6526 Background: Racial and ethnic disparities in access to care and outcomes are well-established and are critical issues across several malignancies, including DLBCL. Previous studies from national registry datasets have shown racial disparities in DLBCL disease characteristics, treatment and outcomes. The VHA is an equal access system providing a unique environment to investigate cancer disparities across the disease continuum. Methods: This is a retrospective chart review of 4033 randomly selected patients with an ICD code for lymphoma treated within the VHA between 01/01/2011 and 12/31/2017. Data abstractors collected baseline patient and disease characteristics and treatment responses for those with an initial diagnosis of DLBCL in that time frame. Survival time was determined via electronic health record query on 11/30/2021. Chi-square tests were used to analyze relationship between race and variables of interest. Cox proportional hazards model was used to estimate hazard ratios (HR) for race and controlling factors. Results: 2141 DLBCL patients met our inclusion criteria. 97% were male. Majority were Non-Hispanic Whites (NHW 75%) followed by Non-Hispanic Blacks (NHB 12.5%), Hispanics (H 5.7%) and others (O 6.8%). NHB were diagnosed at younger median age (63 years) when compared to the NHW, H and O (68 years). There was no statistically significant difference in stage at diagnosis, IPI score, cell of origin (COO) and hit status amongst racial subgroups. Outcomes analysis (Table) revealed similar treatment and response rates, median OS, 1- and 2- year survival across all racial subgroups. However, after adjusting for age, IPI, COO, and exposure to agent orange, and including up to 10-years of survival data, H had 36% lower risk of death (HR=0.64, 95% CI 0.44-0.93) than NHW, while NHB and O had similar outcomes to NHW. Conclusions: This large retrospective study is a continuation of our group’s work (Williams et al, 2020) that doubles the cohort size and confirms that when standard of care therapy is given with equal access to care, short-term treatment and survival outcomes are same for all races. Further studies are needed to analyze risk factors associated with differences in long term outcomes.[Table: see text]
169 Background: Prostate cancer is the most common cancer in men in the United States. Death in prostate cancer patients is often related to other medical conditions and not prostate cancer itself. Hence, it is important to optimize other co-morbidities, such as hyperlipidemia, hypertension, and cardiovascular diseases in these patients. However, there are numerous studies portraying the ability of statins to increase progression free survival and overall survival of prostate cancer. This has led to significant interest of statins having anti-cancer properties and ultimately improving long term outcomes. Methods: This is a retrospective observational study with chart review of 1,011 patients diagnosed with prostate cancer from 1995 to 2010 in a VA Hospital in San Antonio, Texas. Variables included age at diagnosis, statin use, type of statin (1st, 2nd, or 3rd generation), dose of statin (4 dosage levels), length of statin use, time followed in months (from diagnosis to death or end of study period), death, cause of death, and time to first progressive disease. Progressive disease was defined using PSWG2 guidelines which is PSA increase > / = 25% and at least 2ng/dl above the nadir. The Cox proportional hazards regression model was used to estimate the hazard function, with age, co-morbities and other cancers used as a covariate. End points were death by prostate cancer (56), death by any cancer (140), and death by all causes (484). We also looked at the effects of statins on progression free survival of prostate cancer. Results: The hazard ratio (HR) for use of statins and death by prostate cancer was 0.35, 95% confidence interval (CI): 0.20-0.62 (p = 0.0003), indicating that statin use has a statistically significant positive effect at delaying death by prostate cancer. Death by any cancer was significantly affected by statins with a HR of 0.47, 95% CI: 0.32-0.65 (p < 0.0001). Death by all causes was also affected significantly by statins with a HR of 0.64, 95% CI: 0.53-0.78 (p < 0.0001). Length of statin use, shorter versus longer than 4 years, showed an inverse association with our primary end point with a HR of 0.53, 95% CI: 0.40-0.69 (p < 0.0001). Dose level of statin, fourth level vs 1, 2, and 3, also showed an inverse association with our primary end point with a HR of 0.73, 95% CI: 0.57-0.94 (p = 0.014). Lastly, statin exposure significantly increased progression-free survival with a HR of 0.71, 95% CI: 0.53-0.95 (p < 0.021). Conclusions: It is clear that concomitant statin use increases overall survival in patients with prostate cancer, potentially even having anti-cancer protective effects against mortality. Longer duration of statin use and higher dose levels of statins increase length of overall survival in patients with prostate cancer. As mortality is often not due to prostate cancer, more interestingly, statin exposure is also shown to increase progression-free survival.
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