Background Racial outcome disparities have been observed in HNSCC with diminished survival for black patients compared to whites. Methods We retrospectively analyzed 1318 patients with primary HNSCC treated at the UMGCC from 2000 to 2010. Results 65.9% were white, 30.7% were black and 3.3% were of other races. Blacks were less likely to present with oral cavity cancer (OC), and more likely to present with laryngeal or hypopharyngeal cancers. Whites were more likely to have early stage disease, especially in the OC. Black race was independently associated with worse OS in the entire cohort. Blacks had a significantly worse OS amongst OC and oropharyngeal cancers (OPC), with the largest disparity in OPC. However in multivariate analysis race was only still significant in OPC. Conclusion We observed differences by race in distribution of disease site, stage, and OS. Survival disparity in the entire cohort was driven mostly by differences amongst OPC.

Background Immune checkpoint inhibitors (ICIs) represent an appealing treatment for patients with advanced urothelial cancer (aUC) and a poor performance status (PS). However, the benefit of ICIs for patients with a poor PS remains unknown. It was hypothesized that a poor Eastern Cooperative Oncology Group (ECOG) PS (≥2 vs 0‐1) would correlate with shorter overall survival (OS) in patients receiving ICIs. Methods In this retrospective cohort study, clinicopathologic, treatment, and outcome data were collected for patients with aUC who were treated with ICIs at 18 institutions (2013‐2019). The overall response rate (ORR) and OS were compared for patients with an ECOG PS of 0 to 1 and patients with an ECOG PS ≥ 2 at ICI initiation. The association between a new ICI in the last 30 and 90 days of life (DOL) and death location was also tested. Results Of the 519 patients treated with ICIs, 395 and 384 were included in OS and ORR analyses, respectively, with 26% and 24% having a PS ≥ 2. OS was higher in those with a PS of 0 to 1 than those with a PS ≥ 2 who were treated in the first line (median, 15.2 vs 7.2 months; hazard ratio [HR], 0.62; P = .01) but not in subsequent lines (median, 9.8 vs 8.2 months; HR, 0.78; P = .27). ORRs were similar for patients with a PS of 0 to 1 and patients with a PS ≥ 2 in both lines. Of the 288 patients who died, 10% and 32% started ICIs in the last 30 and 90 DOL, respectively. ICI initiation in the last 30 DOL was associated with increased odds of death in a hospital (odds ratio, 2.89; P = .04). Conclusions Despite comparable ORRs, ICIs may not overcome the negative prognostic role of a poor PS, particularly in the first‐line setting, and the initiation of ICIs in the last 30 DOL was associated with hospital death location.

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While we previously reported a striking racial difference in the prevalence of human papillomavirus (HPV) positive oropharyngeal cancer (OPSCC), less is known about differences in outcomes and trends over time in OPSCC by HPV status and race. We conducted a retrospective analysis of 467 OPSCC patients treated at the University of Maryland Greenebaum Cancer Center between 1992 and 2007, of which 200 had tissue available for HPV16 testing. HPV16 positive patients were significantly more likely to be white, with 45.5% of whites and 15.5% of blacks testing positive for HPV16. There was a significant increase in HPV16 positive OPSCC for all patients over time from 15.6% in 1992-1995 to 43.3% in 2004-2007 (p=.01). From 1992-1995, 33% of white patients were HPV16 positive with no black patients positive. From 2004-2007, 17.7% of black patients and 54% of white patients were HPV16 positive. White and black patients with HPV16 positive tumors had an identical and favorable overall survival (OS)(median 8.1 and 8.1 years, respectively ). However among HPV16 negative patients, whites had an improved OS compared to blacks (median 2.3 vs. 0.9 years, respectively, p = .02) including when analyzed in a multivariable Cox regression model. From 1992 to 2007 the percentage of HPV16 positive OPSCCs increased for white patients and was seen for the first time in black patients. While survival for HPV positive black and white patients was similar and favorable, outcomes for HPV negative patients were poor, with blacks having worse survival even after controlling for baseline characteristics.

Although a causal link between chronic inflammation and cancer has been established, the exact molecular mechanism linking inflammation to cancer remains largely unknown. It was previously postulated that molecular switches responsible for cancer cell development, and for infiltration of inflammatory cells into cancer, were divided into a distinct set of intracellular proteins and signaling pathways. However, recent evidence suggests that both tumor cells and tumor-infiltrating immune cells utilize the same kinases, mostly that of Src family, to facilitate cancer development and progression. In the past few years several groups have found that Src activation both in cancer and inflammatory cells is mainly driven by pro-inflammatory cytokines within the tumor microenvironment. Here we evaluate the cross talks between Src kinase pathways in immune cells and cancer cells. We conclude that Src might serve as a critical mechanistic link between inflammation and cancer, mediating and propagating a cycle between immune and tissue cells that can ultimately lead to the development and progression of cancer.