1,721,034 research outputs found

    Potentially Inappropriate Prescribing in Nursing Homes Residents in Tuscany

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    To determine the prevalence of IP in residents of Tuscany Nursing Homes (NHs) using a subset of 10 indicators of STOPP criteri

    Folic acid fortification and cancer risk

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    Roger Bayston and colleagues1 state that, to the best of our knowledge, folic acid does not reduce colorectal cancer risk but neither does it increase it. Although the question surrounding this type of cancer is still debated, we want to underline the possibility that folic acid fortification could have many more beneficial effects than merely those on neural tube defects. Lack of maternal folate supplementation has been associated with an increased risk of childhood leukaemia, possibly resulting from DNA hypomethylation and strand breakage.2 Susceptibility to some types of cancer has been linked to the methylation level of the gene encoding cyclin-dependent kinase inhibitor 2A (CDKN2A), and there seems to be an interesting association between folate concentrations and consequent hypermethylation of such genes.3 Decreased dietary folate has also been associated with epigenetic silencing of CDKN2A in solid tumours, and this relation has been shown to be modified by the MTHFR genotype, suggesting a mechanism of action of folate deficiency in cancer.4 The folate pathways that maintain cell homoeostasis and genomic integrity during cellular division could represent an essential step in our understanding of the biology of cancers. Additional experimental and clinical observations could help clarify the role of folate concentrations and methylation of genes such as CDKN2A in the homoeostasis of normal and malignant blood cells. To avoid the risk of colon cancer, perhaps a genetic analysis of patients could be done to identify individuals with the MTHFR 677TT genotype, which could be the only condition in which high concentrations of folate might promote colon cancer development.5 We declare that we have no conflict of interest

    Unusual association of endometrial cancer and multiple myeloma

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    Abstract OBJECTIVE: Determine whether there is an association between uterine cancer and multiple myeloma. METHODS: Data on second malignancies were obtained for 368 uterine corpus cancer patients treated between 1992 and 2005. Detailed family histories were devised for 192 probands. Diagnoses of multiple myelomas, lymphomas and leukemias in family members were medical record verified. The frequency of multiple myeloma among uterine cancer patients was compared to the female age-adjusted incidence rate of multiple myeloma obtained from the SEER database. The crude rate of multiple myeloma (as well as Hodgkin's, non-Hodgkin's lymphomas and leukemias) among first-degree relatives of patients with uterine cancer was compared to the age-adjusted incidence rate of multiple myeloma in the general population. Descriptive statistics were used to evaluate disease and cohort characteristics. A P value less than 0.05 was considered statistically significant. RESULTS: Two of 368 uterine cancer patients were also diagnosed with multiple myeloma, both at age 50. The observed incidence of multiple myeloma in this cohort (543 per 100,000; 95% CI: 66-1962 per 100,000) represents a 120-fold increase based on predicted incidence (P=0.00014). The frequency of multiple myeloma in first-degree relatives was 2/1351 (148 per 100,000; 95% CI: 14.8-533 per 100,000) which represents a 27-fold increase compared to the general population (P=0.0026). The frequencies of leukemias and lymphomas in these family members on the other hand were not significantly increased (P=0.152 and P=0.218). CONCLUSION: This specific excess frequency of early onset multiple myeloma in endometrial cancer probands and their relatives suggests shared susceptibility

    MDR1 modulates apoptosis in CD34+ leukemic cells

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    Abstract In view of obscure clinical and biological significance of leukemic cells heterogeneity, we studied the efficacy of apoptosis, proliferation, and expression levels of the Bcl-2, MDR1, LRP, and BCRP genes in sorted CD34+ and CD34- subpopulations of childhood AML leukemic samples. In five out of nine cases, CD34+ cells were less sensitive to spontaneous apoptosis and had from 1.2- to 5.0-fold higher expression levels of Bcl-2 (eight of ten) and from 1.5- to 28.7-fold higher expression levels of MDR1 (eight of ten). The expression levels of the LRP gene were from 1.1- to 1.8-fold higher in CD34+ subpopulations (five of ten cases), and the expression levels of the BCRP gene were from 1.1- to 22.4-fold higher in CD34+ leukemic cells (six of ten). In all M4 cases, the expression levels of LRP were higher in the CD34- subpopulation. Significant differences in the patterns of genes expression between patients do not allow us to conclude that the CD34+ fractions have more resistant phenotype than the CD34- subpopulations. Nevertheless, distinctions between CD34+ and CD34- cells may lead to different chemosensitivities between leukemic subpopulations in vivo and may determine the alteration of the leukemic immunophenotype during treatment and in relapse
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