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PubMed1988

Diesel exhaust exposure and mortality among males in the American Cancer Society prospective study.

In 1982, the American Cancer Society enrolled over 1.2 million American men and women in a prospective mortality study of cancer and other causes in relation to different risk factors. The 2-year mortality of 461,981 males aged 40-79 years with known smoking habit has been analyzed in relation to exposure to diesel exhaust (DE) and to employment in selected occupations related to DE exposure. The relative risk (RR) for all causes of death for those exposed was 1.05 (95% confidence interval [CI]: 0.97-1.13). For lung cancer, the RR was 1.18 (95% CI: 0.97-1.44). A dose-response effect was present. Railroad workers, heavy equipment operators, miners, and truck drivers had a higher mortality both for all causes and for lung cancer when compared with subjects with other occupations and no exposure to DE. Truck drivers exposed to DE were not at excess risk of lung cancer if compared with truck drivers unexposed to DE, but a trend of increasing risk with duration of exposure was suggested. DE exposure was also associated with increase in mortality for accidents, cerebrovascular disease, arteriosclerosis, and cirrhosis of the liver. An association based on small numbers was also present for Hodgkin's disease and lymphoid leukemia. No association with chronic non-neoplastic pulmonary diseases or with bladder cancer was found.

Adult↗

PubMed1986

Lung cancer and diesel exhaust: a review.

The evidence from animal studies indicates that organic extracts of diesel particulate are mutagenic and carcinogenic. Of four animal inhalation studies, two have been positive and two have been largely negative. The most recent data indicate that inhalation studies may be positive only with high doses of exhaust. Human studies of diesel-exposed occupations have been inconclusive. These studies have focused on truck drivers, bus drivers and garage workers, railroad workers, and heavy equipment operators. Most human studies have not been able to estimate exposure to diesel exhaust. Negative studies have frequently suffered from insufficient potential latency. Positive studies have often failed to control for smoking, and have sometimes involved confounding occupational exposures. In general, the occupational epidemiology of diesel-exposed workers is made difficult by the fact that many of the suspected toxic components of diesel-exhaust are also present in cigarette smoke and in ambient air. There are two ongoing epidemiologic studies in the United States, focusing on railway workers and truck drivers, which attempt to overcome prior difficulties. Preliminary data from the study of truck drivers indicates an excess of lung cancer among workers in the trucking industry compared to the U.S. population, but these data need to be controlled for smoking and analyzed according to diesel exposure.

Animals↗

PubMed2026

Comprehensive Genomic Analysis of Normal and Cancer Cells Elucidates the Elevated Mutation Burden in Cancer.

Self-renewing normal tissues generate several somatic mutations at each division. Previous studies have reported that cancer cells have more mutations than their normal counterparts. It is not obvious why dramatic differences in mutation burdens between normal tissues and cancers should exist. To fully understand human tumorigenesis, the increase of mutation burden in cancers will have to be understood. Here, we provided a systematic comparison of mutational burdens in normal and cancer cells from five different organs, revealing a four-fold increase of mutation burdens in cancerous vs. non-cancerous cells. Three proposed hypotheses that could account for the increased mutation burdens in cancer are: the classical hypothesis, where driver gene mutations explain the higher mutational burden; the catastrophic hypothesis, where extreme mutational events lead to large-scale genomic alterations; and the tail hypothesis, where differences in baseline mutation rates among individuals account for the differences. Testing through orthogonal observations showed that the observed medians and distributions of mutation burdens in cancers could be explained by the hypotheses to various degrees of significance, and only the tail hypothesis could easily explain the increase in median mutation burdens in the normal tissues of cancer patients compared to the normal tissues of non-cancer patients. Overall, this study characterizes an increased mutation burden across multiple types of cancer compared to normal tissue and provides insights into the contributing factors. A tenable hypothesis proposed in this study involving fundamental differences in baseline mutation rates among individuals could have implications for cancer prevention strategies.

Journal Article↗

PubMed2005

Embedding cancer care within pre-registration nurse education programmes: policy, practice and opportunities for change.

This paper discusses policy and professional drivers which outline the need for, and inclusion of cancer education within pre-registration nursing curricula within the UK. It also evaluates arguments in favour of the development of separate and distinctive cancer modules within nurse training programmes against those advocating a more integrated or thematic approach. The authors suggest that there are advantages and disadvantages to each strategy, and argue that the most important factor irrespective of the approach taken, is that cancer learning outcomes are clearly enunciated within all pre-registration nursing curricula and constructively aligned against teaching, learning and assessment strategies which may encompass a single module or entire programme. The authors then discuss their personal experience of teaching cancer care using both approaches and posit one suggestion for an embedded pre-registration cancer-care curriculum developed as the catalyst for a broader debate on the scope and content of cancer-care education within pre-registration nursing curricula.

Curriculum↗

PubMed2006

A critical assessment of studies on the carcinogenic potential of diesel exhaust.

After decades of research involving numerous epidemiologic studies and extensive investigations in laboratory animals, a causal relationship between diesel exhaust (DE) exposure and lung cancer has not been conclusively demonstrated. Epidemiologic studies of the transportation industry (trucking, busing, and railroad) show a small elevation in lung cancer incidence (relative risks [RRs] generally below 1.5), but a dose response for DE is lacking. The studies are also limited by a lack of quantitative concurrent exposure data and inadequate or lack of controls for potential confounders, particularly tobacco smoking. Furthermore, prior to dieselization, similar elevations in lung cancer incidence have been reported for truck drivers, and in-cab diesel particulate matter (DPM) exposures of truck drivers were comparable to ambient highway exposures. Taken together, these findings suggest that an unidentified occupational agent or lifestyle factor might be responsible for the low elevations in lung cancer reported in the transportation studies. In contrast, underground miners, many of whom experience the highest occupational DPM exposures, generally do not show elevations in lung cancer. Laboratory studies must be interpreted with caution with respect to predicting the carcinogenic potential of DE in humans. Tumors observed in rats following lifetime chronic inhalation of very high levels of DPM may be attributed to species-specific overload mechanisms that lack relevance to humans. Increased tumor incidence was not observed in other species (hamsters or mice) exposed to DPM at very high levels or in rats exposed at lower levels (</=2000 mug/m3). Although DPM contains mutagens, mutagenicity studies in which cells were exposed to concentrated extracts of DPM also have limited application to human risk assessment, because such extracts can be obtained from DPM only by using strong organic solvents, agitation, and heat. Most studies have shown that whole DPM itself is not mutagenic because the adsorbed organic compounds are minimally bioavailable in aqueous-based fluids. In the past two decades, dramatic changes in diesel engine technology (e.g., low-sulfur fuel and exhaust after-treatment) have resulted in >99% reduction in DPM and other quantitative and qualitative changes in the chemical and physical characteristics of diesel exhaust. Thus, the current database, which is focused almost entirely on the potential health effects of traditional diesel exhaust (TDE), has only limited utility in assessing the potential health risks of new-technology diesel exhaust (NTDE). To overcome some of the limitations of the historical epidemiologic database on TDE and to gain further insights into the potential health effects of NTDE, new studies are underway and more studies are planned.

Air Pollutants↗

PubMed2003

Occupational exposures and lung cancer in New Caledonia.

AIMS: To study the associations between occupational exposures and the risk of lung cancer in New Caledonia. METHODS: All cases diagnosed between January 1993 and December 1995 (228 lung cancers) and 305 population controls were included. Detailed information on lifetime job history, smoking, and other potential risk factors was collected by interview. Occupational exposures were assessed from the questionnaires by an industrial hygienist, without knowledge of case-control status. RESULTS: No significant association was found with exposures related to nickel mining and refining, the main industrial activity in the territory. Among men, an excess risk of lung cancer was found for bus and truck drivers. Increased risks were also observed in men with the highest level of cumulative exposure to cleaning products and inorganic fertilisers. Exposure to field dust was associated with lung cancer risk in both sexes, and risk increased with cumulative exposure level. In some areas tremolite asbestos derived from local outcroppings was used as a whitewash. The association between exposure to field dust and lung cancer was limited to men and women exposed to this whitewash-that is, living in areas where the soil may contain tremolite. CONCLUSION: This study shows several associations between occupational exposures and lung cancer. The findings suggest that exposure to tremolite fibres from cultivated fields may increase the risk of lung cancer in New Caledonia.

Adult↗

PubMed2026

Senescent fibroblasts drive CD8+ T cell dysfunction in colorectal cancer via CD36-mediated lipid transfer and peroxidation.

BACKGROUND: Functional exhaustion of tumor-infiltrating CD8+ T cells represents a hallmark of colorectal cancer (CRC) immunosuppression, though its mechanistic drivers remain elusive. Given the established correlation between CRC progression and stromal senescence characterized by pathological lipid accumulation and impaired immunity, we investigated whether and how senescent fibroblasts actively regulate CD8+ T cell dysfunction. METHODS: Single-cell RNA sequencing (scRNA-seq) analysis was conducted to unveil the diverse fibroblast populations and the significant lipid metabolism changes between senescent fibroblasts and non-senescent fibroblasts in human CRC specimens and adjacent normal mucosa. Machine-learning identified senescent fibroblasts with a distinct gene signature. Cell-cell communication analysis was used to evaluate the interactions between senescent fibroblasts and CD8+ T cells in colorectal cancer. Co-culture experiments were conducted among senescent fibroblasts, CD8+ T cells and patient-derived organoids of CRC (CRC-PDOs), with the results evaluated with high-content imaging and propidium iodide/Hoechst 33,342 staining. Flow cytometry, ELISA and lipid pulse-chase with BODIPY FL C16 were performed to detect the alterations of CD8+ T cell cytotoxic function and metabolic status. AOM/DSS-induced CRC mouse model was used to conduct in vivo validation to evaluate whether senolytics could suppress CRC progression. Patients from the Cancer Genome Atlas colorectal cancer cohort were stratified into CD36-high and CD36-low groups by median expression, and drug sensitivity for GDSC2 compounds was predicted computationally using the oncoPredict R package. RESULTS: ScRNA-seq demonstrated the specific cell population presence and divergence of senescent fibroblasts between neoplastic and histologically normal adjacent cell clusters in CRC. Random Forest was employed for cell senescence classification. Feature importance analysis identified five genes as key contributors to the model’s decision process. Cell-cell communication analysis revealed enhanced interactions between senescent fibroblasts and CD8+ T cells in CRC. Co-culture of senescent fibroblasts significantly impaired the cytotoxic functions of CD8+ T cells on CRC-PDOs, which was reflected by the declined proportions of granzyme B (GZMB) + and interferon gamma (IFNγ) + CD8+ T cells and enhanced viability of CRC-PDOs. Mechanistically, the co-culture with senescent fibroblasts promoted the lipid shuttling into CD8+ T cells to induce lipid peroxidation and downstream impairment of cytotoxicity. Furthermore, the inhibition of CD36, the specific scavenger receptor for lipid uptake of CD8+ T cells, effectively suppressed lipid transfer and peroxidation thereby preserving the effector functions of CD8+ T cells and ultimately promoting tumor apoptosis. Complementarily, in vivo senolytic treatment significantly suppressed CRC progression in AOM-DSS CRC mouse models. Top 12 therapeutic agents were identified significantly enhanced predicted efficacy in CD36-high tumors. CONCLUSIONS: Our study identified a substantial population of senescent fibroblasts in human CRC through single cell transcriptomics, machine-learning and clinical biopsies. These senescent fibroblasts impair CD8+ T cell-mediated killing of CRC-PDOs via CD36-dependent lipid transfer, suggesting senolytic targeting of stromal cells as a promising immunotherapeutic strategy for CRC.

Colorectal Neoplasms↗

PubMed2005

Patients' anxiety and expectations: how they influence family physicians' decisions to order cancer screening tests.

OBJECTIVE: To compare the influence of physicians' recommendations and patients' anxiety or expectations on the decision to order four cancer screening tests in clinical situations where guidelines were equivocal: screening for prostate cancer with prostate-specific antigen for men older than 50; breast cancer screening with mammography for women 40 to 49; colorectal cancer screening with fecal occult blood testing; and colorectal cancer screening with colonoscopy for patients older than 40. DESIGN: Cross-sectional mailed survey with clinical vignettes. SETTING: British Columbia, Alberta, Ontario, Quebec, and Prince Edward Island. PARTICIPANTS: Of 600 randomly selected family physicians in active practice approached, 351 responded, but 35 respondents were ineligible (response rate 62%). MAIN OUTCOME MEASURES: Decisions to order cancer screening tests, physicians' perceptions of recommendations, patients' anxiety about cancer, and patients' expectation to be tested. RESULTS: For all screening situations, physicians most likely to order the tests believed that routine screening with the test was recommended; physicians least likely to order tests believed routine screening was not. Patients' expectations or anxiety, however, markedly increased screening by physicians who did not believe that routine screening was recommended. In regression models, the interaction between physicians' recommendations and patients' anxiety or expectation was significant for all four screening tests. When patients had no anxiety or expectations, physicians' beliefs about screening strongly predicted test ordering. Physicians who believed routine screening was recommended ordered the test in most cases regardless of patient characteristics. But patients' anxiety or expectations markedly increased the probability that the test would be ordered. The probability of test ordering went from 0.28 to 0.54 for prostate-specific antigen (odds ratio [OR] = 1.9), from 0.15 to 0.44 for mammography (OR = 2.8), from 0.33 to 0.79 for fecal occult blood testing (OR = 2.4), and from 0.29 to 0.65 for colonoscopy (OR = 2.2). CONCLUSION: Differences in clinical judgment about recommended practice lead to practice variation, but physicians are also influenced by nonmedical factors, such as patients' anxiety and expectations of receiving tests. In terms of magnitude of influence, clinical judgment is more powerful than nonmedical patient factors, but patient factors are also powerful drivers of family physicians' decisions about cancer screening when practice guidelines are equivocal.

Adult↗

PubMed1993

A follow-up study on the mortality of truck drivers.

The aim of this study was to investigate a possible relationship between occupational exposure to vehicle exhaust and cancer risk. For this purpose, a cohort of 14,225 truck drivers was followed throughout a ten-year period with regard to cause-specific mortality. Comparisons were made with another cohort of unskilled male laborers. Both of the occupational groups compared were identified at a census and no supplementary data on individual exposure history were available. The study showed an increased mortality for lung cancer (standardized mortality ratio (SMR) 160, 95% confidence interval (CI) 126-200) and multiple myeloma (SMR 439, 95% CI 142-1,024). It seems likely that exposure to diesel exhaust has contributed to the increased lung cancer risk observed. The possible relationship between multiple myeloma and certain constituents of vehicle exhaust may be worth attention in future investigations.

Adolescent↗

PubMed1999

Medical care consumption in a phase III trial comparing irinotecan with infusional 5-fluorouracil (5-FU) in patients with metastatic colorectal cancer after 5-FU failure.

We evaluated economic implications of treatment with irinotecan, following a RCT which demonstrated significantly increased survival at 1 year with irinotecan (45%) compared to infusional 5-fluorouracil (5-FU) (32%) in patients with metastatic colorectal cancer. Medical care consumption data were collected prospectively alongside the trial, with 256 patients followed for a median of 10 months. Follow-up was prolonged beyond treatment failure and medical care consumption was not protocol driven, enabling a realistic evaluation of economic implications. Medical care consumption associated with chemotherapy administration was lower with irinotecan as compared with infusional 5-FU. The cumulative number of days in hospital due to treatment toxicity and cancer complications, which is the key cost driver, was 14.4 (95% CI: 10.7-18.1) with irinotecan versus 17.5 (95% CI: 11.7-23.3) with infusional 5-FU. Thus, the survival benefit with second-line irinotecan compared to infusional 5-FU in patients with advanced colorectal cancer was achieved without increasing medical care consumption.

Ambulatory Care↗

PubMed2026

A HUWE1 regulatory helix gates ASCL1 degradation through its C-terminal phospho-degron in small cell lung cancer.

Lineage-defining transcription factors are key oncogenic drivers but remain difficult to target pharmacologically due to the absence of ligandable pockets. The molecular rules governing substrate recognition by large HECT ubiquitin ligases also remain incompletely understood, limiting efforts to exploit these enzymes for targeted protein degradation. Here we combine genome-wide CRISPR knockout screening with base editor tiling screens at amino acid resolution, both coupled to an endogenous knock-in reporter of the SCLC lineage oncogenic transcription factor ASCL1, to systematically interrogate the mechanisms governing its degradation. These complementary screens unbiasedly identify the HECT ubiquitin ligase HUWE1 as the dominant regulator of ASCL1 stability in small cell lung cancer (SCLC) and resolve a conserved C-terminal phospho-degron centered on Ser207 and terminal Trp/Phe residues that are required for HUWE1 docking and ubiquitin-mediated degradation. Unexpectedly, base editor screening further uncovers a previously unrecognized regulatory module within HUWE1: a short negatively charged helix that functions as an autoinhibitory gate controlling access of phospho-degron substrates to HUWE1. Charge-flipping mutations within this regulatory helix relieve autoinhibition and accelerate degradation of multiple HUWE1 phospho-degron substrates, including ASCL1 and the canonical HUWE1 substrate DDIT4. Stabilization of ASCL1 through degron disruption paradoxically impairs SCLC proliferation, revealing that dynamic proteasome-coupled turnover is required for transcription factor function. Together, these findings reveal molecular rules governing HUWE1 phospho-degron recognition and identify a regulatory gate controlling substrate engagement. They also illustrate a generalizable strategy for resolving degradation mechanisms of undruggable transcription factors in their endogenous cellular context.

ASCL1↗

PubMed2026

YAP1 induces hepatocellular carcinoma via DNA demethylation rather than by canonical driver gene mutations.

Large-scale genome sequencing analyses have identified driver gene mutations (DGMs) in most cancers as well as their associated tumorigenic mechanisms. However, a small fraction of cancers are not positive for these canonical DGMs, leaving the mechanisms underpinning their formation a mystery. We hypothesized that canonical DGM-negative cancers might be driven by activation of the transcriptional coactivator YAP1 that led to the induction of epigenetic changes. To test this theory, we established a mouse mosaic model of hepatocellular carcinoma (HCC) in which we induced YAP1-TEAD activation in a few hepatocytes. Whole-exome sequencing did not identify canonical DGMs in HCCs, but bisulfite sequencing revealed widespread DNA demethylation leading to the transcriptional activation of multiple oncogenes. Knockdown of the DNA demethylation-promoting gene, Tet1, attenuated HCC formation in these mice. Single-cell spatial transcriptomics identified a Tet1-high subpopulation of HCC cells that interacted with other hepatic cell types. Our mechanistic mouse data align with the observation that YAP1-TEAD-TET1-associated signatures were also elevated in hepatocytes from patients with Fontan-associated liver disease (FALD), a condition associated with the development of HCCs with lower frequencies of canonical DGMs. Our study suggests that the YAP1-TEAD-TET1 axis promotes canonical DGM-negative HCC development, and provides new insights into the molecular processes involved.

Animals↗

PubMed2001

Is optimistic bias influenced by control or delay?

Optimistic bias is a commonly observed but poorly explained phenomenon. Our aim was to determine whether optimistic bias varied according to the nature of the event. Two event characteristics were explored: control and delay. A sample of 100 participants aged 18-30 years was randomly selected from the local residential telephone directory. Respondents were interviewed over the telephone. The highly structured interview schedule assessed respondents' perceptions of their own risk, and the risk of an average person of their age and sex for experiencing four negative life events: developing skin cancer, being involved in a serious car accident as the driver, being involved in a serious car accident as a passenger and having to wear a hearing aid. It also assessed respondents' perceptions of control and delay for each event. Data analysis using a repeated-measures MANOVA showed that optimistic bias occurred for all four events. Optimistic bias was significantly greater for the two events high in control (skin cancer and accident as the driver) than for those low in control (accident as a passenger and hearing aid). Delay was not related to the magnitude of optimistic bias. These findings have implications for health promotion campaigns and self-protective behaviors.

Accidents, Traffic↗

PubMed1983

Malignant lymphomas in road transport workers.

The relative risks of malignant lymphomas among road transport workers were investigated using the National Cancer Registry in England and Wales. Drivers of buses and coaches (OCC unit 120) had increased risks for both Hodgkin's and non-Hodgkin's lymphomas and the drivers of other road passenger vehicles (OCC unit 121) for Hodgkin's lymphomas only. Although the increased risks did not show statistical significance, they corresponded to and reinforced previously described findings based on occupational mortality.

Adolescent↗

PubMed1983

Setting priorities for occupational cancer research and control: synthesis of the results of occupational disease surveillance studies.

The objectives of this paper were 1) to identify occupations with potentially high cancer risk by combining the results of 12 major occupational disease surveillance studies, 2) to develop a quantitative methodology for accomplishing the first objective, and 3) to make recommendations concerning priorities for occupational cancer research and control on the basis of the results of this analysis in conjunction with other available epidemiologic, industrial hygiene, toxicologic, and employment data. It was suggested that the first priority be the investigation and control of occupational exposure to asbestos, particularly in the automobile repair and construction industries. Of the 34 occupational groups found to be at high risk for lung cancer in this analysis, 18 have potential asbestos exposure. The second priority was suggested to be research into the consistent lung-cancer excess found among motor vehicle drivers. This excess may be due to occupational exposure to diesel and gasoline engine exhaust, to cigarette smoking, or to both of these factors.

Adolescent↗

PubMed1995

Tolerability of continuous subcutaneous octreotide used in combination with other drugs.

Continuous subcutaneous infusion of octreotide combined with other drugs has proved to be useful in some circumstances in palliative care setting when theoral route is no longer available. Forty-four patients were administered octreotide alone or in combination with other drugs in the same syringe driver for symptom control in advanced cancer patients. Good tolerability and compatibility were observed without visual drug precipitation for a period of 48 hours at room temperature, the standard clinical situation in patients' homes. Such a combination of drugs administered by the subcutaneous route makes possible the adequate control of symptoms in the final days of life.

Adult↗

PubMed2026

PSMA6 drives non-small cell lung cancer progression by stabilizing NEDD8 and activating NF-κB signaling.

BACKGROUND: Non‑small cell lung cancer (NSCLC) is a major cause of cancer‑associated death globally. Elucidating novel molecular drivers is essential for targeted therapy development. This study sought to investigate the function and regulatory mechanism of proteasome 20S subunit alpha 6 (PSMA6) in NSCLC. METHODS: Proteasome 20S subunit alpha 6 (PSMA6) expression in NSCLC tissues and cells was analyzed using The Cancer Genome Atlas (TCGA) datasets, immunohistochemistry, and Western blotting. Gain- and loss-of-function assays were performed to evaluate its biological functions. Protein interaction assays and functional rescue experiments were conducted to investigate the underlying mechanisms. RESULTS: We found that PSMA6 was significantly upregulated in NSCLC tissues and cell lines and was associated with poor patient prognosis. Functional experiments demonstrated that PSMA6 promoted NSCLC cell proliferation and migration. Mechanistically, PSMA6 activated nuclear factor kappa B (NF-κB) signaling by enhancing p65 nuclear translocation and IκBα phosphorylation. Further investigation revealed that PSMA6 directly interacted with neural precursor cell expressed, developmentally down-regulated 8 (NEDD8) and increased its protein stability without affecting its mRNA level. Importantly, NEDD8 knockdown abolished PSMA6-induced NF-κB activation and malignant phenotypes, confirming that PSMA6 exerts its oncogenic effects through the NEDD8/NF-κB axis. CONCLUSIONS: Our findings identify a novel PSMA6/NEDD8/NF-κB regulatory axis that promotes NSCLC progression and suggest PSMA6 as a potential therapeutic target.

Proteasome 20S subunit alpha 6 (PSMA6)↗

PubMed2026

Access to Guideline-Concordant Oncology Genomic Testing: A Qualitative Study of Black Cancer Patients and Oncology Providers.

Genomic testing is a key component of precision oncology; however, Black patients receive genomic testing at lower rates. The purpose of this qualitative study was to identify individual and health system drivers of genomic testing disparities at a National Cancer Institute-designated comprehensive cancer center. We conducted interviews with 15 oncology providers and 11 Black cancer patients between September 2023 and October 2024. These patients were eligible for genomic testing based on National Comprehensive Cancer Network (NCCN) guidelines, being diagnosed within last 10 years (2014-2023), at least 18 years old, and English-speaking. Providers included oncologists and oncology patient navigators. Topics included motivators, barriers, and knowledge of genomic testing and factors influencing decision-making. The Penchansky and Thomas theoretical framework of healthcare access (e.g., availability, accessibility, accommodation, affordability, and acceptability) guided thematic analysis. Among patients eligible for genomic testing, most participants (n = 7) received genomic testing as part of their cancer treatment based on EMRs, however many patients (n = 7) could not recall discussing genomic testing with their oncologist. Most patients and all providers highlighted affordability as a challenge: patients were concerned about unexpected costs associated with testing, while providers were concerned about costs of matched molecular targeted therapy. Both patients and providers highlighted patient-centered communication to mitigate mistrust and promote patient engagement in care. Despite limited awareness, Black patients view genomic testing positively. Addressing multiple dimensions of access is key to improving system-level processes and ensuring that more patients benefit from lifesaving targeted therapy.

Humans↗