Intracoronary stents can be implanted with a low incidence of stent thrombosis (< 1%) when the stent procedure is guided by intravascular ultrasound. The long-term clinical and angiographic effects, however, have not been reported. This study assesses the 6 month clinical and angiographic results of a consecutive series of patients with intravascular ultrasound guided Palmaz-Schatz stent deployment that were not treated with subsequent anticoagulation after a successful stent implantation procedure. From March, 1993 to April 1994, 411 patients underwent Palmaz-Schatz stent implantation. There were 26 patients that had uncomplicated Palmaz-Schatz stent implantation that were treated with a standard anticoagulation regimen that are not evaluated in this study. Thus, this study includes an assessment of 385 patients that had either a successful intravascular ultrasound guided stent implantation procedure and did not receive post procedure anticoagulation or had a procedural complication. Procedural success was achieved in 369 patients (96%). Clinical success (procedure success without early post procedure event) was achieved in 363 patients (94%). There were 2 acute stent thrombosis events (0.5%) and 1 subacute stent thrombosis (0.3%) in the group of 369 patients with 454 lesions treated without anticoagulation. At 6 month clinical follow-up the incidence of myocardial infarction was 4.9% and the rate of coronary bypass surgery was 6.2%. There was a 2.1% incidence of death. Emergency intervention (emergency angioplasty or bailout stent implantation was necessary in 3 patients (0.8%). The total incidence of repeat percutaneous intervention was 11.4%. By 6 months clinical follow-up, major events had occurred in 19.2% of patients. The angiographic lesion restenosis rate, according to 50% diameter stenosis criteria, was 19%. The incidence of restenosis per patient was 22%. In conclusion, intravascular ultrasound guided Palmaz-Schatz can be performed without subsequent anticoagulation with a low incidence of stent thrombosis and acceptable clinical and angiographic outcome at 6 month clinical follow-up.

Background: Although high doses of ionizing radiation have long been linked to circulatory disease, evidence for an association at lower exposures remains controversial. However, recent analyses suggest excess relative risks at occupational exposure levels

Introduction: Several common breast cancer genetic susceptibility variants have recently been identified. We aimed to determine how these variants combine with a subset of other known risk factors to influence breast cancer risk in white women of European ancestry using case-control studies participating in the Breast Cancer Association Consortium.Methods: We evaluated two-way interactions between each of age at menarche, ever having had a live birth, number of live births, age at first birth and body mass index (BMI) and each of 12 single nucleotide polymorphisms (SNPs) (10q26-rs2981582 (FGFR2), 8q24-rs13281615, 11p15-rs3817198 (LSP1), 5q11-rs889312 (MAP3K1), 16q12-rs3803662 (TOX3), 2q35-rs13387042, 5p12-rs10941679 (MRPS30), 17q23-rs6504950 (COX11), 3p24-rs4973768 (SLC4A7), CASP8-rs17468277, TGFB1-rs1982073 and ESR1-rs3020314). Interactions were tested for by fitting logistic regression models including per-allele and linear trend main effects for SNPs and risk factors, respectively, and single-parameter interaction terms for linear departure from independent multiplicative effects.Results: These analyses were applied to data for up to 26,349 invasive breast cancer cases and up to 32,208 controls from 21 case-control studies. No statistical evidence of interaction was observed beyond that expected by chance. Analyses were repeated using data from 11 population-based studies, and results were very similar.Conclusions: The relative risks for breast cancer associated with the common susceptibility variants identified to date do not appear to vary across women with different reproductive histories or body mass index (BMI). The assumption of multiplicative combined effects for these established genetic and other risk factors in risk prediction models appears justified. © 2010 Milne et al.; licensee BioMed Central Ltd.

Immunosuppression plays a pivotal role in assisting tumors to evade immune destruction and promoting tumor development. We hypothesized that genetic variation in the immunosuppression pathway genes may be implicated in breast cancer tumorigenesis. We included 42,510 female breast cancer cases and 40,577 controls of European ancestry from 37 studies in the Breast Cancer Association Consortium (2015) with available genotype data for 3595 single nucleotide polymorphisms (SNPs) in 133 candidate genes. Associations between genotyped SNPs and overall breast cancer risk, and secondarily according to estrogen receptor (ER) status, were assessed using multiple logistic regression models. Gene-level associations were assessed based on principal component analysis. Gene expression analyses were conducted using RNA sequencing level 3 data from The Cancer Genome Atlas for 989 breast tumor samples and 113 matched normal tissue samples. SNP rs1905339 (A>G) in the STAT3 region was associated with an increased breast cancer risk (per allele odds ratio 1.05, 95 % confidence interval 1.03–1.08; p value = 1.4 × 10−6). The association did not differ significantly by ER status. On the gene level, in addition to TGFBR2 and CCND1, IL5 and GM-CSF showed the strongest associations with overall breast cancer risk (p value = 1.0 × 10−3 and 7.0 × 10−3, respectively). Furthermore, STAT3 and IL5 but not GM-CSF were differentially expressed between breast tumor tissue and normal tissue (p value = 2.5 × 10−3, 4.5 × 10−4 and 0.63, respectively). Our data provide evidence that the immunosuppression pathway genes STAT3,IL5, and GM-CSF may be novel susceptibility loci for breast cancer in women of European ancestry.