I quadri istopatologici extracardiaci nelle intossicazioni acute mortali da eroina e cocaina

We present a measurement of the W-boson-pair production cross section in p (p) over bar collisions at 1.96 TeV center-of-mass energy and the first measurement of the differential cross section as a function of jet multiplicity and leading-jet energy. The W+W- cross section is measured in the final state comprising two charged leptons and neutrinos, where either charged lepton can be an electron or a muon. Using data collected by the CDF experiment corresponding to 9.7 fb(-1) of integrated luminosity, a total of 3027 collision events consistent with W+W- production are observed with an estimated background contribution of 1790 +/- 190 events. The measured total cross section is sigma(p (p) over bar --> W+W-) = 14.0 +/- 0.6(stat)(-1.0)(+1.2)(syst) +/- 0.8(lumi) pb, consistent with the standard model prediction

The FANCM:p.Arg658* truncating variant is associated with risk of triple-negative breast cancer

Breast cancer is a common disease partially caused by genetic risk factors. Germline pathogenic variants in DNA repair genes BRCA1, BRCA2, PALB2, ATM, and CHEK2 are associated with breast cancer risk. FANCM, which encodes for a DNA translocase, has been proposed as a breast cancer predisposition gene, with greater effects for the ER-negative and triple-negative breast cancer (TNBC) subtypes. We tested the three recurrent protein-truncating variants FANCM:p.Arg658*, p.Gln1701*, and p.Arg1931* for association with breast cancer risk in 67,112 cases, 53,766 controls, and 26,662 carriers of pathogenic variants of BRCA1 or BRCA2. These three variants were also studied functionally by measuring survival and chromosome fragility in FANCM−/− patient-derived immortalized fibroblasts treated with diepoxybutane or olaparib. We observed that FANCM:p.Arg658* was associated with increased risk of ER-negative disease and TNBC (OR = 2.44, P = 0.034 and OR = 3.79; P = 0.009, respectively). In a country-restricted analysis, we confirmed the associations detected for FANCM:p.Arg658* and found that also FANCM:p.Arg1931* was associated with ER-negative breast cancer risk (OR = 1.96; P = 0.006). The functional results indicated that all three variants were deleterious affecting cell survival and chromosome stability with FANCM:p.Arg658* causing more severe phenotypes. In conclusion, we confirmed that the two rare FANCM deleterious variants p.Arg658* and p.Arg1931* are risk factors for ER-negative and TNBC subtypes. Overall our data suggest that the effect of truncating variants on breast cancer risk may depend on their position in the gene. Cell sensitivity to olaparib exposure, identifies a possible therapeutic option to treat FANCM-associated tumors