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Article ; Online: Inherited blood cancer predisposition through altered transcription elongation.

Zhao, Jiawei / Cato, Liam D / Arora, Uma P / Bao, Erik L / Bryant, Samuel C / Williams, Nicholas / Jia, Yuemeng / Goldman, Seth R / Nangalia, Jyoti / Erb, Michael A / Vos, Seychelle M / Armstrong, Scott A / Sankaran, Vijay G

Cell

2024 Volume 187, Issue 3, Page(s) 642–658.e19

Abstract: Despite advances in defining diverse somatic mutations that cause myeloid malignancies, a significant heritable component for these cancers remains largely unexplained. Here, we perform rare variant association studies in a large population cohort to ... ...

Abstract	Despite advances in defining diverse somatic mutations that cause myeloid malignancies, a significant heritable component for these cancers remains largely unexplained. Here, we perform rare variant association studies in a large population cohort to identify inherited predisposition genes for these blood cancers. CTR9, which encodes a key component of the PAF1 transcription elongation complex, is among the significant genes identified. The risk variants found in the cases cause loss of function and result in a ∼10-fold increased odds of acquiring a myeloid malignancy. Partial CTR9 loss of function expands human hematopoietic stem cells (HSCs) by increased super elongation complex-mediated transcriptional activity, which thereby increases the expression of key regulators of HSC self-renewal. By following up on insights from a human genetic study examining inherited predisposition to the myeloid malignancies, we define a previously unknown antagonistic interaction between the PAF1 and super elongation complexes. These insights could enable targeted approaches for blood cancer prevention.
MeSH term(s)	Humans ; Hematologic Neoplasms/genetics ; Hematopoietic Stem Cells/metabolism ; Nuclear Proteins/metabolism ; Transcription Factors/genetics ; Phosphoproteins/genetics ; Transcription Elongation, Genetic
Chemical Substances	Nuclear Proteins ; PAF1 protein, human ; Transcription Factors ; CTR9 protein, human ; Phosphoproteins
Language	English
Publishing date	2024-01-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2023.12.016
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article ; Online: Response to Letter to the Editor 'Platelet count: A predictor of sepsis and mortality in severe burns'.

Cato, Liam D / Bishop, Jonathan R B / Moiemen, Naiem

Burns : journal of the International Society for Burn Injuries

2017 Volume 44, Issue 3, Page(s) 729–730

MeSH term(s)	Burns ; Humans ; Platelet Count ; Sepsis
Language	English
Publishing date	2017-12-26
Publishing country	Netherlands
Document type	Letter ; Comment
ZDB-ID	197308-3
ISSN	1879-1409 ; 0305-4179
ISSN (online)	1879-1409
ISSN	0305-4179
DOI	10.1016/j.burns.2017.11.018
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Article ; Online: The association between simple renal cyst and aortic diseases: A systematic review and meta-analysis of observational studies.

Chewcharat, Api / Hamaya, Rikuta / Thongprayoon, Charat / Cato, Liam D / Mao, Michael A / Cheungpasitporn, Wisit

Journal of evidence-based medicine

2020 Volume 13, Issue 4, Page(s) 265–274

Abstract: Objective: The objective of this meta-analysis of observational studies was to evaluate the association between simple renal cysts (SRC) and presence of aortic pathology such as aortic aneurysms and dissection.: Methods: We conducted searches in Ovid ...

Abstract	Objective: The objective of this meta-analysis of observational studies was to evaluate the association between simple renal cysts (SRC) and presence of aortic pathology such as aortic aneurysms and dissection. Methods: We conducted searches in Ovid MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials from January 1960 to August 2019 to identify observational studies that examined the association between SRCs and any aortic diseases, including aortic aneurysms and dissection. Two reviewers independently extracted the data and assessed the risk of bias. The meta-analysis was performed by STATA 14.1. Results: In total, 11 observational studies with 19 719 participants were included in this meta-analysis. Compared to individuals without SRCs, patients with SRCs had higher odds of abdominal aortic aneurysm (AAA) (adjusted OR = 2.61, 95% CI 2.34-2.91, P < 0.001, I Conclusion: SRC is associated with higher odds of aortic diseases including AAA, ascending and descending TAA, type A and type B dissection even after adjusting for confounders.
MeSH term(s)	Aneurysm, Dissecting/etiology ; Aortic Aneurysm/etiology ; Aortic Aneurysm, Abdominal/etiology ; Aortic Aneurysm, Thoracic/etiology ; Aortic Diseases/etiology ; Humans ; Kidney Diseases, Cystic/complications ; Observational Studies as Topic/statistics & numerical data ; Risk Factors
Language	English
Publishing date	2020-05-25
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Systematic Review
ZDB-ID	2474496-7
ISSN	1756-5391 ; 1756-5383
ISSN (online)	1756-5391
ISSN	1756-5383
DOI	10.1111/jebm.12385
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Article ; Online: A noncoding regulatory variant in IKZF1 increases acute lymphoblastic leukemia risk in Hispanic/Latino children.

de Smith, Adam J / Wahlster, Lara / Jeon, Soyoung / Kachuri, Linda / Black, Susan / Langie, Jalen / Cato, Liam D / Nakatsuka, Nathan / Chan, Tsz-Fung / Xia, Guangze / Mazumder, Soumyaa / Yang, Wenjian / Gazal, Steven / Eng, Celeste / Hu, Donglei / Burchard, Esteban González / Ziv, Elad / Metayer, Catherine / Mancuso, Nicholas /

Yang, Jun J / Ma, Xiaomei / Wiemels, Joseph L / Yu, Fulong / Chiang, Charleston W K / Sankaran, Vijay G

Cell genomics

2024 Volume 4, Issue 4, Page(s) 100526

Abstract: Hispanic/Latino children have the highest risk of acute lymphoblastic leukemia (ALL) in the US compared to other racial/ethnic groups, yet the basis of this remains incompletely understood. Through genetic fine-mapping analyses, we identified a new ... ...

Abstract	Hispanic/Latino children have the highest risk of acute lymphoblastic leukemia (ALL) in the US compared to other racial/ethnic groups, yet the basis of this remains incompletely understood. Through genetic fine-mapping analyses, we identified a new independent childhood ALL risk signal near IKZF1 in self-reported Hispanic/Latino individuals, but not in non-Hispanic White individuals, with an effect size of ∼1.44 (95% confidence interval = 1.33-1.55) and a risk allele frequency of ∼18% in Hispanic/Latino populations and <0.5% in European populations. This risk allele was positively associated with Indigenous American ancestry, showed evidence of selection in human history, and was associated with reduced IKZF1 expression. We identified a putative causal variant in a downstream enhancer that is most active in pro-B cells and interacts with the IKZF1 promoter. This variant disrupts IKZF1 autoregulation at this enhancer and results in reduced enhancer activity in B cell progenitors. Our study reveals a genetic basis for the increased ALL risk in Hispanic/Latino children.
MeSH term(s)	Humans ; Child ; Genetic Predisposition to Disease/genetics ; Polymorphism, Single Nucleotide ; Transcription Factors/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Hispanic or Latino/genetics ; Ikaros Transcription Factor/genetics
Chemical Substances	Transcription Factors ; IKZF1 protein, human ; Ikaros Transcription Factor (148971-36-2)
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Journal Article
ISSN	2666-979X
ISSN (online)	2666-979X
DOI	10.1016/j.xgen.2024.100526
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Article ; Online: Shared and distinct genetic etiologies for different types of clonal hematopoiesis.

Brown, Derek W / Cato, Liam D / Zhao, Yajie / Nandakumar, Satish K / Bao, Erik L / Gardner, Eugene J / Hubbard, Aubrey K / DePaulis, Alexander / Rehling, Thomas / Song, Lei / Yu, Kai / Chanock, Stephen J / Perry, John R B / Sankaran, Vijay G / Machiela, Mitchell J

Nature communications

2023 Volume 14, Issue 1, Page(s) 5536

Abstract: Clonal hematopoiesis (CH)-age-related expansion of mutated hematopoietic clones-can differ in frequency and cellular fitness by CH type (e.g., mutations in driver genes (CHIP), gains/losses and copy-neutral loss of chromosomal segments (mCAs), and loss ... ...

Abstract	Clonal hematopoiesis (CH)-age-related expansion of mutated hematopoietic clones-can differ in frequency and cellular fitness by CH type (e.g., mutations in driver genes (CHIP), gains/losses and copy-neutral loss of chromosomal segments (mCAs), and loss of sex chromosomes). Co-occurring CH raises questions as to their origin, selection, and impact. We integrate sequence and genotype array data in up to 482,378 UK Biobank participants to demonstrate shared genetic architecture across CH types. Our analysis suggests a cellular evolutionary trade-off between different types of CH, with LOY occurring at lower rates in individuals carrying mutations in established CHIP genes. We observed co-occurrence of CHIP and mCAs with overlap at TET2, DNMT3A, and JAK2, in which CHIP precedes mCA acquisition. Furthermore, individuals carrying overlapping CH had high risk of future lymphoid and myeloid malignancies. Finally, we leverage shared genetic architecture of CH traits to identify 15 novel loci associated with leukemia risk.
MeSH term(s)	Humans ; Clonal Hematopoiesis/genetics ; Genotype ; Biological Evolution ; Clone Cells ; DNA Modification Methylases
Chemical Substances	DNA Modification Methylases (EC 2.1.1.-)
Language	English
Publishing date	2023-09-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41315-5
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Article: Variant to function mapping at single-cell resolution through network propagation.

Yu, Fulong / Cato, Liam D / Weng, Chen / Liggett, L Alexander / Jeon, Soyoung / Xu, Keren / Chiang, Charleston W K / Wiemels, Joseph L / Weissman, Jonathan S / de Smith, Adam J / Sankaran, Vijay G

bioRxiv : the preprint server for biology

2022

Abstract: With burgeoning human disease genetic associations and single-cell genomic atlases covering a range of tissues, there are unprecedented opportunities to systematically gain insights into the mechanisms of disease-causal variation. However, sparsity and ... ...

Abstract	With burgeoning human disease genetic associations and single-cell genomic atlases covering a range of tissues, there are unprecedented opportunities to systematically gain insights into the mechanisms of disease-causal variation. However, sparsity and noise, particularly in the context of single-cell epigenomic data, hamper the identification of disease- or trait-relevant cell types, states, and trajectories. To overcome these challenges, we have developed the SCAVENGE method, which maps causal variants to their relevant cellular context at single-cell resolution by employing the strategy of network propagation. We demonstrate how SCAVENGE can help identify key biological mechanisms underlying human genetic variation including enrichment of blood traits at distinct stages of human hematopoiesis, defining monocyte subsets that increase the risk for severe coronavirus disease 2019 (COVID-19), and identifying intermediate lymphocyte developmental states that are critical for predisposition to acute leukemia. Our approach not only provides a framework for enabling variant-to-function insights at single-cell resolution, but also suggests a more general strategy for maximizing the inferences that can be made using single-cell genomic data.
Language	English
Publishing date	2022-01-24
Publishing country	United States
Document type	Preprint
DOI	10.1101/2022.01.23.477426
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Article ; Online: Variant to function mapping at single-cell resolution through network propagation.

Yu, Fulong / Cato, Liam D / Weng, Chen / Liggett, L Alexander / Jeon, Soyoung / Xu, Keren / Chiang, Charleston W K / Wiemels, Joseph L / Weissman, Jonathan S / de Smith, Adam J / Sankaran, Vijay G

Nature biotechnology

2022 Volume 40, Issue 11, Page(s) 1644–1653

Abstract: Genome-wide association studies in combination with single-cell genomic atlases can provide insights into the mechanisms of disease-causal genetic variation. However, identification of disease-relevant or trait-relevant cell types, states and ... ...

Abstract	Genome-wide association studies in combination with single-cell genomic atlases can provide insights into the mechanisms of disease-causal genetic variation. However, identification of disease-relevant or trait-relevant cell types, states and trajectories is often hampered by sparsity and noise, particularly in the analysis of single-cell epigenomic data. To overcome these challenges, we present SCAVENGE, a computational algorithm that uses network propagation to map causal variants to their relevant cellular context at single-cell resolution. We demonstrate how SCAVENGE can help identify key biological mechanisms underlying human genetic variation, applying the method to blood traits at distinct stages of human hematopoiesis, to monocyte subsets that increase the risk for severe Coronavirus Disease 2019 (COVID-19) and to intermediate lymphocyte developmental states that predispose to acute leukemia. Our approach not only provides a framework for enabling variant-to-function insights at single-cell resolution but also suggests a more general strategy for maximizing the inferences that can be made using single-cell genomic data.
MeSH term(s)	Humans ; Genome-Wide Association Study/methods ; Polymorphism, Single Nucleotide ; COVID-19/genetics ; Genomics/methods ; Epigenomics
Language	English
Publishing date	2022-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1311932-1
ISSN	1546-1696 ; 1087-0156
ISSN (online)	1546-1696
ISSN	1087-0156
DOI	10.1038/s41587-022-01341-y
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Zs.A 2167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: A genetic disorder reveals a hematopoietic stem cell regulatory network co-opted in leukemia.

Voit, Richard A / Tao, Liming / Yu, Fulong / Cato, Liam D / Cohen, Blake / Fleming, Travis J / Antoszewski, Mateusz / Liao, Xiaotian / Fiorini, Claudia / Nandakumar, Satish K / Wahlster, Lara / Teichert, Kristian / Regev, Aviv / Sankaran, Vijay G

Nature immunology

2022 Volume 24, Issue 1, Page(s) 69–83

Abstract: The molecular regulation of human hematopoietic stem cell (HSC) maintenance is therapeutically important, but limitations in experimental systems and interspecies variation have constrained our knowledge of this process. Here, we have studied a rare ... ...

Abstract	The molecular regulation of human hematopoietic stem cell (HSC) maintenance is therapeutically important, but limitations in experimental systems and interspecies variation have constrained our knowledge of this process. Here, we have studied a rare genetic disorder due to MECOM haploinsufficiency, characterized by an early-onset absence of HSCs in vivo. By generating a faithful model of this disorder in primary human HSCs and coupling functional studies with integrative single-cell genomic analyses, we uncover a key transcriptional network involving hundreds of genes that is required for HSC maintenance. Through our analyses, we nominate cooperating transcriptional regulators and identify how MECOM prevents the CTCF-dependent genome reorganization that occurs as HSCs differentiate. We show that this transcriptional network is co-opted in high-risk leukemias, thereby enabling these cancers to acquire stem cell properties. Collectively, we illuminate a regulatory network necessary for HSC self-renewal through the study of a rare experiment of nature.
MeSH term(s)	Humans ; Hematopoietic Stem Cells ; Leukemia/genetics ; Neoplasms ; Transcription Factors/genetics ; Cell Differentiation/genetics
Chemical Substances	Transcription Factors
Language	English
Publishing date	2022-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-022-01370-4
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 42: Show issues

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Article ; Online: Inpatient burden and mortality of heatstroke in the United States.

Kaewput, Wisit / Thongprayoon, Charat / Petnak, Tananchai / Cato, Liam D / Chewcharat, Api / Boonpheng, Boonphiphop / Bathini, Tarun / Vallabhajosyula, Saraschandra / Cheungpasitporn, Wisit

International journal of clinical practice

2020 Volume 75, Issue 4, Page(s) e13837

Abstract: Background: This study aimed to assess inpatient prevalence, characteristics, outcomes, and resource utilisation of hospitalisation for heatstroke in the United States. Additionally, this study aimed to explore factors associated with in-hospital ... ...

Abstract	Background: This study aimed to assess inpatient prevalence, characteristics, outcomes, and resource utilisation of hospitalisation for heatstroke in the United States. Additionally, this study aimed to explore factors associated with in-hospital mortalities of heatstroke. Methods: The 2003-2014 National Inpatient Sample database was used to identify hospitalised patients with a principal diagnosis of heatstroke. The inpatient prevalence, clinical characteristics, in-hospital treatments, outcomes, length of hospital stay, and hospitalisation cost were studied. Multivariable logistic regression was performed to identify independent factors associated with in-hospital mortality. Results: A total of 3372 patients were primarily admitted for heatstroke, accounting for an overall inpatient prevalence of heatstroke amongst hospitalised patients of 36.3 cases per 1 000 000 admissions in the United States with an increasing trend during the study period (P < .001). Age 40-59 was the most prevalent age group. During the hospital stay, 20% required mechanical ventilation, and 2% received renal replacement therapy. Rhabdomyolysis was the most common complication. Renal failure was the most common end-organ failure, followed by neurological, respiratory, metabolic, hematologic, circulatory, and liver systems. The in-hospital mortality rate of heatstroke hospitalisation was 5% with a decreasing trend during the study period (P < .001). The presence of end-organ failure was associated with increased in-hospital mortality, whereas more recent years of hospitalisation was associated with decreased in-hospital mortality. The median length of hospital stay was 2 days. The median hospitalisation cost was $17 372. Conclusion: The inpatient prevalence of heatstroke in the United States increased, while the in-hospital mortality of heatstroke decreased.
MeSH term(s)	Adult ; Heat Stroke/epidemiology ; Heat Stroke/therapy ; Hospital Mortality ; Hospitalization ; Humans ; Inpatients ; Length of Stay ; Middle Aged ; United States/epidemiology
Language	English
Publishing date	2020-11-29
Publishing country	England
Document type	Journal Article
ZDB-ID	1386246-7
ISSN	1742-1241 ; 1368-5031
ISSN (online)	1742-1241
ISSN	1368-5031
DOI	10.1111/ijcp.13837
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Article ; Online: Impact of Circadian Blood Pressure Pattern on Silent Cerebral Small Vessel Disease: A Systematic Review and Meta-Analysis.

Chokesuwattanaskul, Anthipa / Cheungpasitporn, Wisit / Thongprayoon, Charat / Vallabhajosyula, Saraschandra / Bathini, Tarun / Mao, Michael A / Cato, Liam D / Chokesuwattanaskul, Ronpichai

Journal of the American Heart Association

2020 Volume 9, Issue 12, Page(s) e016299

Abstract: Background Abnormal circadian blood pressure (BP) variations during sleep, specifically the non-dipping (<10% fall in nocturnal BP) and reverse-dipping patterns (rise in nocturnal BP), have been associated with an increased risk of cardiovascular events ... ...

Abstract	Background Abnormal circadian blood pressure (BP) variations during sleep, specifically the non-dipping (<10% fall in nocturnal BP) and reverse-dipping patterns (rise in nocturnal BP), have been associated with an increased risk of cardiovascular events and target organ damage. However, the relationship between abnormal sleep BP variations and cerebral small vessel disease markers is poorly established. This study aims to assess the association between non-dipping and reverse-dipping BP patterns with markers of silent cerebral small vessel disease. Methods and Results MEDLINE, Embase, and Cochrane Databases were searched from inception through November 2019. Studies that reported the odds ratios (ORs) for cerebral small vessel disease markers in patients with non-dipping or reverse-dipping BP patterns were included. Effect estimates from the individual studies were extracted and combined using the random-effect, generic inverse variance method of DerSimonian and Laird. Twelve observational studies composed of 3497 patients were included in this analysis. The reverse-dipping compared with normal dipping BP pattern was associated with a higher prevalence of white matter hyperintensity with a pooled adjusted OR of 2.00 (95% CI, 1.13-2.37; I
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Asymptomatic Diseases ; Blood Pressure ; Cerebral Small Vessel Diseases/diagnostic imaging ; Cerebral Small Vessel Diseases/epidemiology ; Cerebral Small Vessel Diseases/physiopathology ; Circadian Rhythm ; Female ; Humans ; Male ; Middle Aged ; Neuroimaging ; Observational Studies as Topic ; Risk Assessment ; Risk Factors ; Time Factors
Language	English
Publishing date	2020-06-01
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Systematic Review
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.119.016299
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