity measures for directed graphs have never been applied on a large scale.Peer reviewe

The orbit-polynomial

Research on the structural complexity of networks has produced many useful results in graph theory and applied disciplines such as engineering and data analysis. This paper is intended as a further contribution to this area of research. Here we focus on measures designed to compare graphs with respect to symmetry. We do this by means of a novel characteristic of a graph G, namely an 'orbit polynomial.' A typical term of this univariate polynomial is of the form czn, where c is the number of orbits of size n of the automorphism group of G. Subtracting the orbit polynomial from 1 results in another polynomial that has a unique positive root, which can serve as a relative measure of the symmetry of a graph. The magnitude of this root is indicative of symmetry and can thus be used to compare graphs with respect to that property. In what follows, we will prove several inequalities on the unique positive roots of orbit polynomials corresponding to different graphs, thus showing differences in symmetry. In addition,we present numerical results relating to several classes of graphs for the purpose of comparing the new symmetry measure with existing ones. Finally, it is applied to a set of isomers of the chemical compound adamantane C10H16. We believe that the measure can be quite useful for tackling applications in chemistry, bioinformatics, and structure-oriented drug design.Peer reviewe

A Genomewide Search for Quantitative-Trait Loci Underlying Asthma

A genomewide screen for quantitative-trait loci (QTLs) that underlie asthma was performed on 533 Chinese families with asthma, by the unified Haseman-Elston method. Nine asthma-related phenotypes were studied, including forced expiratory volume in 1 s (FEV(1)), forced vital capacity (FVC), airway responsiveness as indicated by methacholine (MTCH)-challenge test, serum total immunoglobulin E (TIgE), serum-specific immunoglobulin E, eosinophil count in peripheral blood, and skin-prick tests with three different allergens (cockroach, Dermatophagoides pteronyssinus, and D. farinae). Our study showed significant linkage between airway responsiveness to MTCH and D2S1780 on chromosome 2 (P<.00002) and provided suggestive evidence (P<.002) for six additional possible QTLs: D10S1435 and D22S685, for FEV(1); D16S412, for FVC; D19S433, for airway responsiveness to MTCH; D1S518, for TIgE; and D4S1647, for skin reactivity to cockroach. No significant or suggestive evidence of linkage for the other four traits was found