Lung cancer is still the leading cause of death from cancer worldwide primarily because of the fact that most lung cancers are diagnosed at advanced stages. Overexpression of the high mobility group protein HMGA2 has been observed in a variety of malignant tumors and often correlates with poor prognosis. Herein, HMGA2 expression levels were analyzed in matching cancerous and non-cancerous lung samples of 17 patients with adenocarcinoma (AC) and 17 patients with squamous cell carcinoma (SCC) with real-time quantitative RT-PCR (qRT-PCR). Transcript levels were compared to results obtained by immunohistochemistry (IHC). HMGA2 expression was detectable by qRT-PCR in all samples tested and varied from 5422 to 16 991 545 copies per 250 ng total RNA in the carcinoma samples and from 289 to 525 947 copies in the non-cancerous tissue samples. In 33/34 non-small cell lung cancer (NSCLC) samples tested, an overexpression of HMGA2 was revealed with statistically highly significant differences between non-neoplastic and tumor samples for both AC (P < 0.0001) as well as for SCC (P < 0.0001). Expression varies strongly and is increased up to 911-fold for AC and up to 2504-fold for SCC, respectively, with statistically significant higher increase in SCC (P < 0.05). The results presented herein indicate that HMGA2 overexpression is a common event in NSCLC and could serve as molecular marker for lung cancer.

We quantified lipoprotein(a) [Lp(a)] immunochemically in young (less than 46 y) male survivors of myocardial infarction and in age-matched controls recruited from participants of the Prospective Cardiovascular Münster (PROCAM) study. We further determined apolipoprotein E polymorphism and measured triglycerides, total cholesterol, high- and low-density lipoprotein cholesterol (HDL and LDL), and apolipoproteins AI, AII, and B in the serum of these subjects. Lp(a) concentrations in serum were not correlated with other well-recognized risk factors for early myocardial infarction such as apolipoproteins AI and B, LDL cholesterol, and HDL cholesterol. Apolipoprotein E polymorphism did not affect Lp(a) concentrations, but had a major influence on apolipoprotein B concentration. Lp(a) concentrations were not influenced by age. Our data suggest that (a) an increased concentration of Lp(a) constitutes an independent risk factor for early myocardial infarction and (b) the concentrations of Lp(a) and LDL cholesterol (apolipoprotein B) in serum are under separate metabolic control.

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In the Prospective Cardiovascular Münster (PROCAM) study, serum lipoprotein(a) [Lp(a)] and its relationship to pro- and anticoagulatory as well as fibrinolytic indices were determined in a large group of employees: 864 men (m) and 373 women (f), ages 16-65 years. Univariate statistical analysis showed Lp(a) concentration to be associated with fibrinogen concentrations in both sexes (m: r = 0.08, P less than 0.05; f: r = 0.20, P less than 0.001), but not with euglobulin fibrinolysis activity, tissue-type plasminogen activator, plasminogen activator inhibitor type 1 (PAI-1), or the split products of cross-linked fibrin (d-dimer). In women only, Lp(a) was significantly correlated with antithrombin III (r = 0.15, P less than 0.01) and Protein C (r = 0.17, P less than 0.01). Further sex-related differences were seen in the relationship between Lp(a) and age (m: r = 0.05; f: r = 0.23, P less than 0.001) and body mass index (m: r = 0.01; f: r = 0.19, P less than 0.001), primarily as a consequence of remarkable differences of Lp(a) concentrations between postmenopausal (mean = 79.4 mg/L) and premenopausal women (mean = 51.5 mg/L, P = 0.001). Multiple-regression analysis demonstrated a significant negative correlation of Lp(a) to PAI-1 (m: beta = -0.12, P less than 0.01; f: beta = -0.14, P less than 0.05) and a positive correlation to cholesterol (m: beta = 0.18, P less than 0.001; f: beta = 0.17, P less than 0.01) and systolic blood pressure (m: beta = 0.08, P less than 0.05; f: beta = 0.11, P less than 0.05).

This crossover study investigated the effects of two fat-reduced diets, one rich in monounsaturated fatty acids (MUFAs), the other rich in polyunsaturated fatty acids (PUFAs), on serum lipid profiles in 38 healthy young adults initially on a typical western diet. After being randomly assigned to two groups, the subjects received the MUFA or PUFA diet for 3-wk and then the other diet for 3 wk. Both test diets led to significant reductions in serum cholesterol, LDL cholesterol, and HDL cholesterol (P less than 0.001). Both reduced apolipoprotein B (P less than 0.001) and apolipoprotein A-I concentrations (P less than 0.01 for the MUFA, P less than 0.001 for the PUFA diet). Apolipoprotein A-I was significantly higher on the MUFA than on the PUFA diet. The ratio of apolipoprotein A-I to B significantly increased on both diets. Thus, a low-fat, MUFA-rich diet is as effective as a low-fat, PUFA-rich diet in lowering total and LDL cholesterol, but both also lowered HDL cholesterol concentrations. The MUFA-rich diet may be more advantageous than the PUFA-rich one because it does not lower apolipoprotein A-I concentrations as much as the PUFA-rich diet.