A community-based trial of educational interventions with fecal immunochemical tests for colorectal cancer screening uptake among blacks in community settings

BACKGROUND

Intervention studies among individuals in diverse community settings are needed to reduce health disparities in colorectal cancer (CRC) screening and mortality rates. The current study compared the efficacy of 2 intervention conditions promoting CRC screening among black individuals.

METHODS

Black individuals ages 50 to 75 years (N = 330) were recruited in community settings in 4 Tampa Bay counties. After obtaining consent and conducting a baseline interview to assess sociodemographic and health-related variables, participants received either a culturally targeted CRC photonovella booklet plus a fecal immunochemical test (FIT) kit or a standard CRC screening brochure plus an FIT kit. The primary outcome was FIT kit screening uptake.

RESULTS

FIT screening uptake at 6 months was 86.7% overall (90.3% in the brochure group and 81.9% in the photonovella group). Controlling for baseline between-group differences, there was no influence of intervention on FIT kit uptake (P = .756). Significant predictors of not returning an FIT kit included being unable to work (P = .010), having higher religious belief scores (P = .015), and living farther from the cancer center (P = .015).

CONCLUSIONS

Providing FIT kits and educational print materials to black individuals in community settings resulted in high rates of CRC screening. The study also identified subgroups of participants who were less likely to return an FIT kit and provides insight for future interventions. Cancer 2016. © 2016 American Cancer Society.

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Correction

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In This Issue

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Issue Information

Cover of this issue. Localization of Pragmin to focal adhesions. See also Senda, Y., et al. (pages 972–980 of this issue).

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Myasthenic crisis and polymyositis induced by one dose of nivolumab

An 80-year-old man, who developed multiple lymph node and skin metastasis of malignant melanoma, received nivolumab monotherapy. Two weeks after the first dose, he experienced anorexia and fatigue, and suffered from progressive, severe dyspnea and muscle weakness. We diagnosed him with myocarditis, myositis, and myasthenic crisis induced by nivolumab. We commenced steroid therapy, immune absorption therapy, plasma exchange therapy, and i.v. immunoglobulin therapy, and succeeded in saving his life. Because his serum level of anti-acetylcholine receptor antibodies in a sample collected before nivolumab treatment were positive and were elevated significantly after nivolumab, we suspected that nivolumab triggered a severe autoimmune response, which progressed subclinical myasthenia gravis to myasthenic crisis. We carried out T cell receptor repertoire analysis using next-generation sequencing technologies and identified infiltration of clonally expanded T cell populations in the skeletal muscle after nivolumab treatment, implying a very strong T cell immune response against muscular cells. To avoid severe immune-related adverse events, the exclusion of patients with subclinical autoimmune disease is very important for treatment with immune checkpoint inhibitors.

Myasthenic crisis and polymyositis were induced by one dose of nivolumab. We performed T cell receptor repertoire analysis using the next-generation sequencing technologies and identified infiltration of clonally expanded T cell populations in the skeletal muscle tissue after the nivolumab treatment, implying the very strong T cell immune response against muscular cells

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HBx mutations promote hepatoma cell migration through the Wnt/β-catenin signaling pathway

Abstract

HBx mutations (T1753V, A1762T, G1764A, T1768A) are frequently observed in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Aberrant activation of the Wnt/β-catenin signaling pathway is involved in the development of HCC. However, activation of the Wnt/β-catenin signaling pathway by HBx mutants has not been studied in hepatoma cells or HBV-associated HCC samples.In this study, we examined the effects of HBx mutants on the migration and proliferation of HCC cellsand evaluated the activation of Wnt/β-catenin signaling in HBx-transfected HCC cells and HBV-related HCC tissues. We found that HBx mutants (T, A, TA, and Combo) promoted the migration and proliferation of hepatoma cells. The HBx Combo mutantpotentiated TOP-luc activityand increased nuclear translocation ofβ-catenin.Moreover, the HBxCombo mutant increased and stabilizedβ-catenin levels through inactivation of GSK-3β, resulting in upregulation of downstream target genes such as c-Myc, CTGF, and WISP2. Enhanced activation of Wnt/β-catenin was found in HCC tissues with HBx TA and Combo mutations. Knockdown of β-catenin effectively abrogated cell migration and proliferation stimulated by the HBx TA and Combo mutants. Our results indicate that HBx mutants, especially the Combo mutant, allow constitutive activation of the Wnt signaling pathway and may play a pivotal role in HBV-associated hepatocarcinogenesis.

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A splicing variant of TERT identified by GWAS interacts with menopausal estrogen therapy in risk of ovarian cancer

ABSTRACT

Menopausal estrogen-alone therapy (ET) is a well-established risk factor for serous and endometrioid ovarian cancer. Genetics also plays a role in ovarian cancer, which is partly attributable to 18 confirmed ovarian cancer susceptibility loci identified by genome-wide association studies. The interplay among these loci, ET use, and ovarian cancer risk has yet to be evaluated. We analyzed data from 1,414 serous cases, 337 endometrioid cases, and 4,051 controls across 10 case-control studies participating in the Ovarian Cancer Association Consortium (OCAC). Conditional logistic regression was used to determine the association between the confirmed susceptibility variants and risk of serous and endometrioid ovarian cancer among ET users and non-users separately and to test for statistical interaction. A splicing variant in TERT, rs10069690, showed a statistically significant interaction with ET use for risk of serous ovarian cancer (p_int=0.013). ET users carrying the T allele had a 51% increased risk of disease (OR=1.51, 95% CI 1.19-1.91), which was stronger for long-term ET users of 10+ years (OR=1.85, 95% CI 1.28-2.66, p_int=0.034). Non-users showed essentially no association (OR=1.08, 95% CI 0.96-1.21). Two additional genomic regions harboring rs7207826 (C allele) and rs56318008 (T allele) also had significant interactions with ET use for the endometrioid histotype (p_int=0.021 and p_int=0.037, respectively). Hence, a total of three confirmed susceptibility variants were identified whose associations with ovarian cancer risk are modified by ET exposure; follow-up is warranted given that these interactions are not adjusted for multiple comparisons. These findings, if validated, may elucidate the mechanism of action of these loci. This article is protected by copyright. All rights reserved.

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