The combined effects of rs2046210 and rs4784227.

a<p>Adjusted by age, BMI, age at menarche, age at first live birth, menopausal status and family history breast cancer where appropriate.</p>b<p>The risk allele included rs2046210-A and rs4784227-T.</p><p>The combined effects of rs2046210 and rs4784227.</p

Distributions of selected characteristics in breast cancer cases and healthy-control cases.

a<p>Unnatural menopause include hysterectomy operation and other status.</p><p>Distributions of selected characteristics in breast cancer cases and healthy-control cases.</p

Stratified analyses on associations among rs2046210 and rs4784227 and risk of breast cancer.

a<p>Counting genotypes as ranking variables.</p>b<p>Derived from additive model with an adjustment by age, BMI, age at menarche, age at first live birth, menopausal status and family history breast cancer where appropriate.</p>c<p><i>P</i> for heterogeneity test.</p><p>Stratified analyses on associations among rs2046210 and rs4784227 and risk of breast cancer.</p

Logistic regression analyses on associations among rs2046210, rs4784227 and risk of breast cancer.

a<p>Reference allele/risk allele.</p>b<p>Adjusted by age, BMI, age at menarche, age at first live birth, menopausal status and family history of breast cancer where appropriate.</p>c<p><i>P</i> trend for genotypes between cases and controls.</p>d<p>Two-sided χ² test for differences in frequency distribution of alleles between cases and controls.</p>e<p>Two-sided χ² test for differences in frequency distribution of combined genotypes(dominant model) between cases and controls.</p><p>Logistic regression analyses on associations among rs2046210, rs4784227 and risk of breast cancer.</p

Additional file 1 of Healthy lifestyles, systemic inflammation and breast cancer risk: a mediation analysis

Supplementary Material 1: Supplementary Table 1. The construction of HLI Supplementary Table 2. The levels of inflammation markers and the risk of breast cancer among women from the UK Biobank Supplementary Table 3. The levels of inflammation markers and the risk of breast cancer by menopausal status Supplementary Table 4. The levels of inflammation markers and the risk of breast cancer grouped by 2 years entering the cohort Supplementary Table 5. The associations between HLI and inflammation markers Supplementary Table 6. The associations between individual components of HLI and inflammation markers Supplementary Table 7. Independent and joint effects of HLI and inflammation markers on breast cancer risk Supplementary Table 8. The association between HLI and the risk of breast cancer by menopausal status Supplementary Table 9. The associations between individual components of HLI and breast cancer risk among overall, premenopausal, and postmenopausal women in UK Biobank Supplementary Table 10. The mediation analysis of the inflammation markers in the association between HLI and breast cancer risk Supplementary Table 11. Mediating effects of inflammation markers on the association between diet score and breast cancer risk Supplementary Table 12. Mediating effects of inflammation markers on the association between physical activity and breast cancer risk Supplementary Table 13. Mediating effects of inflammation markers on the association between BMI and breast cancer risk Supplementary Table 14. Mediating effects of inflammation markers on the association between WC and breast cancer risk Supplementary Table 15. Mediating effects of inflammation markers on the association between smoking and breast cancer risk Supplementary Figure 1. The associations between levels of CRP, LMR, SII, CAR, CLR, MHR and NHR and breast cancer were evaluated on a continuous scale with restricted cubic spline curves based on cox regression with four knots. Solid lines are multivariable adjusted odds ratios, with dashed lines showing 95% confidence intervals. Blue curves show the fraction of breast cancer with different levels of inflammation marker

Efficacy and safety of neoadjuvant therapy for triple-negative breast cancer: a Bayesian network meta-analysis

Numerous studies have concentrated on neoadjuvant therapies for treating triple-negative breast cancer (TNBC) that improve the pathological complete response (pCR) rate but remain controversial. We conducted a network meta-analysis (NMA) to objectively explore the efficacy and safety of different neoadjuvant regimens. Phase II/III randomized clinical trials that compared different neoadjuvant therapies for TNBC were included. NMA and pairwise meta-analysis were performed using WinBUGS (version 1.4.3) and Review Manager 5.3. Forty-four studies with 8459 patients met the eligibility criteria. The NMA of pCR showed that programmed cell death Protein-1 and programmed cell death Ligand-1 inhibitors (PD-1/PD-L1), bevacizumab (Bev), zoledronic acid (ZOL), and platinum salts plus poly polymerase inhibitors (Pt+PARPi) may be favorable for TNBC neoadjuvant therapy. Chemotherapy combined with platinum salts or nanoparticle albumin-bound paclitaxel (Nab-p) has additional beneficial effects. However, neo-type drugs may also have increased toxicity. PD-1/PD-L1, Bev, ZOL, and Pt+ PARPi-containing regimens improved the pCR rate compared to traditional chemotherapy, including anthracyclines and taxanes. Chemotherapy with platinum salts or Nab-p improved the pCR rate. Nevertheless, the balance between efficacy and toxicity should be evaluated rigorously. PD-1/PD-L1-containing regimens appear to be the most favorable for TNBC neoadjuvant therapy, with good efficacy and tolerance.</p

X chromosome inactivation analysis.

<p>After digestion with or without Hpa II, DNA was used to amplify a polymorphic CAG repeat within the androgen receptor (AR) gene. The size of the allele is determined by the number of repeats. The area under the peak indicates the degree of amplification of that allele. II5 and II3 inherited the allele 276 from their mother (I 1) and allele 265 from their father, II7 inherited the other allele 286 from I 1. After digestion with Hpa II, their paternal allele was predominantly amplified and represented the inactive. In contrast, III2 inherited the allele 276 from her mother (II3), which was predominantly amplified and represented the inactive. Thus four of them showed skewing of XCI (XCI ratio≥80∶20).</p

Alignment of ALDP proteins in different species.

<p>The black bar indicates the position of p.283H in the ALDP sequence.</p

Biochemical findings^a.

a<p>VLCFAs normal ranges: C26 0.378–0.642 µmol/L; C24/C22 0.606–1.16; C26/C22 0.011–0.023.</p>b<p>unit: µmol/L.</p

XCI pattern of X-ALD carriers, related noncarriers and normal controls.

<p>XCI pattern of X-ALD carriers, related noncarriers and normal controls.</p