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  1. Article ; Online: Pulmonary Artery Mass in a Patient With Tuberculous Pericarditis.

    Churchill, Jessica L / Ard, Kevin L / Roh, Jason D / Lu, Michael T

    CASE (Philadelphia, Pa.)

    2019  Volume 3, Issue 1, Page(s) 2–5

    Language English
    Publishing date 2019-01-02
    Publishing country United States
    Document type Case Reports
    ISSN 2468-6441
    ISSN (online) 2468-6441
    DOI 10.1016/j.case.2018.11.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Intrinsic and Extrinsic Contributors to the Cardiac Benefits of Exercise.

    Hastings, Margaret H / Castro, Claire / Freeman, Rebecca / Abdul Kadir, Azrul / Lerchenmüller, Carolin / Li, Haobo / Rhee, James / Roh, Jason D / Roh, Kangsan / Singh, Anand P / Wu, Chao / Xia, Peng / Zhou, Qiulian / Xiao, Junjie / Rosenzweig, Anthony

    JACC. Basic to translational science

    2023  Volume 9, Issue 4, Page(s) 535–552

    Abstract: Among its many cardiovascular benefits, exercise training improves heart function and protects the heart against age-related decline, pathological stress, and injury. Here, we focus on cardiac benefits with an emphasis on more recent updates to our ... ...

    Abstract Among its many cardiovascular benefits, exercise training improves heart function and protects the heart against age-related decline, pathological stress, and injury. Here, we focus on cardiac benefits with an emphasis on more recent updates to our understanding. While the cardiomyocyte continues to play a central role as both a target and effector of exercise's benefits, there is a growing recognition of the important roles of other, noncardiomyocyte lineages and pathways, including some that lie outside the heart itself. We review what is known about mediators of exercise's benefits-both those intrinsic to the heart (at the level of cardiomyocytes, fibroblasts, or vascular cells) and those that are systemic (including metabolism, inflammation, the microbiome, and aging)-highlighting what is known about the molecular mechanisms responsible.
    Language English
    Publishing date 2023-10-18
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2452-302X
    ISSN (online) 2452-302X
    DOI 10.1016/j.jacbts.2023.07.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Targeting Age-Related Pathways in Heart Failure.

    Li, Haobo / Hastings, Margaret H / Rhee, James / Trager, Lena E / Roh, Jason D / Rosenzweig, Anthony

    Circulation research

    2020  Volume 126, Issue 4, Page(s) 533–551

    Abstract: During aging, deterioration in cardiac structure and function leads to increased susceptibility to heart failure. The need for interventions to combat this age-related cardiac decline is becoming increasingly urgent as the elderly population continues to ...

    Abstract During aging, deterioration in cardiac structure and function leads to increased susceptibility to heart failure. The need for interventions to combat this age-related cardiac decline is becoming increasingly urgent as the elderly population continues to grow. Our understanding of cardiac aging, and aging in general, is limited. However, recent studies of age-related decline and its prevention through interventions like exercise have revealed novel pathological and cardioprotective pathways. In this review, we summarize recent findings concerning the molecular mechanisms of age-related heart failure and highlight exercise as a valuable experimental platform for the discovery of much-needed novel therapeutic targets in this chronic disease.
    MeSH term(s) Aged ; Aging/genetics ; Aging/metabolism ; Aging/physiology ; Exercise/physiology ; Gene Expression Regulation, Developmental ; Heart/physiopathology ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Heart Failure/prevention & control ; Humans ; MicroRNAs/genetics ; Myocardium/metabolism ; Signal Transduction/genetics ; Signal Transduction/physiology
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2020-02-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.119.315889
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Animal Models of Exercise From Rodents to Pythons.

    Hastings, Margaret H / Herrera, Jonathan J / Guseh, J Sawalla / Atlason, Bjarni / Houstis, Nicholas E / Abdul Kadir, Azrul / Li, Haobo / Sheffield, Cedric / Singh, Anand P / Roh, Jason D / Day, Sharlene M / Rosenzweig, Anthony

    Circulation research

    2022  Volume 130, Issue 12, Page(s) 1994–2014

    Abstract: Acute and chronic animal models of exercise are commonly used in research. Acute exercise testing is used, often in combination with genetic, pharmacological, or other manipulations, to study the impact of these manipulations on the cardiovascular ... ...

    Abstract Acute and chronic animal models of exercise are commonly used in research. Acute exercise testing is used, often in combination with genetic, pharmacological, or other manipulations, to study the impact of these manipulations on the cardiovascular response to exercise and to detect impairments or improvements in cardiovascular function that may not be evident at rest. Chronic exercise conditioning models are used to study the cardiac phenotypic response to regular exercise training and as a platform for discovery of novel pathways mediating cardiovascular benefits conferred by exercise conditioning that could be exploited therapeutically. The cardiovascular benefits of exercise are well established, and, frequently, molecular manipulations that mimic the pathway changes induced by exercise recapitulate at least some of its benefits. This review discusses approaches for assessing cardiovascular function during an acute exercise challenge in rodents, as well as practical and conceptual considerations in the use of common rodent exercise conditioning models. The case for studying feeding in the Burmese python as a model for exercise-like physiological adaptation is also explored.
    MeSH term(s) Animals ; Boidae/genetics ; Cardiovascular Physiological Phenomena ; Models, Animal ; Physical Conditioning, Animal/physiology ; Rodentia
    Language English
    Publishing date 2022-06-09
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.122.320247
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Coronary Microvascular Function Following Severe Preeclampsia.

    Honigberg, Michael C / Economy, Katherine E / Pabón, Maria A / Wang, Xiaowen / Castro, Claire / Brown, Jenifer M / Divakaran, Sanjay / Weber, Brittany N / Barrett, Leanne / Perillo, Anna / Sun, Anina Y / Antoine, Tajmara / Farrohi, Faranak / Docktor, Brenda / Lau, Emily S / DeFaria Yeh, Doreen / Natarajan, Pradeep / Sarma, Amy A / Weisbrod, Robert M /
    Hamburg, Naomi M / Ho, Jennifer E / Roh, Jason D / Wood, Malissa J / Scott, Nandita S / Di Carli, Marcelo F

    Hypertension (Dallas, Tex. : 1979)

    2024  

    Abstract: Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating proangiogenic and antiangiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of ... ...

    Abstract Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating proangiogenic and antiangiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia-associated cardiovascular risk.
    Methods: Women with singleton pregnancies complicated by severe antepartum-onset preeclampsia and a comparator group with normotensive deliveries underwent cardiac positron emission tomography within 4 weeks of delivery. A control group of premenopausal, nonpostpartum women was also included. Myocardial flow reserve, myocardial blood flow, and coronary vascular resistance were compared across groups. sFlt-1 (soluble fms-like tyrosine kinase receptor-1) and PlGF (placental growth factor) were measured at imaging.
    Results: The primary cohort included 19 women with severe preeclampsia (imaged at a mean of 15.3 days postpartum), 5 with normotensive pregnancy (mean, 14.4 days postpartum), and 13 nonpostpartum female controls. Preeclampsia was associated with lower myocardial flow reserve (β, -0.67 [95% CI, -1.21 to -0.13];
    Conclusions: In this exploratory cross-sectional study, we observed reduced coronary microvascular function in the early postpartum period following preeclampsia, suggesting that systemic microvascular dysfunction in preeclampsia involves coronary microcirculation. Further research is needed to establish interventions to mitigate the risk of preeclampsia-associated cardiovascular disease.
    Language English
    Publishing date 2024-04-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.124.22905
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Coronary Microvascular Function Following Severe Preeclampsia.

    Honigberg, Michael C / Economy, Katherine E / Pabón, Maria A / Wang, Xiaowen / Castro, Claire / Brown, Jenifer M / Divakaran, Sanjay / Weber, Brittany N / Barrett, Leanne / Perillo, Anna / Sun, Anina Y / Antoine, Tajmara / Farrohi, Faranak / Docktor, Brenda / Lau, Emily S / Yeh, Doreen DeFaria / Natarajan, Pradeep / Sarma, Amy A / Weisbrod, Robert M /
    Hamburg, Naomi M / Ho, Jennifer E / Roh, Jason D / Wood, Malissa J / Scott, Nandita S / Carli, Marcelo F Di

    medRxiv : the preprint server for health sciences

    2024  

    Abstract: Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating pro- and anti-angiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia- ... ...

    Abstract Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating pro- and anti-angiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia-associated cardiovascular risk.
    Methods: Women with singleton pregnancies complicated by severe antepartum-onset preeclampsia and a comparator group with normotensive deliveries underwent cardiac positron emission tomography (PET) within 4 weeks of delivery. A control group of pre-menopausal, non-postpartum women was also included. Myocardial flow reserve (MFR), myocardial blood flow (MBF), and coronary vascular resistance (CVR) were compared across groups. Soluble fms-like tyrosine kinase receptor-1 (sFlt-1) and placental growth factor (PlGF) were measured at imaging.
    Results: The primary cohort included 19 women with severe preeclampsia (imaged at a mean 16.0 days postpartum), 5 with normotensive pregnancy (mean 14.4 days postpartum), and 13 non-postpartum female controls. Preeclampsia was associated with lower MFR (
    Conclusions: In this exploratory study, we observed reduced coronary microvascular function in the early postpartum period following severe preeclampsia, suggesting that systemic microvascular dysfunction in preeclampsia involves the coronary microcirculation. Further research is needed to establish interventions to mitigate risk of preeclampsia-associated cardiovascular disease.
    Language English
    Publishing date 2024-03-05
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.04.24303728
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Placental senescence pathophysiology is shared between peripartum cardiomyopathy and preeclampsia in mouse and human.

    Roh, Jason D / Castro, Claire / Yu, Andy / Rana, Sarosh / Shahul, Sajid / Gray, Kathryn J / Honigberg, Michael C / Ricke-Hoch, Melanie / Iwamoto, Yoshiko / Yeri, Ashish / Kitchen, Robert / Guerra, Justin Baldovino / Hobson, Ryan / Chaudhari, Vinita / Chang, Bliss / Sarma, Amy / Lerchenmüller, Carolin / Al Sayed, Zeina R / Diaz Verdugo, Carmen /
    Xia, Peng / Skarbianskis, Niv / Zeisel, Amit / Bauersachs, Johann / Kirkland, James L / Karumanchi, S Ananth / Gorcsan, John / Sugahara, Masataka / Damp, Julie / Hanley-Yanez, Karen / Ellinor, Patrick T / Arany, Zoltan / McNamara, Dennis M / Hilfiker-Kleiner, Denise / Rosenzweig, Anthony

    Science translational medicine

    2024  Volume 16, Issue 743, Page(s) eadi0077

    Abstract: Peripartum cardiomyopathy (PPCM) is an idiopathic form of pregnancy-induced heart failure associated with preeclampsia. Circulating factors in late pregnancy are thought to contribute to both diseases, suggesting a common underlying pathophysiological ... ...

    Abstract Peripartum cardiomyopathy (PPCM) is an idiopathic form of pregnancy-induced heart failure associated with preeclampsia. Circulating factors in late pregnancy are thought to contribute to both diseases, suggesting a common underlying pathophysiological process. However, what drives this process remains unclear. Using serum proteomics, we identified the senescence-associated secretory phenotype (SASP), a marker of cellular senescence associated with biological aging, as the most highly up-regulated pathway in young women with PPCM or preeclampsia. Placentas from women with preeclampsia displayed multiple markers of amplified senescence and tissue aging, as well as overall increased gene expression of 28 circulating proteins that contributed to SASP pathway enrichment in serum samples from patients with preeclampsia or PPCM. The most highly expressed placental SASP factor, activin A, was associated with cardiac dysfunction or heart failure severity in women with preeclampsia or PPCM. In a murine model of PPCM induced by cardiomyocyte-specific deletion of the gene encoding peroxisome proliferator-activated receptor γ coactivator-1α, inhibiting activin A signaling in the early postpartum period with a monoclonal antibody to the activin type II receptor improved heart function. In addition, attenuating placental senescence with the senolytic compound fisetin in late pregnancy improved cardiac function in these animals. These findings link senescence biology to cardiac dysfunction in pregnancy and help to elucidate the pathogenesis underlying cardiovascular diseases of pregnancy.
    MeSH term(s) Humans ; Pregnancy ; Female ; Mice ; Animals ; Pre-Eclampsia ; Peripartum Period ; Placenta ; Cardiomyopathies ; Heart Failure ; Transcription Factors ; Heart Diseases
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2024-04-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.adi0077
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  8. Article ; Online: Genetic Associations of Circulating Cardiovascular Proteins With Gestational Hypertension and Preeclampsia.

    Schuermans, Art / Truong, Buu / Ardissino, Maddalena / Bhukar, Rohan / Slob, Eric A W / Nakao, Tetsushi / Dron, Jacqueline S / Small, Aeron M / Cho, So Mi Jemma / Yu, Zhi / Hornsby, Whitney / Antoine, Tajmara / Lannery, Kim / Postupaka, Darina / Gray, Kathryn J / Yan, Qi / Butterworth, Adam S / Burgess, Stephen / Wood, Malissa J /
    Scott, Nandita S / Harrington, Colleen M / Sarma, Amy A / Lau, Emily S / Roh, Jason D / Januzzi, James L / Natarajan, Pradeep / Honigberg, Michael C

    JAMA cardiology

    2024  Volume 9, Issue 3, Page(s) 209–220

    Abstract: Importance: Hypertensive disorders of pregnancy (HDPs), including gestational hypertension and preeclampsia, are important contributors to maternal morbidity and mortality worldwide. In addition, women with HDPs face an elevated long-term risk of ... ...

    Abstract Importance: Hypertensive disorders of pregnancy (HDPs), including gestational hypertension and preeclampsia, are important contributors to maternal morbidity and mortality worldwide. In addition, women with HDPs face an elevated long-term risk of cardiovascular disease.
    Objective: To identify proteins in the circulation associated with HDPs.
    Design, setting, and participants: Two-sample mendelian randomization (MR) tested the associations of genetic instruments for cardiovascular disease-related proteins with gestational hypertension and preeclampsia. In downstream analyses, a systematic review of observational data was conducted to evaluate the identified proteins' dynamics across gestation in hypertensive vs normotensive pregnancies, and phenome-wide MR analyses were performed to identify potential non-HDP-related effects associated with the prioritized proteins. Genetic association data for cardiovascular disease-related proteins were obtained from the Systematic and Combined Analysis of Olink Proteins (SCALLOP) consortium. Genetic association data for the HDPs were obtained from recent European-ancestry genome-wide association study meta-analyses for gestational hypertension and preeclampsia. Study data were analyzed October 2022 to October 2023.
    Exposures: Genetic instruments for 90 candidate proteins implicated in cardiovascular diseases, constructed using cis-protein quantitative trait loci (cis-pQTLs).
    Main outcomes and measures: Gestational hypertension and preeclampsia.
    Results: Genetic association data for cardiovascular disease-related proteins were obtained from 21 758 participants from the SCALLOP consortium. Genetic association data for the HDPs were obtained from 393 238 female individuals (8636 cases and 384 602 controls) for gestational hypertension and 606 903 female individuals (16 032 cases and 590 871 controls) for preeclampsia. Seventy-five of 90 proteins (83.3%) had at least 1 valid cis-pQTL. Of those, 10 proteins (13.3%) were significantly associated with HDPs. Four were robust to sensitivity analyses for gestational hypertension (cluster of differentiation 40, eosinophil cationic protein [ECP], galectin 3, N-terminal pro-brain natriuretic peptide [NT-proBNP]), and 2 were robust for preeclampsia (cystatin B, heat shock protein 27 [HSP27]). Consistent with the MR findings, observational data revealed that lower NT-proBNP (0.76- to 0.88-fold difference vs no HDPs) and higher HSP27 (2.40-fold difference vs no HDPs) levels during the first trimester of pregnancy were associated with increased risk of HDPs, as were higher levels of ECP (1.60-fold difference vs no HDPs). Phenome-wide MR analyses identified 37 unique non-HDP-related protein-disease associations, suggesting potential on-target effects associated with interventions lowering HDP risk through the identified proteins.
    Conclusions and relevance: Study findings suggest genetic associations of 4 cardiovascular disease-related proteins with gestational hypertension and 2 associated with preeclampsia. Future studies are required to test the efficacy of targeting the corresponding pathways to reduce HDP risk.
    MeSH term(s) Pregnancy ; Female ; Humans ; Hypertension, Pregnancy-Induced ; Pre-Eclampsia/physiopathology ; Cardiovascular Diseases/complications ; Genome-Wide Association Study ; Precision Medicine/adverse effects ; HSP27 Heat-Shock Proteins
    Chemical Substances HSP27 Heat-Shock Proteins
    Language English
    Publishing date 2024-01-04
    Publishing country United States
    Document type Journal Article ; Comment
    ISSN 2380-6591
    ISSN (online) 2380-6591
    DOI 10.1001/jamacardio.2023.4994
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  9. Article ; Online: Restoration of Cardiomyogenesis in Aged Mouse Hearts by Voluntary Exercise.

    Lerchenmüller, Carolin / Vujic, Ana / Mittag, Sonja / Wang, Annie / Rabolli, Charles P / Heß, Chiara / Betge, Fynn / Rangrez, Ashraf Y / Chaklader, Malay / Guillermier, Christelle / Gyngard, Frank / Roh, Jason D / Li, Haobo / Steinhauser, Matthew L / Frey, Norbert / Rothermel, Beverly / Dieterich, Christoph / Rosenzweig, Anthony / Lee, Richard T

    Circulation

    2022  Volume 146, Issue 5, Page(s) 412–426

    Abstract: Background: The human heart has limited capacity to generate new cardiomyocytes and this capacity declines with age. Because loss of cardiomyocytes may contribute to heart failure, it is crucial to explore stimuli of endogenous cardiac regeneration to ... ...

    Abstract Background: The human heart has limited capacity to generate new cardiomyocytes and this capacity declines with age. Because loss of cardiomyocytes may contribute to heart failure, it is crucial to explore stimuli of endogenous cardiac regeneration to favorably shift the balance between loss of cardiomyocytes and the birth of new cardiomyocytes in the aged heart. We have previously shown that cardiomyogenesis can be activated by exercise in the young adult mouse heart. Whether exercise also induces cardiomyogenesis in aged hearts, however, is still unknown. Here, we aim to investigate the effect of exercise on the generation of new cardiomyocytes in the aged heart.
    Methods: Aged (20-month-old) mice were subjected to an 8-week voluntary running protocol, and age-matched sedentary animals served as controls. Cardiomyogenesis in aged hearts was assessed on the basis of
    Results: Cardiomyogenesis was observed at a significantly higher frequency in exercised compared with sedentary aged hearts on the basis of the detection of mononucleated/diploid
    Conclusions: Our data demonstrate that voluntary running in part restores cardiomyogenesis in aged mice and suggest that pathways associated with circadian rhythm may play a role in physiologically stimulated cardiomyogenesis.
    MeSH term(s) Animals ; Calcineurin/metabolism ; Humans ; Infant ; Mice ; Myocytes, Cardiac/cytology ; Physical Conditioning, Animal ; Thymidine/metabolism
    Chemical Substances Calcineurin (EC 3.1.3.16) ; Thymidine (VC2W18DGKR)
    Language English
    Publishing date 2022-07-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.121.057276
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: POU2F3 in SCLC: Clinicopathologic and Genomic Analysis With a Focus on Its Diagnostic Utility in Neuroendocrine-Low SCLC.

    Baine, Marina K / Febres-Aldana, Christopher A / Chang, Jason C / Jungbluth, Achim A / Sethi, Shenon / Antonescu, Cristina R / Travis, William D / Hsieh, Min-Shu / Roh, Mee Sook / Homer, Robert J / Ladanyi, Marc / Egger, Jacklynn V / Lai, W Victoria / Rudin, Charles M / Rekhtman, Natasha

    Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

    2022  Volume 17, Issue 9, Page(s) 1109–1121

    Abstract: Introduction: POU2F3 is a recent marker of a small cell lung carcinoma (SCLC) subtype related to chemosensory tuft cells (SCLC-P). The characteristics of SCLC-P have not been fully defined, and the data on POU2F3 expression in other lung tumors are ... ...

    Abstract Introduction: POU2F3 is a recent marker of a small cell lung carcinoma (SCLC) subtype related to chemosensory tuft cells (SCLC-P). The characteristics of SCLC-P have not been fully defined, and the data on POU2F3 expression in other lung tumors are scarce.
    Methods: We screened 254 SCLC for POU2F3 expression and comprehensively analyzed histopathologic, genomic, and clinical characteristics of POU2F3-positive tumors. We also explored POU2F3 expression in other major lung cancer types (n = 433) and a targeted set of potential diagnostic mimics of SCLC (n = 123).
    Results: POU2F3 was expressed in 30 of 254 (12%) SCLC and was strongly associated with low expression of standard neuroendocrine markers (synaptophysin, chromogranin A, CD56, INSM1). Notably, POU2F3 was expressed in 75% of SCLC with entirely negative or minimal neuroendocrine marker expression (15/20) and was helpful in supporting the diagnosis of SCLC in such cases. Broad targeted next-generation sequencing revealed that SCLC-P (n = 12) exhibited enrichment in several alterations, including PTEN inactivation, MYC amplifications, and 20q13 amplifications, but similar rates of RB1 and TP53 alterations as other SCLC (n = 155). Beyond SCLC, POU2F3 expression was exclusively limited to large cell neuroendocrine carcinoma (12%) and basaloid squamous cell carcinoma (22%).
    Conclusions: This is the largest cohort of SCLC-P clinical samples to date, where we describe the diagnostic utility of POU2F3 in a challenging subset of SCLC with low or absent expression of standard neuroendocrine markers. The distinct genomic alterations in SCLC-P may offer a novel avenue for therapeutic targeting. The role of POU2F3 in a narrow subset of other lung cancer types warrants further study.
    MeSH term(s) Biomarkers, Tumor ; Carcinoma, Large Cell ; Carcinoma, Neuroendocrine ; Genomics ; Humans ; Lung Neoplasms ; Octamer Transcription Factors ; Repressor Proteins ; Small Cell Lung Carcinoma
    Chemical Substances Biomarkers, Tumor ; Octamer Transcription Factors ; POU2F3 protein, human ; Repressor Proteins ; INSM1 protein, human (147955-03-1)
    Language English
    Publishing date 2022-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2432037-7
    ISSN 1556-1380 ; 1556-0864
    ISSN (online) 1556-1380
    ISSN 1556-0864
    DOI 10.1016/j.jtho.2022.06.004
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