Quantum Monte Carlo Calculations of Pion Scattering from Li

We show that the neutron and proton transition densities predicted by recent quantum Monte Carlo calculations for A=6,7 nuclei are consistent with pion scattering from 6Li and 7Li at energies near the Delta resonance. This has provided a microscopic understanding of the enhancement factors for quadrople excitations, which were needed to describe pion inelastic scattering within the nuclear shell model of Cohen and Kurath.Comment: 10 pages, REVTeX, 3 postscript figures; added calculation of elastic and inelastic pion scattering from 6Li at multiple energie

Proton-proton bremsstrahlung below and above pion-threshold: the influence of the Δ\Delta-isobar

The proton-proton bremsstrahlung is investigated within a coupled-channel model with the $\Delta$ degree of freedom. The model is consistent with the $NN$ scattering up to 1 GeV and the $\gamma N\Delta$ vertex determined in the study of pion photoproduction reactions. It is found that the $\Delta$ excitation can significantly improve the agreements with the $pp \rightarrow pp\gamma$ at $E_{lab}=280$ MeV. Predictions at $E_{lab}=550$ and $800$ MeV are presented for future experimental tests.Comment: 26 pages Revtex, 12 figures are available from the authors upon request ([email protected]

Pentaquark baryon production at the Relativistic Heavy Ion Collider

Production of pentaquark $\Theta^+$ baryons in central relativistic heavy ion collisions is studied in a kinetic model. Assuming that a quark-gluon plasma is produced in the collisions, we first determine the number of $\Theta^+$ produced from the quark-gluon plasma using a parton coalescence model, and then take into consideration its production and absorption in subsequent hadronic matter via the reactions $KN\leftrightarrow\Theta$, $KN\leftrightarrow\pi\Theta$, and \piN\leftrightarrow\bar K\Theta. We find that although the final $\Theta^+$ number is affected by hadronic interactions, it remains sensitive to the initial number of $\Theta^+$ produced from the quark-gluon plasma, particularly in the case of a small $\Theta^+$ width as imposed by the $K^+N$ and $K^+d$ scattering data. Because of small baryon chemical potential in the hot dense matter produced in these collisions, the number of produced anti-$\Theta$ is only slightly smaller than that of $\Theta^+$.Comment: 6 pages, 2 figures, revised version, to appear in PL

Dynamical coupled-channel model of meson production reactions in the nucleon resonance region

A dynamical coupled-channel model is presented for investigating the nucleon resonances in the meson production reactions induced by pions and photons. The model is based on an energy-independent Hamiltonian which is derived from a set of Lagrangians by using a unitary transformation method. By applying the projection operator techniques,we derive a set of coupled-channel equations which satisfy the unitarity conditions within the channel space spanned by the considered two-particle meson-baryon states and the three-particle $\pi\pi N$ state. We present and explain in detail a numerical method based on a spline-function expansion for solving the resulting coupled-channel equations which contain logarithmically divergent one-particle-exchange driving terms resulted from the $\pi\pi N$ unitarity cut. We show that this driving term can generate rapidly varying structure in the reaction amplitudes associated with the unstable particle channels. It also has large effects in determining the two-pion production cross sections. Our results indicate that cautions must be taken to interpret the $N^*$ parameters extracted from using models which do not include $\pi\pi N$ cut effects.Comment: 73 pages, 20 figure

Three-body decay of the d* dibaryon

Under certain circumstances, a three-body decay width can be approximated by an integral involving a product of two off-shell two-body decay widths. This ``angle-average'' approximation is used to calculate the $\pi NN$ decay width of the $d^*(J^\pi=3^+, T=0)$ dibaryon in a simple $\Delta^2$ model for the most important Feynman diagrams describing pion emissions with baryon-baryon recoil and meson retardation. The decay width is found to be about 0.006 (0.07, 0.5) MeV at the $d^*$ mass of 2065 (2100, 2150) MeV for input dynamics derived from the Full Bonn potential. The smallness of this width is qualitatively understood as the result of the three-body decay being ``third forbidden''. The concept of $\ell$ forbiddenness and the threshold behavior of a three-body decay are further studied in connection with the $\pi NN$ decay of the dibaryon $d'(J^\pi=0^-, T=0 or 2)$ where the idea of unfavorness has to be introduced. The implications of these results are briefly discussed.Comment: 15 pages, RevTeX, two-column journal style, six figure

FGF receptor genes and breast cancer susceptibility: results from the Breast Cancer Association Consortium

Background:Breast cancer is one of the most common malignancies in women. Genome-wide association studies have identified FGFR2 as a breast cancer susceptibility gene. Common variation in other fibroblast growth factor (FGF) receptors might also modify risk. We tested this hypothesis by studying genotyped single-nucleotide polymorphisms (SNPs) and imputed SNPs in FGFR1, FGFR3, FGFR4 and FGFRL1 in the Breast Cancer Association Consortium. Methods:Data were combined from 49 studies, including 53 835 cases and 50 156 controls, of which 89 050 (46 450 cases and 42 600 controls) were of European ancestry, 12 893 (6269 cases and 6624 controls) of Asian and 2048 (1116 cases and 932 controls) of African ancestry. Associations with risk of breast cancer, overall and by disease sub-type, were assessed using unconditional logistic regression. Results:Little evidence of association with breast cancer risk was observed for SNPs in the FGF receptor genes. The strongest evidence in European women was for rs743682 in FGFR3; the estimated per-allele odds ratio was 1.05 (95 confidence interval=1.02-1.09, P=0.0020), which is substantially lower than that observed for SNPs in FGFR2. Conclusion:Our results suggest that common variants in the other FGF receptors are not associated with risk of breast cancer to the degree observed for FGFR2. © 2014 Cancer Research UK

The BRCA2 c.68-7T > A variant is not pathogenic : A model for clinical calibration of spliceogenicity

Although the spliceogenic nature of the BRCA2 c.68-7T > A variant has been demonstrated, its association with cancer risk remains controversial. In this study, we accurately quantified by real-time PCR and digital PCR (dPCR), the BRCA2 isoforms retaining or missing exon 3. In addition, the combined odds ratio for causality of the variant was estimated using genetic and clinical data, and its associated cancer risk was estimated by case-control analysis in 83,636 individuals. Co-occurrence in trans with pathogenic BRCA2 variants was assessed in 5,382 families. Exon 3 exclusion rate was 4.5-fold higher in variant carriers (13%) than controls (3%), indicating an exclusion rate for the c.68-7T > A allele of approximately 20%. The posterior probability of pathogenicity was 7.44x10(-115). There was neither evidence for increased risk of breast cancer (OR 1.03; 95% CI 0.86-1.24) nor for a deleterious effect of the variant when co-occurring with pathogenic variants. Our data provide for the first time robust evidence of the nonpathogenicity of the BRCA2 c.68-7T > A. Genetic and quantitative transcript analyses together inform the threshold for the ratio between functional and altered BRCA2 isoforms compatible with normal cell function. These findings might be exploited to assess the relevance for cancer risk of other BRCA2 spliceogenic variants.Peer reviewe

Fine-Scale Mapping of the 5q11.2 Breast Cancer Locus Reveals at Least Three Independent Risk Variants Regulating MAP3K1

Peer reviewe

Identification of independent association signals and putative functional variants for breast cancer risk through fine-scale mapping of the 12p11 locus.

BACKGROUND: Multiple recent genome-wide association studies (GWAS) have identified a single nucleotide polymorphism (SNP), rs10771399, at 12p11 that is associated with breast cancer risk. METHOD: We performed a fine-scale mapping study of a 700 kb region including 441 genotyped and more than 1300 imputed genetic variants in 48,155 cases and 43,612 controls of European descent, 6269 cases and 6624 controls of East Asian descent and 1116 cases and 932 controls of African descent in the Breast Cancer Association Consortium (BCAC; http://bcac.ccge.medschl.cam.ac.uk/ ), and in 15,252 BRCA1 mutation carriers in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). Stepwise regression analyses were performed to identify independent association signals. Data from the Encyclopedia of DNA Elements project (ENCODE) and the Cancer Genome Atlas (TCGA) were used for functional annotation. RESULTS: Analysis of data from European descendants found evidence for four independent association signals at 12p11, represented by rs7297051 (odds ratio (OR) = 1.09, 95 % confidence interval (CI) = 1.06-1.12; P = 3 × 10(-9)), rs805510 (OR = 1.08, 95 % CI = 1.04-1.12, P = 2 × 10(-5)), and rs1871152 (OR = 1.04, 95 % CI = 1.02-1.06; P = 2 × 10(-4)) identified in the general populations, and rs113824616 (P = 7 × 10(-5)) identified in the meta-analysis of BCAC ER-negative cases and BRCA1 mutation carriers. SNPs rs7297051, rs805510 and rs113824616 were also associated with breast cancer risk at P < 0.05 in East Asians, but none of the associations were statistically significant in African descendants. Multiple candidate functional variants are located in putative enhancer sequences. Chromatin interaction data suggested that PTHLH was the likely target gene of these enhancers. Of the six variants with the strongest evidence of potential functionality, rs11049453 was statistically significantly associated with the expression of PTHLH and its nearby gene CCDC91 at P < 0.05. CONCLUSION: This study identified four independent association signals at 12p11 and revealed potentially functional variants, providing additional insights into the underlying biological mechanism(s) for the association observed between variants at 12p11 and breast cancer risk.UK funding includes Cancer Research UK and NIH.This is the final version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s13058-016-0718-

Fine-Scale Mapping of the 4q24 Locus Identifies Two Independent Loci Associated with Breast Cancer Risk

Background: A recent association study identified a common variant (rs9790517) at 4q24 to be associated with breast cancer risk. Independent association signals and potential functional variants in this locus have not been explored. Methods: We conducted a fine-mapping analysis in 55,540 breast cancer cases and 51,168 controls from the Breast Cancer Association Consortium. Results: Conditional analyses identified two independent association signals among women of European ancestry, represented by rs9790517 [conditional P = 2.51 × 10−4; OR, 1.04; 95% confidence interval (CI), 1.02–1.07] and rs77928427 (P = 1.86 × 10−4; OR, 1.04; 95% CI, 1.02–1.07). Functional annotation using data from the Encyclopedia of DNA Elements (ENCODE) project revealed two putative functional variants, rs62331150 and rs73838678 in linkage disequilibrium (LD) with rs9790517 (r2 ≥ 0.90) residing in the active promoter or enhancer, respectively, of the nearest gene, TET2. Both variants are located in DNase I hypersensitivity and transcription factor–binding sites. Using data from both The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), we showed that rs62331150 was associated with level of expression of TET2 in breast normal and tumor tissue. Conclusion: Our study identified two independent association signals at 4q24 in relation to breast cancer risk and suggested that observed association in this locus may be mediated through the regulation of TET2. Impact: Fine-mapping study with large sample size warranted for identification of independent loci for breast cancer risk