4 research outputs found
Insurance coverage, stage at diagnosis, and time to treatment following dependent coverage and Medicaid expansion for men with testicular cancer.
IntroductionWe sought to assess the impact of Affordable Care Act Dependent Care Expansion (ACA-DCE), which allowed dependent coverage for adults aged 19-25, and Medicaid expansion on outcomes for men with testicular cancer.MethodsUsing a US-based cancer registry, we performed adjusted difference-in-difference (DID) analyses comparing outcomes between men aged 19-25 (n = 8,026) and 26-64 (n = 33,303) pre- (2007-2009) and post-ACA-DCE (2011-2016) and between men in states that expanded Medicaid (n = 2,296) to men in those that did not (n = 2,265)pre- (2011-2013) and post-Medicaid expansion (2015-2016).ResultsIn ACA-DCE analysis, rates of uninsurance decreased (DID -5.64, 95% confidence interval [CI] -7.23 to -4.04%, pConclusionsMen with testicular cancer had lower uninsurance rates and decreased time to delivery of chemotherapy or radiotherapy following ACA-DCE and Medicaid expansions. Time to orchiectomy and stage at diagnosis did not change following either insurance expansion
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Inflammatory bowel disease induces inflammatory and pre-neoplastic changes in the prostate.
BackgroundInflammatory bowel disease (IBD) has been implicated as a risk factor for prostate cancer, however, the mechanism of how IBD leads to prostate tumorigenesis is not known. Here, we investigated whether chronic intestinal inflammation leads to pro-inflammatory changes associated with tumorigenesis in the prostate.MethodsUsing clinical samples of men with IBD who underwent prostatectomy, we analyzed whether prostate tumors had differences in lymphocyte infiltrate compared to non-IBD controls. In a mouse model of chemically-induced intestinal inflammation, we investigated whether chronic intestinal inflammation could be transferred to the wild-type mouse prostate. In addition, mouse prostates were evaluated for activation of pro-oncogenic signaling and genomic instability.ResultsA higher proportion of men with IBD had T and B lymphocyte infiltration within prostate tumors. Mice with chronic colitis showed significant increases in prostatic CD45 + leukocyte infiltration and elevation of three pro-inflammatory cytokines-TIMP-1, CCL5, and CXCL1 and activation of AKT and NF-kB signaling pathways. Lastly, mice with chronic colitis had greater prostatic oxidative stress/DNA damage, and prostate epithelial cells had undergone cell cycle arrest.ConclusionsThese data suggest chronic intestinal inflammation is associated with an inflammatory-rich, pro-tumorigenic prostatic phenotype which may explain how gut inflammation fosters prostate cancer development in men with IBD