Effects of MAD2L1 or BUB1 depletion on the phenotype of MDA-MB-231 cancer cells <i>in vitro</i>.

<p>A) MAD2L1 protein expression by western blot analysis, β-actin used as control. B) Knockdown of <i>MAD2L1</i> expression inhibited cell proliferation. C) Knockdown of <i>MAD2L1</i> expression inhibited cell migration. D) Knockdown of <i>MAD2L1</i> expression inhibited cell invasion. E) Representative pictures of cell migration and invasion before and after knockdown. F) BUB1 protein expression by western blot analysis, β-actin used as control. G) Knockdown of <i>BUB1</i> expression inhibited cell proliferation. H) Knockdown of <i>BUB1</i> expression inhibited cell migration. I) Knockdown of <i>BUB1</i> expression inhibited cell invasion. J) Representative pictures of cell migration and invasion before and after knockdown. * = P<0.001.</p

Biological and Clinical Significance of <i>MAD2L1</i> and <i>BUB1</i>, Genes Frequently Appearing in Expression Signatures for Breast Cancer Prognosis

<div><p>To investigate the biologic relevance and clinical implication of genes involved in multiple gene expression signatures for breast cancer prognosis, we identified 16 published gene expression signatures, and selected two genes, <i>MAD2L1</i> and <i>BUB1</i>. These genes appeared in 5 signatures and were involved in cell-cycle regulation. We analyzed the expression of these genes in relation to tumor features and disease outcomes. <i>In vitro</i> experiments were also performed in two breast cancer cell lines, MDA-MB-231 and MDA-MB-468, to assess cell proliferation, migration and invasion after knocking down the expression of these genes. High expression of these genes was found to be associated with aggressive tumors and poor disease-free survival of 203 breast cancer patients in our study, and the association with survival was confirmed in an online database consisting of 914 patients. <i>In vitro</i> experiments demonstrated that lowering the expression of these genes by siRNAs reduced tumor cell growth and inhibited cell migration and invasion. Our investigation suggests that MAD2L1 and BUB1 may play important roles in breast cancer progression, and measuring the expression of these genes may assist the prediction of breast cancer prognosis.</p></div

Characteristics of selected pancreatic cancer cases and controls, case-control study in urban Shanghai.

<p>^aContinuous variables were expressed as median (interquartile) and categorical variables were expressed as frequency(percentage among cases or controls).</p><p>^b<i>P</i>-value were calculated from student’s t test for continuous variables and χ²-test for categorical variables.</p><p>^c<i>P</i>-value were calculated from Fisher’s exact test.</p><p>^d<i>P</i>-value were calculated from student’s t test for log₁₀ transformed standardized PGE-M.</p><p>Characteristics of selected pancreatic cancer cases and controls, case-control study in urban Shanghai.</p

Association of urinary PGE-M levels and risk of pancreatic cancer.

<p>Abbreviation: OR, odds ratio; CI, confidence interval; Cr, creatinine.</p><p>^abasic model: adjusted for gender and age.</p><p>^bfull model: adjusted for gender, age, education levels, family history of pancreatic cancer, and diabetes history (three categories: no diabetes history, diagnosed less than 3 years before interview, diagnosed at least 3 years before interview).</p><p>Association of urinary PGE-M levels and risk of pancreatic cancer.</p

Kaplan-Meier survival curves by different levels of <i>MAD2L1</i> and <i>BUB1</i> expression in the GOBO database.

<p>A) Overall survival (OS) by low, medium and high <i>MAD2L1</i> expression; B) Relapse-free survival (RFS) by low, medium and high <i>MAD2L1</i> expression; C) Overall survival (OS) by low, medium and high <i>BUB1</i> expression; (D) Relapse-free survival (RFS) by low, medium and high <i>BUB1</i> expression.</p

Kaplan-Meier survival curves by different levels of <i>MAD2L1</i> and <i>BUB1</i> expression in 203 breast cancer patients.

<p>A) Overall survival (OS) by low, medium and high <i>MAD2L1</i> expression; B) Relapse-free survival (RFS) by low, medium and high <i>MAD2L1</i> expression; C) Overall survival (OS) by low, medium and high <i>BUB1</i> expression; (D) Relapse-free survival (RFS) by low, medium and high <i>BUB1</i> expression.</p

Combined effects of PGE-M and some a priori factors on risk for pancreatic cancer.

<p>Adjusted ORs for pancreactic cancer according to the tertiles of PGE-M and diabetes status (A), meat intake (B), vegetables/fruits intake (C), and current aspirin usage (D). Adjusted for gender and age. Diabetes History was considered positive for self-reported diabetes diagnosed at least 3 years before interview.</p

Urinary Prostaglandin E₂ Metabolite and Pancreatic Cancer Risk: Case-Control Study in Urban Shanghai

<div><p>Pancreatic cancer has been increasing in importance in Shanghai over the last four decades. The etiology of the disease is still unclear. Evidence suggests that the COX-2 pathway, an important component of inflammation, may be involved in the disease. We aimed to evaluate the association between urinary prostaglandin E₂ metabolite (PGE-M) level and risk of pancreatic cancer. From a recent population-based case-control study in Shanghai, 200 pancreatic ductal adenocarcinoma cases and 200 gender- and age- frequency matched controls were selected for the present analysis. Urinary PGE-M was measured with a liquid chromatography/mass spectrometric assay. Adjusted unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). A positive association was observed between PGE-M leve and pancreatic cancer risk: OR = 1.63 (95% CI 1.01–2.63) for the third tertile compared to the first. Though the interactions were not statistically significant, the associations tended to be stronger among subjects with diabetes history (OR = 3.32; 95% CI 1.20–9.19) and higher meat intake (OR = 2.12; 95% CI 1.10–4.06). The result suggests that higher urinary PGE-M level may be associated with increased risk of pancreatic ductal adenocarcinoma.</p></div

Multivariate-Adjusted Hazard Ratios (HRs) and 95% CIs for cancer-specific death (due to lymphoma) by stage and age group in Nine SEER Registries during 1990–2014 period.

<p>Multivariate-Adjusted Hazard Ratios (HRs) and 95% CIs for cancer-specific death (due to lymphoma) by stage and age group in Nine SEER Registries during 1990–2014 period.</p

Forest plots showing Multivariate-Adjusted Hazard Ratios (HRs) and 95%CIs for cancer-specific death (due to lymphoma) by race and year of Diagnosis in 9 SEER Registries (1990–2014).

<p>HL: Hodgkin’s Lymphoma; NHL: Non-Hodgkin’s Lymphoma; HR: Hazard ratio.</p