Patient-Provider Discussion About Lung Cancer Screening by Race and Ethnicity: Implications for Equitable Uptake of Lung Cancer Screening.

BACKGROUND: Physician-patient discussions regarding lung cancer screening (LCS) are uncommon and its racial and ethnic disparities are under-investigated. We examined the racial and ethnic disparities in the trends and frequency of LCS discussion among the LCS-eligible United States (US) population. METHODS: We analyzed data from the Health Information National Trends Survey from 2014 to 2020. LCS-eligible individuals were defined as adults aged 55 to 80 years old who have a current or former smoking history. We estimated the trends and frequency of LCS discussions and adjusted the probability of having an LCS discussion by racial and ethnic groups. RESULTS: Among 2136 LCS-eligible participants (representing 22.7 million US adults), 12.9% (95% CI, 10.9%-15%) reported discussing LCS with their providers in the past year. The frequency of LCS discussion was lowest among non-Hispanic White participants (12.3%, 95% CI, 9.9%-14.7%) compared to other racial and ethnic groups (14.1% in Hispanic to 15.3% in non-Hispanic Black). A significant increase over time was only observed among non-Hispanic Black participants (10.1% in 2014 to 22.1% in 2020; P = .05) and non-Hispanic Whites (8.5% in 2014 to 14% in 2020; P = .02). In adjusted analyses, non-Hispanic Black participants (14.6%, 95% CI, 12.3%-16.7%) had a significantly higher probability of LCS discussion than non-Hispanic Whites (12.1%, 95% CI, 11.4%-12.7%). CONCLUSION: Patient-provider LCS discussion was uncommon in the LCS-eligible US population. Non-Hispanic Black individuals were more likely to have LCS discussions than other racial and ethnic groups. There is a need for more research to clarify the discordance between LCS discussions and the actual screening uptake in this population.

MicroRNA-302b targets Mcl-1 and inhibits cell proliferation and induces apoptosis in malignant pleural mesothelioma cells.

MicroRNAs belonging to the miR-302 family are emerging as key players in the control of cell growth, and maintaining pluripotency during cell fate determination and differentiation in embryonic stem cells. However, the mechanisms whereby ephA2/ephirnA1 signaling regulates miR-302b expression and attenuates malignant pleural mesothelioma (MPM) cell growth are not known. Our study identified a novel mechanism of ephrin-A1 mediated anti-oncogenic signaling in MPM. Ephrin-A1 treatment up regulates miR-302b expression in MPM cells and attenuates cell proliferation and tumorsphere formation via repression of myeloid cell leukemia-1 (Mcl-1). The expression of miR-302b was analyzed by qPCR, the expression of Mcl-1 was analyzed by RT-PCR, immuno-blotting and Immunofluorescence staining. To confirm that ephrin-A1 regulates the expression of Mcl-1 mRNA through miR-302b up regulation, cells were transfected with and without miR-302b and miR-302b inhibitor prior to ephrinA1 treatment. The cell proliferation and tumorsphere formation was measured by WST-1 and matrigel assays respectively. In addition, to confirm the binding of miR-302b to the 3'UTR of Mcl-1 Luciferase assay was performed. Ephrin-A1 treatment induced several fold increases of miR-302b expression in MM cells. In ephrin-A1 treated MM cells, Mcl-1 expression was significantly down regulated when compared to control. Moreover, ephrin-A1 activation significantly inhibited MM cell proliferation and tumorsphere growth. Furthermore, ephrinA1 and miR-302b induced apoptosis in MM cells. The present data suggests that ephrin-A1 induces the expression of miR-302b in MM cells which targets Mcl-1 thereby inhibits MM tumorsphere growth by inducing apoptosis.