RESUMO
BACKGROUND: No adjuvant treatment has been established for patients who remain at high risk for hepatocellular carcinoma recurrence after curative-intent resection or ablation. We aimed to assess the efficacy of adjuvant atezolizumab plus bevacizumab versus active surveillance in patients with high-risk hepatocellular carcinoma. METHODS: In the global, open-label, phase 3 IMbrave050 study, adult patients with high-risk surgically resected or ablated hepatocellular carcinoma were recruited from 134 hospitals and medical centres in 26 countries in four WHO regions (European region, region of the Americas, South-East Asia region, and Western Pacific region). Patients were randomly assigned in a 1:1 ratio via an interactive voice-web response system using permuted blocks, using a block size of 4, to receive intravenous 1200 mg atezolizumab plus 15 mg/kg bevacizumab every 3 weeks for 17 cycles (12 months) or to active surveillance. The primary endpoint was recurrence-free survival by independent review facility assessment in the intention-to-treat population. This trial is registered with ClinicalTrials.gov, NCT04102098. FINDINGS: The intention-to-treat population included 668 patients randomly assigned between Dec 31, 2019, and Nov 25, 2021, to either atezolizumab plus bevacizumab (n=334) or to active surveillance (n=334). At the prespecified interim analysis (Oct 21, 2022), median duration of follow-up was 17·4 months (IQR 13·9-22·1). Adjuvant atezolizumab plus bevacizumab was associated with significantly improved recurrence-free survival (median, not evaluable [NE]; [95% CI 22·1-NE]) compared with active surveillance (median, NE [21·4-NE]; hazard ratio, 0·72 [adjusted 95% CI 0·53-0·98]; p=0·012). Grade 3 or 4 adverse events occurred in 136 (41%) of 332 patients who received atezolizumab plus bevacizumab and 44 (13%) of 330 patients in the active surveillance group. Grade 5 adverse events occurred in six patients (2%, two of which were treatment related) in the atezolizumab plus bevacizumab group, and one patient (<1%) in the active surveillance group. Both atezolizumab and bevacizumab were discontinued because of adverse events in 29 patients (9%) who received atezolizumab plus bevacizumab. INTERPRETATION: Among patients at high risk of hepatocellular carcinoma recurrence following curative-intent resection or ablation, recurrence-free survival was improved in those who received atezolizumab plus bevacizumab versus active surveillance. To our knowledge, IMbrave050 is the first phase 3 study of adjuvant treatment for hepatocellular carcinoma to report positive results. However, longer follow-up for both recurrence-free and overall survival is needed to assess the benefit-risk profile more fully. FUNDING: F Hoffmann-La Roche/Genentech.
Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , Adulto , Humanos , Bevacizumab/uso terapêutico , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/cirurgia , Conduta Expectante , Protocolos de Quimioterapia Combinada Antineoplásica , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/cirurgiaRESUMO
Differences in cancer genomes between racial groups may impact tumor biology and health disparities. However, the discovery of race-associated mutations is constrained by the limited representation and sample size of different racial groups in prior genomic studies. We evaluated the influence of race on the frequency of gene mutations using the Genomics, Evidence, Neoplasia, Information, Exchange database, a large genomic dataset aggregated from clinical sequencing. Matched cohort analyses were used to identify histology-specific race-associated mutations including increased TERT promoter mutations in Black and Asian patients with gliomas and bladder cancers, and a decreased frequency of mutations in DNA repair pathway genes and subunits of the SWI/SNF chromatin complex in Asian and Black patients across multiple cancer types. The distribution of actionable mutations in oncogenes was also race-specific, demonstrating how targeted therapies may have a disparate impact on racial groups. Down-sampling analyses indicate that larger sample sizes are likely to discover more race-associated mutations. These results provide a resource to understand differences in cancer genomes between racial groups which may inform the design of clinical studies and patient recruitment strategies in biomarker trials.
Assuntos
Grupos Raciais , Neoplasias da Bexiga Urinária , Humanos , Mutação , Grupos Raciais/genética , Neoplasias da Bexiga Urinária/genética , Biomarcadores , Estudos de CoortesRESUMO
BACKGROUND AND AIMS: Immunotherapies have altered the treatment paradigm in HCC. Surrogate and modified endpoints are used to assess early success in clinical studies and guide clinical practice. We sought to determine whether surrogate endpoints and modifications to the conventional criteria for tumor response (RECIST), including modified RECIST (mRECIST) and immune-modified RECIST (imRECIST), are valid measures to predict overall survival (OS) in HCC treated with immunotherapies. APPROACH AND RESULTS: We performed an individual-level post hoc analysis of patients treated with atezolizumab and bevacizumab in the IMbrave150 trial (N = 279) and a cross-sectional analysis of a multicenter real-world patient cohort treated with immunotherapy (N = 328). Landmark analyses showed that objective response rates by RECIST were associated with greater OS including among Child-Pugh A and B patients and among patients treated with immunotherapies in the first- or second-line setting (IMbrave150: HR 0.24, 95% CI, 0.17-0.33; RW: HR 0.25, 95% CI, 0.15-0.43). Objective response rates by mRECIST or imRECIST were not associated with the greater predictive power of OS benefit (mRECIST: HR 0.30, 95% CI, 0.22-0.42; imRECIST: HR 0.36, 95% CI, 0.30-0.51). Progression-free survival determined by RECIST was only moderately correlated with OS, and this association was not improved using mRECIST or imRECIST. CONCLUSIONS: Our results clarify the utility of surrogate and modified endpoints in HCC treated with immunotherapies and support the use of RECIST objective response rates as an appropriate signal-finding measure for the evaluation of emerging treatments. Contrary to their intended purpose, mRECIST and imRECIST did not provide meaningful improvements in predicting OS benefits.
Assuntos
Antineoplásicos , Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/patologia , Antineoplásicos/uso terapêutico , Estudos Transversais , ImunoterapiaRESUMO
Inactivating mutations in the exonuclease domain of POLE induce somatic hypermutation resulting in a high tumor mutation burden (TMB) and are associated with immune checkpoint inhibitor (ICI) benefit. POLE mutations outside the exonuclease domain predicted to be deleterious are also observed in cancers, but it is unknown whether they are similarly associated with response to ICIs. We present a patient with hepatocellular carcinoma with a rare POLE mutation (V1368M) outside the exonuclease-domain predicted to be deleterious, a low TMB (1 mut/Mb), and microsatellite stability, who demonstrated an exceptional response to pembrolizumab. To support the generalizability of this finding, an analysis of 1278 patients with advanced cancers harboring low or intermediate TMB treated with ICIs showed that missense non-exonuclease domain POLE mutations were associated with greater overall survival. In contrast, among patients with advanced cancers without ICI exposure, POLE mutations were not associated with overall survival. These results demonstrate that a subset of missense POLE mutations may represent predictive biomarkers independent of TMB. Pathogenic POLE mutations outside the exonuclease domain may result in altered functions beyond DNA replication and proofreading which render cancers sensitive to ICIs.
Assuntos
Exonucleases , Neoplasias , Biomarcadores Tumorais/genética , Exonucleases/genética , Humanos , Imunoterapia , Mutação , Neoplasias/tratamento farmacológico , Neoplasias/genéticaRESUMO
Advanced hepatocellular carcinoma (HCC) is responsive to immune checkpoint inhibitors, but there are currently no known biomarkers to predict treatment benefit. Blood TMB (bTMB) estimation via circulating tumor DNA (ctDNA) profiling can provide a convenient means to estimate HCC TMB. Here we provide the first landscape of bTMB in advanced HCC using a commercially available next-generation sequencing assay, show that it is approximately three times as high as matched tissue TMB, and show that bTMB correlates with NAFLD cirrhosis etiology and the presence of genomic alterations in HTERT and TP53. These results lay the foundation for subsequent studies evaluating bTMB as an immune therapy predictive biomarker in HCC.
Assuntos
Carcinoma Hepatocelular , DNA Tumoral Circulante , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/patologia , DNA Tumoral Circulante/genética , Biomarcadores Tumorais/genética , Sequenciamento de Nucleotídeos em Larga Escala/métodos , MutaçãoRESUMO
Journal editors are gatekeepers of knowledge, and pharmaceutical industry payments to oncology editors have not been previously characterized. We performed a cross-sectional study of nonresearch industry payments to editors of 26 oncology research journals. A total of 433 editors were eligible for inclusion in the CMS Open Payments database from 2013 to 2018. A total of 80% of eligible editors had nonresearch payments, and the mean value of payments per editor was $106,778, which has increased over time. Only 5 out of 26 journals disclosed editor conflicts of interest and 3 of these journals reported at least one editor with no nonresearch industry payments but were found to have nonresearch payments. There was a positive correlation between journal impact factor and the average payment per editor for each journal. Our study shows the high prevalence and lack of transparency of nonresearch industry payments to oncology editors. Higher impact journals appear to be associated with greater nonresearch industry payments.
Assuntos
Conflito de Interesses , Médicos , Estudos Transversais , Indústria Farmacêutica , Humanos , Oncologia , Estados UnidosRESUMO
BACKGROUND AND AIMS: Foreign body ingestions (FoBIs) are a common cause for medical attention. However, trends and patterns of adult FoBIs as well as associations with clinical comorbidities and behavioral attributes have not been elucidated beyond single institutional experiences. METHODS: We utilized survey data from the National Electronic Injury Surveillance System to examine fundamental characteristics of adult FoBIs involving consumer products between 2000 and 2017 across the United States. Data regarding the circumstances of FoBIs were abstracted from narrative data. Relationships among time, intent, demographics, and behavioral attributes were assessed using regression analyses, accounting for survey structure. RESULTS: Adult FoBIs have increased in incidence over the past 2 decades from 3 to 5.3 per 100,000 persons. Examination of consumer products revealed that jewelry (15.4%), nails (7.2%), and toothpicks (6.9%) were the most commonly ingested products. The most common products ingested varied over time, and the number of unique consumer product categories ingested increased from 103 to 143 in the time period studied. Intentional ingestions accounted for 14% of adult FoBIs and frequently involved plastic bagging (13.6%), batteries (13%), nails (10.1%), and desk supplies (6.8%). Adjusted regression analyses demonstrated that compared with accidental FoBIs, intentional FoBIs have increased over time. Intentional FoBIs were more frequently associated with younger age, substance abuse, police custody, and mental and cognitive illnesses relative to accidental FoBIs. CONCLUSIONS: Our results indicate that adult FoBIs are an increasing burden of disease in the United States with social, psychiatric, and behavioral contributors to this trend.
Assuntos
Lesões Acidentais/epidemiologia , Corpos Estranhos/epidemiologia , Trato Gastrointestinal , Comportamento Autodestrutivo/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Intoxicação Alcoólica/epidemiologia , Alcoolismo/epidemiologia , Transporte Intracorporal de Contrabando/estatística & dados numéricos , Demência/epidemiologia , Ingestão de Alimentos , Fontes de Energia Elétrica , Feminino , Humanos , Deficiência Intelectual/epidemiologia , Joias , Modelos Logísticos , Masculino , Transtornos Mentais/epidemiologia , Pessoa de Meia-Idade , Numismática , Razão de Chances , Crescimento Demográfico , Prisioneiros/estatística & dados numéricos , Fatores de Risco , Transtornos Relacionados ao Uso de Substâncias/epidemiologia , Estados Unidos/epidemiologia , Adulto JovemAssuntos
Antineoplásicos , Carcinoma Hepatocelular , Neoplasias Hepáticas , Quinolinas , Humanos , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Compostos de Fenilureia/efeitos adversos , Quinolinas/uso terapêutico , Antineoplásicos/uso terapêutico , Receptor ErbB-2 , Receptores ErbB/genéticaRESUMO
Extensive sequencing efforts of cancer genomes such as The Cancer Genome Atlas (TCGA) have been undertaken to uncover bona fide cancer driver genes which has enhanced our understanding of cancer and revealed therapeutic targets. However, the number of driver gene mutations is bounded, indicating that there must be a point when further sequencing efforts will be excessive. We found that there was a significant positive correlation between sample size and identified driver gene mutations across 33 cancers sequenced by the TCGA, which is expected if additional sequencing is still leading to the identification of more driver genes. However, the rate of new cancer driver genes being discovered with larger samples is declining rapidly. Our analysis provides a general guide for determining which cancer types would likely benefit from additional sequencing efforts, particularly those with relatively high rates of cancer driver gene discovery. Our results argue that past strategies of indiscriminately sequencing as many specimens as possible for all cancer types is becoming inefficient. In addition, without significant investments into applying our knowledge of cancer genomes, we risk sequencing more cancer genomes for the sake of sequencing rather than meaningful patient benefit.
Assuntos
Genes Neoplásicos , Neoplasias/genética , Animais , HumanosRESUMO
Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease associated with immunocompromised states. We describe a case of PML, which developed after prolonged ibrutinib use and a low burden of chronic lymphocytic leukemia disease. The delay in diagnosis of the patient despite multiple presentations to medical providers across different facilities suggests that there is a lack of awareness of PML as a potential complication of ibrutinib. Treatments with postulated anti-John Cunningham polyomavirus agents and IL-2 were ineffective, likely due to the advanced state of the patient's disease. Although recent evidence indicates that ibrutinib may enhance cell-mediated immunity, consistent with elevated CD4+ and CD8+ T cells and appropriate T-cell response to mitogens in the patient, ibrutinib-mediated inhibition of the humoral function may contribute to PML pathogenesis. As the duration of ibrutinib use is often indefinite, and the number of indications for ibrutinib continues to grow, recognition and further evaluation of the link between PML and ibrutinib is warranted.
Assuntos
Antineoplásicos/efeitos adversos , Leucemia Linfocítica Crônica de Células B/tratamento farmacológico , Leucoencefalopatia Multifocal Progressiva/induzido quimicamente , Inibidores de Proteínas Quinases/efeitos adversos , Pirazóis/efeitos adversos , Pirimidinas/efeitos adversos , Adenina/análogos & derivados , Idoso , Progressão da Doença , Evolução Fatal , Feminino , Humanos , Leucemia Linfocítica Crônica de Células B/diagnóstico , Leucemia Linfocítica Crônica de Células B/enzimologia , Leucemia Linfocítica Crônica de Células B/imunologia , Leucoencefalopatia Multifocal Progressiva/diagnóstico por imagem , Leucoencefalopatia Multifocal Progressiva/imunologia , Leucoencefalopatia Multifocal Progressiva/terapia , Imageamento por Ressonância Magnética , PiperidinasAssuntos
Docentes/estatística & dados numéricos , Estupro/estatística & dados numéricos , Sexismo/estatística & dados numéricos , Assédio Sexual/estatística & dados numéricos , Pesquisa Biomédica , Feminino , Humanos , Masculino , Escolas para Profissionais de Saúde/organização & administração , Universidades/organização & administraçãoRESUMO
Immunotherapy has revolutionized the standard of care in multiple aspects of oncology. Given successes in the setting of unresectable hepatocellular carcinoma (HCC) and the advantages of neoadjuvant therapy, many trials are demonstrating the safety and feasibility of combination of immune checkpoint inhibitors (ICIs)/tyrosine kinases in patients with resectable HCC. Numerous clinical trials are currently investigating the role of different immune modulators either as monotherapy or as combination therapy in the neoadjuvant setting. Key questions that remain to be addressed include efficacy, safety, predictive biomarkers, and length of treatment.
Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Terapia Neoadjuvante , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/cirurgia , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/cirurgia , Terapia Combinada , ImunoterapiaRESUMO
Background: A useful clinical biomarker requires not only association but also a consistent temporal relationship. For instance, chemotherapy-induced neutropenia and epidermal growth-factor inhibitor-related acneiform rash both occur within weeks of treatment initiation, thereby providing information prior to efficacy assessment. Although immune checkpoint inhibitor (ICI)-associated immune-related adverse events (irAE) have been associated with therapeutic benefit, irAE may have delayed and highly variable onset. To determine whether ICI efficacy and irAE could serve as clinically useful biomarkers for predicting each other, we determined the temporal relationship between initial efficacy assessment and irAE onset in a diverse population treated with ICI. Methods: Using two-sided Fisher exact and Cochran-Armitage tests, we determined the relative timing of initial efficacy assessment and irAE occurrence in a cohort of 155 ICI-treated patients (median age 68 years, 40% women). Results: Initial efficacy assessment was performed a median of 50 days [interquartile range (IQR) 39-59 days] after ICI initiation; median time to any irAE was 77 days (IQR 28-145 days) after ICI initiation. Median time to first irAE was 42 days (IQR 20-88 days). Overall, 58% of any irAE and 47% of first irAE occurred after initial efficacy assessment. For clinically significant (grade ≥2) irAE, 60% of any and 53% of first occurred after initial efficacy assessment. The likelihood of any future irAE did not differ according to response (45% for complete or partial response vs. 47% for other cases; P=1). In landmark analyses controlling for clinical and toxicity follow-up, patients demonstrating greater tumor shrinkage at initial efficacy assessment were more likely to develop future grade ≥2 (P=0.05) and multi-organ (P=0.02) irAE. Conclusions: In contrast to that seen with chemotherapy and molecularly targeted therapies, the temporal relationship between ICI efficacy and toxicity is complex and bidirectional. In practice, neither parameter can be routinely relied on as a clinical biomarker to predict the other.
Assuntos
Biomarcadores , Inibidores de Checkpoint Imunológico , Neoplasias , Humanos , Feminino , Masculino , Idoso , Inibidores de Checkpoint Imunológico/efeitos adversos , Inibidores de Checkpoint Imunológico/uso terapêutico , Pessoa de Meia-Idade , Neoplasias/tratamento farmacológico , Neoplasias/imunologia , Neoplasias/terapia , Imunoterapia/efeitos adversos , Imunoterapia/métodos , Resultado do Tratamento , Fatores de TempoRESUMO
Immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 or its ligand (PD-1/L1) have expanded the treatment landscape against cancers but are effective in only a subset of patients. Tumor mutation burden (TMB) is postulated to be a generic determinant of ICI-dependent tumor rejection. Here we describe the association between TMB and survival outcomes among microsatellite-stable cancers in a real-world clinicogenomic cohort consisting of 70,698 patients distributed across 27 histologies. TMB was associated with survival benefit or detriment depending on tissue and treatment context, with eight cancer types demonstrating a specific association between TMB and improved outcomes upon treatment with anti-PD-1/L1 therapies. Survival benefits were noted over a broad range of TMB cutoffs across cancer types, and a dose-dependent relationship between TMB and outcomes was observed in a subset of cancers. These results have implications for the use of cancer-agnostic and universal TMB cutoffs to guide the use of anti-PD-1/L1 therapies, and they underline the importance of tissue context in the development of ICI biomarkers.
Assuntos
Antígeno B7-H1 , Biomarcadores Tumorais , Inibidores de Checkpoint Imunológico , Mutação , Neoplasias , Receptor de Morte Celular Programada 1 , Humanos , Neoplasias/genética , Neoplasias/tratamento farmacológico , Neoplasias/imunologia , Inibidores de Checkpoint Imunológico/uso terapêutico , Antígeno B7-H1/antagonistas & inibidores , Antígeno B7-H1/genética , Receptor de Morte Celular Programada 1/antagonistas & inibidores , Prognóstico , Biomarcadores Tumorais/genética , Instabilidade de Microssatélites , Feminino , Repetições de Microssatélites , MasculinoRESUMO
Somatic mutations in non-malignant tissues are selected for because they confer increased clonal fitness. However, it is uncertain whether these clones can benefit organ health. Here, ultra-deep targeted sequencing of 150 liver samples from 30 chronic liver disease patients revealed recurrent somatic mutations. PKD1 mutations were observed in 30% of patients, whereas they were only detected in 1.3% of hepatocellular carcinomas (HCCs). To interrogate tumor suppressor functionality, we perturbed PKD1 in two HCC cell lines and six in vivo models, in some cases showing that PKD1 loss protected against HCC, but in most cases showing no impact. However, Pkd1 haploinsufficiency accelerated regeneration after partial hepatectomy. We tested Pkd1 in fatty liver disease, showing that Pkd1 loss was protective against steatosis and glucose intolerance. Mechanistically, Pkd1 loss selectively increased mTOR signaling without SREBP-1c activation. In summary, PKD1 mutations exert adaptive functionality on the organ level without increasing transformation risk.
Assuntos
Carcinoma Hepatocelular , Cirrose Hepática , Neoplasias Hepáticas , Mutação , Canais de Cátion TRPP , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/metabolismo , Animais , Canais de Cátion TRPP/genética , Canais de Cátion TRPP/metabolismo , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/metabolismo , Camundongos , Cirrose Hepática/genética , Cirrose Hepática/metabolismo , Cirrose Hepática/patologia , Fígado Gorduroso/genética , Fígado Gorduroso/metabolismo , Fígado Gorduroso/patologia , Masculino , Serina-Treonina Quinases TOR/metabolismo , Camundongos Endogâmicos C57BL , Linhagem Celular Tumoral , Feminino , Transdução de SinaisRESUMO
The interaction between antigens and antibodies (B cell receptors, BCRs) is the key step underlying the function of the humoral immune system in various biological contexts. The capability to profile the landscape of antigen-binding affinity of a vast number of BCRs will provide a powerful tool to reveal novel insights at unprecedented levels and will yield powerful tools for translational development. However, current experimental approaches for profiling antibody-antigen interactions are costly and time-consuming, and can only achieve low-to-mid throughput. On the other hand, bioinformatics tools in the field of antibody informatics mostly focus on optimization of antibodies given known binding antigens, which is a very different research question and of limited scope. In this work, we developed an innovative Artificial Intelligence tool, Cmai, to address the prediction of the binding between antibodies and antigens that can be scaled to high-throughput sequencing data. Cmai achieved an AUROC of 0.91 in our validation cohort. We devised a biomarker metric based on the output from Cmai applied to high-throughput BCR sequencing data. We found that, during immune-related adverse events (irAEs) caused by immune-checkpoint inhibitor (ICI) treatment, the humoral immunity is preferentially responsive to intracellular antigens from the organs affected by the irAEs. In contrast, extracellular antigens on malignant tumor cells are inducing B cell infiltrations, and the infiltrating B cells have a greater tendency to co-localize with tumor cells expressing these antigens. We further found that the abundance of tumor antigen-targeting antibodies is predictive of ICI treatment response. Overall, Cmai and our biomarker approach filled in a gap that is not addressed by current antibody optimization works nor works such as AlphaFold3 that predict the structures of complexes of proteins that are known to bind.
RESUMO
Introduction: Racial and ethnic disparities in the presentation and outcomes of lung cancer are widely known. To evaluate potential factors contributing to these observations, we measured systemic immune parameters in Black and White patients with lung cancer. Methods: Patients scheduled to receive cancer immunotherapy were enrolled in a multi-institutional prospective biospecimen collection registry. Clinical and demographic information were obtained from electronic medical records. Pre-treatment peripheral blood samples were collected and analyzed for cytokines using a multiplex panel and for immune cell populations using mass cytometry. Differences between Black and White patients were determined and corrected for multiple comparisons. Results: A total of 187 patients with non-small cell lung cancer (Black, 19; White, 168) were included in the analysis. There were no significant differences in baseline characteristics between Black and White patients. Compared to White patients, Black patients had significantly lower levels of CCL23 and CCL27, and significantly higher levels of CCL8, CXCL1, CCL26, CCL25, CCL1, IL-1 b, CXCL16, and IFN-γ (all P <0.05, FDR<0.1). Black patients also exhibited greater populations of non-classical CD16+ monocytes, NKT-like cells, CD4+ cells, CD38+ monocytes, and CD57+ gamma delta T cells (all P <0.05). Conclusions: Black and White patients with lung cancer exhibit several differences in immune parameters, with Black patients exhibiting greater levels of numerous pro-inflammatory cytokines and cell populations. The etiology and clinical significance of these differences warrant further evaluation.