Tracing the evolution of dust obscured star-formation and accretion back to the reionisation epoch with SPICA

Our current knowledge of star formation and accretion luminosity at high-redshift (z>3-4), as well as the possible connections between them, relies mostly on observations in the rest-frame ultraviolet (UV), which are strongly affected by dust obscuration. Due to the lack of sensitivity of past and current infrared (IR) instrumentation, so far it has not been possible to get a glimpse into the early phases of the dust-obscured Universe. Among the next generation of IR observatories, SPICA, observing in the 12-350 micron range, will be the only facility that can enable us to make the required leap forward in understanding the obscured star-formation rate and black-hole accretion rate densities (SFRD and BHARD, respectively) with respect to what Spitzer and Herschel achieved in the mid- and far-IR at z<3. In particular, SPICA will have the unique ability to trace the evolution of the obscured SFRD and BHARD over cosmic time, from the peak of their activity back to the reionisation epoch (i.e., 3 < z < 6 - 7), where its predecessors had severe limitations. Here we discuss the potential of both deep and shallow photometric surveys performed with the SPICA mid-IR instrument (SMI), enabled by the very low level of impact of dust obscuration in a band centred at 34 micron. These unique unbiased photometric surveys that SPICA will perform will be followed up by observations both with the SPICA spectrometers and with other facilities at shorter and longer wavelengths, with the aim to fully characterise the evolution of AGNs and star-forming galaxies after re-ionisation

BRCA2 Polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

Q1Q1Artículo Original1-10Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormonerelated cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10-6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations