Cigarette smoking cannot fully explain the epidemiologic characteristics of lung cancer in Taiwanese women, who smoke rarely but have lung cancer relatively often. In a previous study, the authors suspected that exposure to fumes from cooking oils was an important risk factor for lung cancer in Taiwanese women nonsmokers in the Republic of China. In a new case-control study conducted in 1993-1996, they further explored the association of oil fumes with lung cancer in women. Two sets of controls were used concurrently. The subjects were 131 nonsmoking incident cases with newly diagnosed and histologically confirmed primary carcinoma of the lung, 252 hospital controls hospitalized for causes unrelated to diseases of smoking, and 262 community controls; all controls were women nonsmokers matched by age and date of interview. Details on cooking conditions and habits were collected, in addition to other epidemiologic data. Lung cancer risk increased with the number of meals per day to about threefold for women who cooked these meals each day. The risk was also greater if women usually waited until fumes were emitted from the cooking oil before they began cooking (adjusted odds ratios = 2.0-2.6) and if they did not use a fume extractor (adjusted odds ratios = 3.2-12.2). These results suggest that a proportion of lung cancer may be attributable to the habit of waiting until the cooking oil has been heated to a high temperature before cooking the food.

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Abstract-Genes contributing to common forms of hypertension are largely unknown. A number of studies in humans and in animal models have revealed associations between insulin resistance, dyslipidemia, and elevated hypertension. To identify genes contributing to blood pressure (BP) variation associated with insulin-resistant dyslipidemia, we conducted a genome-wide scan for BP in a set of 18 Dutch families exhibiting the common lipid disorder familial combined hyperlipidemia. Our results reveal a locus on chromosome 4 that exhibits a significant lod score of 3.9 with systolic BP. In addition, this locus also appears to influence plasma free fatty acid levels (lodϭ2.4). After adjustment for age and gender, the lod score for systolic BP increased to 4.6, whereas the lod score for free fatty acid levels did not change. The chromosome 4 locus contains an attractive candidate gene, ␣-adducin, which has been associated with altered BP in animal studies and in some human populations. However, we found no evidence for an association between 2 intragenic ␣-adducin polymorphisms and systolic BP in this sample. We also observed suggestive evidence for linkage (lodϭ1.8) of diastolic BP to the lipoprotein lipase gene locus on chromosome 8p, supporting a finding previously observed in a separate insulin-resistant population. In addition, we also obtained suggestive evidence for linkage of systolic BP (lodϭ2.4) and plasma apolipoprotein B levels (lodϭ2.0) to a locus on proximal chromosome 19p. In conclusion, our genome scan results support the existence of multiple genetic factors that can influence both BP and plasma lipid parameters. Key Words: genetics Ⅲ hypertension, essential Ⅲ dyslipidemia Ⅲ genome scan Ⅲ linkage analysis S ignificant progress has been made in elucidating the genetic basis for certain mendelian forms of hypertension, but the genetic factors contributing to essential hypertension are largely unknown. 1,2 A number of candidate gene studies and genome scans have been conducted but with varying results. [3][4][5][6] The variation in these latter linkage results could be due the different racial make-up of the study populations and/or the underlying genetic heterogeneity of essential hypertension, which can clearly confound genefinding efforts.One strategy to reduce genetic heterogeneity is to stratify the study population by hypertension that is associated with other pathophysiologic processes, such as insulin-resistant dyslipidemia. A number of studies, those of Williams and colleagues 7 in particular, have revealed associations between hyperlipidemia, insulin resistance, and elevated blood pressure (BP). These studies led to the definition of a condition similar to the metabolic syndrome termed familial dyslipidemic hypertension (FDH), involving a clustering of traits, including central obesity, lipid abnormalities, hypertension, and elevated fasting insulin levels. Several studies have demonstrated a high degree of heritability of this trait, which occurs in Ϸ1% of the general population but in Ϸ12% of pat...

Genomic aberrations are of predominant importance to the biology and clinical outcome of patients with acute myelogenous leukemia (AML), and conventional karyotype-based risk classifications are routinely used in clinical decision making in AML. One of the known limitations of cytogenetic analysis is the inability to detect genomic abnormalities less than 5 Mb in size, and it is currently unclear whether overcoming this limitation with high-resolution genomic single-nucleotide polymorphism (SNP) array analysis would be clinically relevant. Furthermore, given the heterogeneity of molecular mechanisms/ aberrations that underlie the conventional karyotype-based risk classifications, it is likely that further refinements in genomic risk prognostication can be achieved. In this study, we analyzed flow cytometersorted, AML blast-derived, and paired, buccal DNA from 114 previously untreated prospectively enrolled AML patients for acquired genomic copy number changes and loss of heterozygosity using Affymetrix SNP 6.0 arrays, and we corre-

Our results demonstrate that a major gene determining fasting insulin is located on chromosome 7q. Linkage of BP, HOMA, and leptin levels to the same region suggests this locus may broadly influence traits associated with IR and supports a genetic basis for phenotypic associations in IR syndrome.