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Certain Cancers (certain + cancers)
Selected AbstractsFolate deficiency in human peripheral blood lymphocytes induces chromosome 8 aneuploidy but this effect is not modified by riboflavinENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2010Juan Ni Abstract Chromosome 8 aneuploidy is a common event in certain cancers but whether folate (F) deficiency induces chromosome 8 aneuploidy is not known. Furthermore the impact of riboflavin (R) deficiency, which may alter activity of a key enzyme in folate metabolism, on these events is unknown. Therefore, the aim of our research was to test the following hypotheses: (a) F deficiency induces chromosome 8 aneuploidy; (b) chromosome 8 aneuploidy is affected by F deficiency to a similar degree as chromosome 17 and (c) R deficiency aggravates the risk of aneuploidy caused by F deficiency. These hypotheses were tested in long-term cultures of lymphocytes from twenty female healthy volunteers (aged 30,48 years). Lymphocytes were cultured in each of the four possible combinations of low (L) and high (H) F (LF, 20 nmol/L, HF 200 nmol/L, respectively) and L and H R (LR 1 nmol/L, HR 500 nmol/L, respectively) media (LFLR, LFHR, HFLR, HFHR) for 9 days. Chromosomes 8 and 17 aneuploidy was measured in mononucleated (MONO) and cytokinesis-blocked binucleated (BN) cells using dual-color fluorescence in situ hybridization (FISH) with fluorescent centromeric probes specific for chromosomes 8 and 17. Culture in LF media (LFLR or LFHR) induced significant and similar increases in frequencies of aneuploidy of chromosomes 8 and 17 (P < 0.001) relative to culture in HF media (HFLR or HFHR). There was no significant effect of R concentration on aneuploidy frequency for either chromosome. We conclude that F deficiency is a possible cause of chromosome 8 aneuploidy. Environ. Mol. Mutagen. 2010. © 2009 Wiley-Liss, Inc. [source] Probiotics and their fermented food products are beneficial for healthJOURNAL OF APPLIED MICROBIOLOGY, Issue 6 2006S. Parvez Abstract Probiotics are usually defined as microbial food supplements with beneficial effects on the consumers. Most probiotics fall into the group of organisms' known as lactic acid-producing bacteria and are normally consumed in the form of yogurt, fermented milks or other fermented foods. Some of the beneficial effect of lactic acid bacteria consumption include: (i) improving intestinal tract health; (ii) enhancing the immune system, synthesizing and enhancing the bioavailability of nutrients; (iii) reducing symptoms of lactose intolerance, decreasing the prevalence of allergy in susceptible individuals; and (iv) reducing risk of certain cancers. The mechanisms by which probiotics exert their effects are largely unknown, but may involve modifying gut pH, antagonizing pathogens through production of antimicrobial compounds, competing for pathogen binding and receptor sites as well as for available nutrients and growth factors, stimulating immunomodulatory cells, and producing lactase. Selection criteria, efficacy, food and supplement sources and safety issues around probiotics are reviewed. Recent scientific investigation has supported the important role of probiotics as a part of a healthy diet for human as well as for animals and may be an avenue to provide a safe, cost effective, and ,natural' approach that adds a barrier against microbial infection. This paper presents a review of probiotics in health maintenance and disease prevention. [source] Statins, stem cells, and cancerJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2009Kalamegam Gauthaman Abstract The statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) were proven to be effective antilipid agents against cardiovascular disease. Recent reports demonstrate an anticancer effect induced by the statins through inhibition of cell proliferation, induction of apoptosis, or inhibition of angiogenesis. These effects are due to suppression of the mevalonate pathway leading to depletion of various downstream products that play an essential role in cell cycle progression, cell signaling, and membrane integrity. Recent evidence suggests a shared genomic fingerprint between embryonic stem cells, cancer cells, and cancer stem cells. Activation targets of NANOG, OCT4, SOX2, and c-MYC are more frequently overexpressed in certain tumors. In the absence of bona fide cancer stem cell lines, human embryonic stem cells, which have similar properties to cancer and cancer stem cells, have been an excellent model throwing light on the anticancer affects of various putative anticancer agents. It was shown that key cellular functions in karyotypically abnormal colorectal and ovarian cancer cells and human embryonic stem cells are inhibited by the statins and this is mediated via a suppression of this stemness pathway. The strategy for treatment of cancers may thus be the targeting of a putative cancer stem cell within the tumor with specific agents such as the statins with or without chemotherapy. The statins may thus play a dual prophylactic role as a lipid-lowering drug for the prevention of heart disease and as an anticancer agent to prevent certain cancers. This review examines the relationship between the statins, stem cells, and certain cancers. J. Cell. Biochem. 106: 975,983, 2009. © 2009 Wiley-Liss, Inc. [source] Association between body weight and periodontal infectionJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2008Pekka Ylöstalo Abstract Background: Besides being a risk factor for cardiovascular diseases, certain cancers and type II diabetes, obesity has been suggested to be a risk factor for periodontitis. A number of epidemiological studies have studied the association between obesity and periodontitis, but the results have been partly inconclusive. The aim of this study was to examine the association of body weight with periodontal infection. Material and Methods: The association between body weight and periodontal infection was examined using a nationally representative Health 2000 Health Examination Survey. The study was based on a subpopulation of dentate non-diabetic subjects aged 30,49 (n=2841). Periodontal infection was measured by the number of teeth with periodontal pockets of 4 mm or deeper and 6 mm or deeper. Body weight was measured using body mass index (BMI). Results: We detected a weak exposure,response association of BMI with teeth with deepened periodontal pockets after controlling for smoking habits by restricting the sample to subjects who have never smoked and for other potential confounders by including them in the multivariate models. Conclusions: The results showed an association between body weight and periodontal infection among the non-diabetic, non-smoking population aged 30,49. Additional research is needed to determine the nature of this association. [source] HYDROLYSIS OF ISOFLAVONE GLYCOSIDES IN SOY MILK BY ,-GALACTOSIDASE AND ,-GLUCOSIDASEJOURNAL OF FOOD BIOCHEMISTRY, Issue 1 2009THUY T. PHAM ABSTRACT The objective of this study was to assess the potential of pure ,-galactosidase and ,-glucosidase for hydrolyzing isoflavone glycosides to aglycones in soy milk. Both pure ,-galactosidase and ,-glucosidase were added at various concentrations (0.5, 1.0, 2.0 and 4.0 U/mL) to soy milk made from 4% soy protein isolate and incubated at 37C for up to 240 min. Isoflavones were quantified using high-performance liquid chromatography. The isoflavone contents of soy milk before and after autoclaving were also compared. ,-Glucosidase and ,-galactosidase were both able to hydrolyze the ,-glucosidic linkages in isoflavone glycosides. A range of 43.3 to 77.2% of the total isoflavone glycosides was hydrolyzed at various ,-galactosidase concentrations. The ,-glucosidase hydrolyzed isoflavone glycosides more efficiently than ,-galactosidase. At the most diluted ,-glucosidase concentration (0.5 U/mL), 86.6% of isoflavone glycosides were hydrolyzed to aglycones at 240 min. PRACTICAL APPLICATIONS Isoflavone glycosides, which are mainly found in the bean family, are the inactive forms of isoflavones. However, aglycones, which are the nonsugar component of a glycoside molecule that results from hydrolysis of the isoflavone glycosides, are the biologically active forms. Because of their similarity to female hormone, they are considered a "natural way" to relieve the menopausal symptoms as they prevent certain cancers and improve bone health. Only a small amount of the total isoflavones, however, exists in the aglycone forms in nature. A novel method to produce aglycones from natural isoflavones is highly important. ,-Glucosidase has been claimed to be the only enzyme which is able to hydrolyze isoflavone glycosides to aglycones. However, other enzymes could hydrolyze isoflavone glycosides more efficiently and could be easier to produce. This paper investigates the ability of ,-galactosidase to biotransform isoflavone glycosides to aglycones, as the source of the enzyme is abundant. [source] The cell migration protein Grb7 associates with transcriptional regulator FHL2 in a Grb7 phosphorylation-dependent mannerJOURNAL OF MOLECULAR RECOGNITION, Issue 1 2009Sharareh Siamakpour-Reihani Abstract Grb7 is an adaptor molecule that can mediate signal transduction from multiple cell surface receptors to various downstream signaling pathways. Grb7, along with Grb10 and Grb14, make up the Grb7 protein family. This protein family has been shown to be overexpressed in certain cancers and cancer cell lines. Grb7 and a receptor tyrosine kinase (RTK), erbB2, are overexpressed in 20,30% of breast cancers. Grb7 overexpression has been linked to enhanced cell migration and metastasis, though the participants in these pathways have not been determined. In this study, we report that Grb7 interacts with four and half lim domains isoform 2 (FHL2), a transcription regulator with an important role in oncogenesis, including breast cancer. Additionally, in yeast 2-hybrid (Y2H) assays, we show that the interaction is specific to the Grb7 RA and PH domains. We have also demonstrated that full-length (FL) Grb7 and FHL2 interact in mammalian cells and that Grb7 must be tyrosine phosphorylated for this interaction to occur. Immunofluorescent microscopy demonstrates possible co-localization of Grb7 and FHL2. A model with supporting NMR evidence of Grb7 autoinhibition is proposed. Copyright © 2008 John Wiley & Sons, Ltd. [source] Lycopene content differs among red-fleshed watermelon cultivars,JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 10 2001Penelope Perkins-Veazie Abstract Lycopene, a carotenoid, has antioxidant properties that may reduce the incidence of certain cancers. Watermelon (Citrullus lanatus (Thunb) Matsum & Nakai) is a natural source of lycopene, with a reported average content of 48.7,µg,g,1 fresh weight based on samples taken from retail produce. This study demonstrated the variability of lycopene content in 11 red-fleshed watermelon cultivars grown at one location, representing seedless, open-pollinated and hybrid types, and in commercially shipped hybrid and seedless melons, representing seasonal production periods. Tristimulus colorimeter a* and chroma values were positively correlated with lycopene values, but linear or quadratic regressions of colorimeter data against lycopene values were not significant. Tristimulus colorimeter readings from cut melons were compared to amounts of lycopene extracted from the same melons. Lycopene content varied widely among cultivars, with four cultivars having mean values greater than 65.0,µg,g,1 fresh weight. Seedless types sampled tended to have higher amounts of lycopene (>50.0,µg,g,1 fresh weight) than seeded types. Watermelon lycopene content changed for some cultivars with production season. Published in 2001 for SCI by John Wiley & Sons, Ltd [source] Risk factors for venous thrombosis in medical inpatients: validation of a thrombosis risk scoreJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 12 2004N. A. Zakai Summary.,Background/objectives:,The occurrence of and risk factors for venous thrombosis (VT) complicating hospital admission in unselected medical inpatients have not been widely studied. Patients and methods:,In a 400-bed teaching hospital we identified all cases of VT complicating hospital admission between September 2000 and September 2002 using discharge codes and chart review. Controls were randomly selected adult inpatients frequency matched to cases for medical service. Results:,The incidence of VT complicating hospital admission was 7.6 per 1000 admissions. On average, VT was diagnosed on the fifth hospital day. The median age of the 65 cases and 123 controls was 68 years and 45% were men. Cases had a 4-fold higher death rate than controls [95% confidence interval (CI) 1.9, 8.8]. At admission, trauma within 3 months, leg edema, pneumonia, platelet count > 350 × 103 mm,3 and certain cancers were associated with risk of VT. Age, body mass index, and acute myocardial infarction were not associated with VT risk. One of three published VT risk models was able to risk stratify patients and was associated with a 2.6-fold increased risk of VT (95% CI 1.3, 5.5). Use of VT prophylaxis did not differ in cases and controls; prophylaxis was used <,1/3 of hospital days in 52% of patients. Conclusions:,VT was common among medical inpatients. Of the risk factors identified, elevated platelet count has not been previously reported. Only one of three published risk scores was associated with risk of inpatient VT. Future study should improve upon risk prediction models for in-hospital VT among medical patients. [source] Antioxidant and other biological activities of phenols from olives and olive oilMEDICINAL RESEARCH REVIEWS, Issue 1 2002Francesco Visioli Abstract Olive oil is the principal source of fats in the Mediterranean diet, which has been associated with a lower incidence of coronary heart disease and certain cancers. Phenolic compounds, e.g., hydroxytyrosol and oleuropein, in extra-virgin olive oil are responsible for its peculiar pungent taste and for its high stability. Recent findings demonstrate that olive oil phenolics are powerful antioxidants, both in vitro and in vivo, and possess other potent biological activities that could partially account for the observed healthful effects of the Mediterranean diet. © 2001 John Wiley & Sons, Inc. Med Res Rev, 22, No. 1, 65,75, 2002 [source] The grain, the wholegrain and nothing but the grain: the science behind wholegrain and the reduced risk of heart disease and cancerNUTRITION BULLETIN, Issue 4 2000David P. Richardson Summary Wholegrain foods are important sources of nutrients and phytoprotective substances that are in short supply in our diet. Encouraging the public to increase consumption of wholegrain foods imparts a positive health message and could contribute towards the achievement of reduced fat and increased fibre intakes. More recent research suggests that the health benefits of wholegrain foods are derived from more than just the fibre. Wholefoods, such as fruit and vegetables and wholegrains, deliver ,packages' of constituents that may work synergistically to promote health. Wholegrain foods, particularly cereals, have been shown to be protective against coronary heart disease, certain cancers and diabetes. At least one daily serving of wholegrain food is associated with reduced risk of disease and there may be further benefits with increasing intake. A greater consumption of wholegrain foods has important public health implications, and would be an attractive and prudent food-based dietary strategy, targeted at the whole population. [source] Vegetarian Diets and Weight StatusNUTRITION REVIEWS, Issue 4 2006Susan E. Berkow PhD The increasing global health problems of overweight and obesity are associated with coronary heart disease, hypertension, diabetes, osteoarthritis, and certain cancers, among other health concerns. Vegetarian diets are associated with reduced body weight, lower incidence of certain chronic disease, and lower medical costs compared with non-vegetarian diets. We reviewed the literature to ascertain the extent to which and by what mechanism(s) a plant-based diet may mediate body weight. [source] Selenium Accumulation in Plant FoodsNUTRITION REVIEWS, Issue 6 2005John W. Finley PhD Selenium (Se) is an essential nutrient, and Se deficiency is associated with disease conditions and general impairment of the immune system. Supplementation of Se to humans already consuming the RDA may help to prevent certain cancers. A convincing argument can be made for augmenting the food supply with Se, and Se-enhanced plants may be the best means of accomplishing this. Plants accumulate varying amounts of Se in different chemical forms; some plants accumulate Se in direct relationship to the amount available from the soil, whereas others (Se-accumulators) may accumulate Se in concentrations many orders of magnitude above that in the soil. There are many different chemical forms of Se in plants, and the form partially dictates the metabolism of Se by the animal that consumes the plant. The Se content and the chemical form of Se withinplants may be altered by manipulation of plant genetics or by agricultural production conditions. However, attempts to maximize Se in plants may have unintended consequences and must be carefully monitored. [source] Epidemiology of cancer in adolescents,PEDIATRIC BLOOD & CANCER, Issue 3 2002Charles Stiller MA Abstract In western populations, the annual incidence rate of cancer among adolescents aged 15,19 years is around 150,200 per million, intermediate between the rates for older children and young adults. The most frequent diagnostic groups are acute leukemia, lymphomas, central nervous system tumors, bone and soft tissue sarcomas, germ cell tumors, thyroid carcinoma, and malignant melanoma. While the causes of most cancers in teenagers are still unknown, health education and promotion and public health programs offer some scope for prevention among people of this age group. Reduction in sun exposure should lead to a reduction in incidence of melanoma, and elimination of hepatitis B in regions where it is endemic should result in a decrease in hepatic carcinoma. Five-year survival of patients diagnosed around 1990 exceeded 70% in the USA and UK. Entry to clinical trials appears to be much less frequent for adolescents with cancer than for children. There is some evidence that higher survival is associated with entry to trials or centralized treatment for certain cancers in this age group. Med Pediatr Oncol 2002;39:149,155. © 2002 Wiley-Liss, Inc. [source] Inhibition of NF-,B activation with designed ankyrin-repeat proteins targeting the ubiquitin-binding/oligomerization domain of NEMOPROTEIN SCIENCE, Issue 9 2007Emanuel Wyler Abstract The link between the NF-,B signal transduction pathway and cancer is now well established. Inhibiting this pathway is therefore a promising approach in the treatment of certain cancers through a pro-apoptotic effect in malignant cells. Owing to its central role in the pathway, the I,B kinase (IKK) complex is a privileged target for designing inhibitors. Previously, we showed that oligomerization of NEMO is necessary for IKK activation and defined a minimal oligomerization domain (CC2-LZ) for NEMO, and we developed NEMO peptides inhibiting NF-,B activation at the level of the IKK complex. To improve the low-affinity inhibitors, we used ribosome display to select small and stable proteins with high affinity against the individual CC2-LZ because the entire NEMO protein is poorly soluble. Several binders with affinities in the low nanomolar range were obtained. When expressed in human cells, some of the selected molecules, despite their partial degradation, inhibited TNF-,-mediated NF-,B activation while having no effect on the basal activity. Controls with a naive library member or null plasmid had no effect. Furthermore, we could show that this NF-,B inhibition occurs through a specific interaction between the binders and the endogenous NEMO, resulting in decreased IKK activation. These results indicate that in vitro selections with the NEMO subdomain alone as a target may be sufficient to lead to interesting compounds that are able to inhibit NF-,B activation. [source] How race becomes biology: Embodiment of social inequalityAMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue 1 2009Clarence C. Gravlee Abstract The current debate over racial inequalities in health is arguably the most important venue for advancing both scientific and public understanding of race, racism, and human biological variation. In the United States and elsewhere, there are well-defined inequalities between racially defined groups for a range of biological outcomes,cardiovascular disease, diabetes, stroke, certain cancers, low birth weight, preterm delivery, and others. Among biomedical researchers, these patterns are often taken as evidence of fundamental genetic differences between alleged races. However, a growing body of evidence establishes the primacy of social inequalities in the origin and persistence of racial health disparities. Here, I summarize this evidence and argue that the debate over racial inequalities in health presents an opportunity to refine the critique of race in three ways: 1) to reiterate why the race concept is inconsistent with patterns of global human genetic diversity; 2) to refocus attention on the complex, environmental influences on human biology at multiple levels of analysis and across the lifecourse; and 3) to revise the claim that race is a cultural construct and expand research on the sociocultural reality of race and racism. Drawing on recent developments in neighboring disciplines, I present a model for explaining how racial inequality becomes embodied,literally,in the biological well-being of racialized groups and individuals. This model requires a shift in the way we articulate the critique of race as bad biology. Am J Phys Anthropol 2009. © 2009 Wiley-Liss, Inc. [source] Angiogenesis: now and then,APMIS, Issue 7-8 2004CARLA COSTA Angiogenesis or new blood vessel formation plays an essential role during embryogenesis, adult vascular remodeling and in several pathological disorders, as in tumor development. Although sprouting of blood vessels is the principal angiogenic mechanism, additional ones, such as the recruitment of bone marrow-derived cells, have recently been described. These processes are controlled by several molecules, although members of the VEGF family of angiogenic factors and its receptors seem to be the main mediators. Initially, VEGF receptors were described as endothelial specific; however, further studies have reported their presence in several types of cells of non-endothelial origin, such as tumor cells. This VEGF receptor altered expression has suggested an angiogenesis-independent growth advantage mechanism on certain types of cancers by the generation of autocrine loops. A possible role in tumorigenesis and a potential novel target in cancer therapy have been hypothesized. Detection of other receptors and molecules considered to be angiogenic players has also been observed on tumor cells. Currently, their clinical significance as well as their potential as therapeutic targets for the treatment of certain cancers is being evaluated, having in mind the future development of promising mechanism-based therapies. The aspects mentioned above are the main focus of this review, which aims to throw light on recent findings respecting angiogenesis and novel therapeutic approaches. [source] Gastrin-releasing peptide: Different forms, different functionsBIOFACTORS, Issue 1 2009Joseph Ischia Abstract All forms of the neuropeptide gastrin-releasing peptide (GRP) are derived from the precursor proGRP1-125. Amidated GRP18-27, which together with amidated GRP1-27 was long thought to be the only biologically relevant product of the GRP gene, is involved in a multitude of physiological functions and acts as a mitogen, morphogen, and proangiogenic factor in certain cancers. Recently, GRP has been implicated in several psychiatric conditions, in the maintenance of circadian rhythm, in spinal transmission of the itch sensation, and in inflammation and wound repair. The actions of GRP are mediated by the GRP receptor. Over the last decade, nonamidated peptides derived from proGRP, such as the glycine-extended form GRP18-28 and recombinant and synthetic fragments from proGRP31-125, have been shown to be biologically active in a range of tissues and in cancer cell lines. While GRP18-28 acts via the GRP receptor, the identity of the receptor for proGRP31-125 and its fragments has not yet been established. Nonamidated fragments are also present in normal tissues and in various cancers. In fact, proGRP31-98 is the most sensitive serum biomarker in patients with small cell lung cancer and is a significant predictor of poor survival in patients with advanced prostate cancer. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Vitamin D and systemic cancer: is this relevant to malignant melanoma?BRITISH JOURNAL OF DERMATOLOGY, Issue 2 2002J.E. Osborne Summary 1,25-dihydroxyvitamin D3[1,25(OH)2D3] is a well-known potent regulator of cell growth and differentiation and there is recent evidence of an effect on cell death, tumour invasion and angiogenesis, which makes it a candidate agent for cancer regulation. The classical synthetic pathway of 1,25(OH)2D3 involves 25- and 1,-hydroxylation of vitamin D3, in the liver and kidney, respectively, of absorbed or skin-synthesized vitamin D3. There is recent focus on the importance in growth control of local metabolism of 1,25(OH)2D3, which is a function of local tissue synthetic hydroxylases and particularly the principal catabolizing enzyme, 24-hydroxylase. The classical signalling pathway of 1,25(OH)2D3 employs the vitamin D nuclear receptor (VDR), which is a transcription factor for 1,25(OH)2D3 target genes. Effects of this pathway include inhibition of cellular growth and invasion. Cytoplasmic signalling pathways are increasingly being recognized, which similarly may regulate growth and differentiation but also apoptosis. 1,25(OH)2D3 has a major inhibitory effect on the G1/S checkpoint of the cell cycle by upregulating the cyclin dependent kinase inhibitors p27 and p21, and by inhibiting cyclin D1. Indirect mechanisms include upregulation of transforming growth factor-, and downregulation of the epidermal growth factor receptor. 1,25(OH)2D3 may induce apoptosis either indirectly through effects on the insulin-like growth receptor and tumour necrosis factor-, or more directly via the Bcl-2 family system, the ceramide pathway, the death receptors (e.g. Fas) and the stress-activated protein kinase pathways (Jun N terminal kinase and p38). Inhibition of tumour invasion and metastasis potential has been demonstrated and mechanisms include inhibition of serine proteinases, metalloproteinases and angiogenesis. The lines of evidence for an effect of vitamin D3 in systemic cancer are the laboratory demonstration of relevant effects on cellular growth, differentiation, apoptosis, malignant cell invasion and metastasis; epidemiological findings of an association of the occurrence and outcome of cancers with derangements of vitamin D3/1,25(OH)2D3 and the association of functional polymorphisms of the VDR with the occurrence of certain cancers. In addition, vitamin D3 analogues are being developed as cancer chemotherapy agents. There is accumulating evidence that the vitamin D3/1,25(OH)2D3/VDR axis is similarly important in malignant melanoma (MM). MM cells express the VDR, and the antiproliferative and prodifferentiation effects of 1,25(OH)2D3 have been shown in cultured melanocytes, MM cells and MM xenografts. Recently, an inhibitory effect on the spread of MM cells has been demonstrated, low serum levels of 1,25(OH)2D3 have been reported in MM patients and the VDR polymorphisms have been shown to be associated with both the occurrence and outcome of MM. The relationship between solar irradiation and MM is more complex than for the systemic cancers. As in other cancers, there is evidence of a protective effect of vitamin D3 in MM, but ultraviolet radiation, which is a principal source of vitamin D3, is mutagenic. Further work is necessary on the influence of serum vitamin D3 levels on the occurrence and prognosis of MM, the effects of sun protection measures on serum vitamin D3 levels in temperate climates and epidemiological studies on geographical factors and skin type on the prognosis of MM. Meanwhile, it would seem mandatory to ensure an adequate vitamin D3 status if sun exposure were seriously curtailed, certainly in relation to carcinoma of breast, prostate and colon and probably also MM. [source] Hormone replacement therapy and lung cancer risk in ChineseCANCER, Issue 8 2007Kuan-Yu Chen MD Abstract BACKGROUND. The association between hormone replacement therapy (HRT) and a reduced lung cancer risk has been reported in previous studies. There is a high female to male ratio in Chinese lung cancer patients, and female patients have different clinicopathological characteristics compared with Western patient populations. The authors investigated whether HRT may reduce lung cancer risk in Taiwan. METHODS. The authors used a case-control study design to investigate 826 women with lung cancer and 531 healthy controls. Personal interviews based on a structured questionnaire were performed to collect information on HRT use of at least 3 months, age, ethnicity, active and passive smoking, exposure to air pollution, cooking or incense fumes, body mass index (BMI), menopause, and family history of cancers. RESULTS. HRT use was associated with reduced lung cancer risk with a multivariate, adjusted odds ratio of 0.70 (95% CI, 0.53,0.94; P = .019). HRT use was associated with reduced odds ratio of lung cancer in all subset analyses stratified by histology, active and passive cigarette smoking, BMI, history of incense burning, cooking, and motorcycle riding, as well as family history of certain cancers. CONCLUSIONS. This study confirmed that HRT is associated with a reduced lung cancer risk. The results appeared to be applicable to Chinese female population groups. Cancer 2007. © 2007 American Cancer Society. [source] | ||||||||||||||||