Prevalence of Targetable Mutations in Black Patients With Lung Cancer: A Systematic Review and Meta-Analysis

Costa, Philippos Apolinário; Saul, Eduardo Edelman; Paul, Yonette; Iyer, Sunil; Silva, Laércio Lopes da; Tamariz, Leonardo; Lopes, Gilberto

doi:10.1200/op.20.00961

Cited by 14 publications

(11 citation statements)

References 39 publications

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“…This is partially due to the persistent inequity of inclusion of racial and ethnic minority groups in large whole-exome sequencing studies or in studies centered on known genetic mutations for lung cancer, including EGFR (OMIM 131550), ALK (OMIM 105590), ROS1 (OMIM 165020), and BRAF (OMIM 164757). 7,56,57 For instance, there is a need to better understand how different facets of structural racism may drive unequal biologic risk due to gene-environment associations and drive inequities in the development of lung cancer. 57…”

Section: Private Industrymentioning

confidence: 99%

“…[1][2][3][4][5][6] Todate,researchonthepotential contributors to these racial and ethnic disparities in the developmentoflungcancerhaveprimarilyfocusedondifferencesintobaccorelatedbehaviorsorgeneticdifferencesamongraces,despiteracebeing a social construct and not a biologic phenomenon. [7][8][9][10] For instance, researchfocusedonincreasedlungcancerriskamongnon-HispanicBlack/ African American groups has primarily focused on different smoking patterns or tobacco products used compared with White groups. [11][12][13] Furthermore, the higher rates of nonsmoker lung cancer among racial and ethnic minority groups, including Asian or Pacific Islander, Hispanic or Latino, or non-Hispanic Black/African American compared with non-Hispanic White individuals in the US, have mostly been posited as the result of different genetic risk.…”

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Structural Racism and Lung Cancer Risk

Bonner,

Curley,

Love

et al. 2024

JAMA Oncol

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ImportanceStructural racism is associated with persistent inequities in health and health outcomes in the US for racial and ethnic minority groups. This review summarizes how structural racism contributes to differential population-level exposure to lung cancer risk factors and thus disparate lung cancer risk across different racial and ethnic groups.ObservationsA scoping review was conducted focusing on structural racism and lung cancer risk for racial and ethnic minority groups. The domains of structural racism evaluated included housing and built environment, occupation and employment, health care, economic and educational opportunity, private industry, perceived stress and discrimination, and criminal justice involvement. The PubMed, Embase, and MedNar databases were searched for English-language studies in the US from January 1, 2010, through June 30, 2022. The review demonstrated that racial and ethnic minority groups are more likely to have environmental exposures to air pollution and known carcinogens due to segregation of neighborhoods and poor housing quality. In addition, racial and ethnic minority groups were more likely to have exposures to pesticides, silica, and asbestos secondary to higher employment in manual labor occupations. Furthermore, targeted marketing and advertisement of tobacco products by private industry were more likely to occur in neighborhoods with more racial and ethnic minority groups. In addition, poor access to primary care services and inequities in insurance status were associated with elevated lung cancer risk among racial and ethnic minority groups. Lastly, inequities in tobacco use and cessation services among individuals with criminal justice involvement had important implications for tobacco use among Black and Hispanic populations.Conclusions and RelevanceThe findings suggest that structural racism must be considered as a fundamental contributor to the unequal distribution of lung cancer risk factors and thus disparate lung cancer risk across different racial and ethnic groups. Additional research is needed to better identify mechanisms contributing to inequitable lung cancer risk and tailor preventive interventions.

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Section: Private Industrymentioning

confidence: 99%

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confidence: 99%

Structural Racism and Lung Cancer Risk

Bonner,

Curley,

Love

et al. 2024

JAMA Oncol

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“…Guidry et al's deconvolution of LUAD heterogeneity by integrating well established genetic and molecular analysis platforms with DNA methylation analysis may address demonstrative health disparities that exist in cancer care. Currently, there is no consensus around the prevalence of oncogenic driver mutations in Blacks as driver mutations are not well defined in this demographic when compared to their White and Asian counterparts (15,17).…”

Section: Keap1mentioning

confidence: 99%

CLOCK’ing differences in DNA methylation signatures to understand the molecular etiology of lung cancer

Neely¹,

Yang²,

Marconett³

2023

Transl Lung Cancer Res

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Lung adenocarcinoma (LUAD) is the most commonly diagnosed form of non-small cell lung cancer, and is associated with high frequency of tumor recurrence, severe malignancy and vast heterogeneity (1). Moreover, this histological diversity is compounded by the LUAD tumor microenvironment's (TME) extensive cellular diversity and accompanying immune infiltration patterns. These properties have been linked to unpredictable tumor recurrence, poor patient response to therapy, and mortality (2). Integrative application of existing tools and methods geared towards understanding epigenetic contributions to LUAD heterogeneity is imperative to answering these questions (3).In the recent issue of Clinical Cancer Research, Guidry et al. repurposed established DNA methylation patterns associated with cellular age to define signatures that can act as an index for distinct subtypes of LUAD (4). In establishing the relationship between epigenetic signatures and LUAD subtypes, they were able to ascribe phenotypic and molecular characteristics to each subclassification, including enrichment for oncogenic driver mutations and immune composition of the TME (5-9). Further to this, Guidry drew correlations between immune microenvironment composition, ethnic background and patient smoking history.Previous studies have utilized genome-wide methylation alterations within LUAD to define relevant subtypes. These investigations yielded three [3] major DNA methylation classifications in LUAD; CpG-island methylation phenotype (CIMP)-low, CIMP-intermediate, and CIMPhigh (10). DNA methylation patterns have also been associated with TME molecular characteristics and immune cell composition within LUAD tumors (11). The study by Guidry et al., improves on these associations by refining genome-wide methylation patterning to the 353 CpG sites within the Horvath DNA methylation CLOCK (6). The authors were then able to use methylation levels at these sites to subdivide LUAD into six [6] distinct subgroups, each associated with distinct pathologic and molecular features of LUAD. Subgroups with higher DNAm age were associated with better patient survival and specific oncogenic driver mutations.Aberrant oncogenic driver gene expression plays an integral role in tumorigenesis and progression in LUAD. To understand the relationship between DNAm-defined LUAD subclusters and oncogenic drivers, Guidy et al. conducted mutational analysis on tumor samples and focused on established LUAD oncogenic driver mutations

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“…We particularly note Dr Costa's report showing lower rates of targetable mutations among Black patients with lung cancer and Dr O'Neill's suggestion that existing prognostic markers may carry different significance for Black and White patient populations diagnosed with head and neck cancer. 1,2 The relationship between genetics and race is complex, as race is a social construct, yet we see somatic genomic differences in tumors between racial and ethnic groups. These may be driven by epigenetic changes from centuries of systemic racism and social determinants of health, rather than intrinsic biologic differences.…”

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confidence: 99%