Introduction
We 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.
Methods
Using 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).
Results
In ACA-DCE analysis, rates of uninsurance decreased (DID -5.64, 95% confidence interval [CI] -7.23 to -4.04%, p<0.001) among patients aged 19–25 relative to older patients aged 26–64. There was no significant DID in advanced stage at diagnosis (stage≥II; p = 0.6) or orchiectomy more than 14 days after diagnosis (p = 0.6). For patients who received chemotherapy or radiotherapy as their first course of treatment, treatment greater than 60 days after diagnosis decreased (DID -4.84%, 95% CI -8.22 to -1.45%, p = 0.005) among patients aged 19–25 relative to patients aged 26–64. In Medicaid expansion states, rates of uninsurance decreased (DID -4.20%, 95% CI -7.67 to -0.73%, p = 0.018) while patients receiving chemotherapy or radiotherapy greater than 60 days after diagnosis decreased (DID -8.76, 95% CI -17.13 to -0.38%, p = 0.040) compared to rates in non-expansion states. No significant DIDs were seen for stage (p = 0.8) or time to orchiectomy (p = 0.1).
Conclusions
Men 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.
Background: Inflammatory 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.
Methods:Using 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.Results: A 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.Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
Author Contributions: Mr Jain-Poster and Dr Johnson had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
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