Tumor Genomic Profile Is Associated With Arterial Thromboembolism Risk in Patients With Solid Cancer - Original Research

Sep 28, 2026

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Patients with cancer have an elevated risk of arterial thromboembolism (ATE), yet little is known about how cancer-specific somatic genomic alterations affect that risk. A retrospective cohort evaluated tumor genetic alterations from adults with solid cancers tested in 2014–2016. ATE was defined using electronic medical record assessments and followed for up to one year. KRAS and STK11 alterations independently increased ATE risk, supporting a need to clarify underlying mechanisms.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages10

Reading Time25 min

AccessFree to download

Abstract

Background

Objectives

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JA CC: CAR D IO ON CO L O GY V O L . 5 , N O . 2 , 2 0 2 3 ª 2 0 23 T H E A UTH O RS . P UBL I S H ED BY ELS E V I E R ON BEHA LF OF T H E A MERICA N CO LL EG E O F C AR DI O L O G Y F O U ND AT I O N . T H I S I S AN O P EN ACCE SS A R T I CLE U ND ER TH E C C BY-NC-N D L IC E NS E ( [http:/ /creati v e com mon s . o rg/licen s es/b y-n c-n d/ 4 . 0/](http:/ /creati v e com mon s . o rg/licen s es/b y-n c-n d/ 4 . 0/) ) . MINI-FOCUS ISSUE: BLEEDING, THROMBOSIS, AND ATRIAL FIBRILLATION ORIGINAL RESEARCH Tumor Genomic Proﬁle Is Associated With Arterial Thromboembolism Risk in Patients With Solid Cancer Stephanie Feldman, MD,a,* Dipti Gupta, MD, MPH,a,* Babak B. Navi, MD, MS,b,c Ka-Wai Grace Ho, MD,c Peter Willeit, MD, MPHIL, PHD,d,e Sean Devlin, PHD,f Kelly L. Bolton, MD, PHD,a Maria E. Arcila, MD,g Simon Mantha, MD, MPHa | ABSTRACT | | | --- | --- | BACKGROUND Patients with cancer have an increased risk for arterial thromboembolism (ATE) . Scant data exist about the impact of cancer-speciﬁc genomic alterations on the risk for ATE. OBJECTIVES The aim of this study was to determine whether individual solid tumor somatic genomic alterationsinﬂuence the incidence of ATE. METHODS A retrospective cohort study was conducted using tumor genetic alteration data from adults with solid cancers who underwent Memorial Sloan Kettering–Integrated Mutation Proﬁling of Actionable Cancer Targets testing between 2014 and 2016 . The primary outcome, ATE, was deﬁned as myocardial infarction, coronary revascularization, ischemic stroke, peripheral arterial occlusion, or limb revascularization and identiﬁed through systematic electronic medical record assessments. Patients were followed from date of tissue-matched blood control accession to ﬁrst ATE event or death, for up to 1 year. Cause-speciﬁc Cox proportional hazards regression was used to determine HRs of ATE for individual genes adjusted for pertinent clinical covariates. RESULTS Among 11,871 eligible patients, 74% had metastatic disease, and there were 160 ATE events. A signiﬁcantly increased risk for ATE independent of tumor type was noted for the KRAS oncogene (HR: 1.98; 95% CI: 1.34-2.94; multiplicity-adjusted P ¼ 0.015) and the STK11 tumor suppressor gene (HR: 2.51; 95% CI: 1.44-4.38; multiplicity-adjusted P ¼ 0. 015) . CONCLUSIONS In a large genomic tumor-proﬁling registry of patients with solid cancers, alterations in KRAS and STK11 were associated with an increased risk for ATE independent of cancer type. Further investigation is needed to elucidate the mechanism by which these mutations contribute to ATE in this high-risk population. (J Am Coll Cardiol CardioOnc 2023;5:246–255) © 2023 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license ([http://creativecommons.org/licenses/by-nc-nd/4.0/](http://creativecommons.org/licenses/by-nc-nd/4.0/)). From the aDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA; bDepartment of Neurology and the Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York, USA; cDepartment of Neurology, Memorial Sloan Kettering Cancer Center, New York, New York, USA; dClinical Epidemiology Team, Medical University of Innsbruck, Innsbruck, Austria; eDepartment of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom; fDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA; and the gDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA. *Drs Feldman and Gupta are joint ﬁrst authors. The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center. Manuscr

FAQs

What question does the study address about cancer and ATE risk?

The study determines whether individual solid tumor somatic genomic alterations influence the incidence of arterial thromboembolism in patients with solid cancer.

How was ATE defined and identified in the study?

ATE was defined as myocardial infarction, coronary revascularization, ischemic stroke, peripheral arterial occlusion, or limb revascularization and identified through systematic electronic medical record assessments.

Which gene alterations were associated with increased ATE risk?

Alterations in KRAS and STK11 were associated with a significantly increased risk of ATE independent of tumor type.

Sep 28, 2026

Uploaded by Asher