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Institution

St. Jude Children's Research Hospital

HealthcareMemphis, Tennessee, United States
About: St. Jude Children's Research Hospital is a healthcare organization based out in Memphis, Tennessee, United States. It is known for research contribution in the topics: Population & Virus. The organization has 9344 authors who have published 19233 publications receiving 1233399 citations. The organization is also known as: St. Jude Children's Hospital & St. Jude Hospital.


Papers
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Journal ArticleDOI
TL;DR: An overview of the diverging roles of inflammasomes in cancer is presented and its targeting potential in anticancer therapy is discussed.
Abstract: Inflammasomes are molecular platforms that assemble upon sensing various intracellular stimuli. Inflammasome assembly leads to activation of caspase 1, thereby promoting the secretion of bioactive interleukin-1β (IL-1β) and IL-18 and inducing an inflammatory cell death called pyroptosis. Effectors of the inflammasome efficiently drive an immune response, primarily providing protection against microbial infections and mediating control over sterile insults. However, aberrant inflammasome signalling is associated with pathogenesis of inflammatory and metabolic diseases, neurodegeneration and malignancies. Chronic inflammation perpetuated by inflammasome activation plays a central role in all stages of tumorigenesis, including immunosuppression, proliferation, angiogenesis and metastasis. Conversely, inflammasome signalling also contributes to tumour suppression by maintaining intestinal barrier integrity, which portrays the diverse roles of inflammasomes in tumorigenesis. Studies have underscored the importance of environmental factors, such as diet and gut microbiota, in inflammasome signalling, which in turn influences tumorigenesis. In this Review, we deliver an overview of the interplay between inflammasomes and tumorigenesis and discuss their potential as therapeutic targets.

383 citations

Journal ArticleDOI
TL;DR: To eliminate cancer health disparities, it will be necessary to facilitate access to, and utilisation of, health services to all individuals, and to address structural inequities, including racism, that disproportionally affect racial/ethnic minorities in the USA.
Abstract: There are well-established disparities in cancer incidence and outcomes by race/ethnicity that result from the interplay between structural, socioeconomic, socio-environmental, behavioural and biological factors. However, large research studies designed to investigate factors contributing to cancer aetiology and progression have mainly focused on populations of European origin. The limitations in clinicopathological and genetic data, as well as the reduced availability of biospecimens from diverse populations, contribute to the knowledge gap and have the potential to widen cancer health disparities. In this review, we summarise reported disparities and associated factors in the United States of America (USA) for the most common cancers (breast, prostate, lung and colon), and for a subset of other cancers that highlight the complexity of disparities (gastric, liver, pancreas and leukaemia). We focus on populations commonly identified and referred to as racial/ethnic minorities in the USA-African Americans/Blacks, American Indians and Alaska Natives, Asians, Native Hawaiians/other Pacific Islanders and Hispanics/Latinos. We conclude that even though substantial progress has been made in understanding the factors underlying cancer health disparities, marked inequities persist. Additional efforts are needed to include participants from diverse populations in the research of cancer aetiology, biology and treatment. Furthermore, to eliminate cancer health disparities, it will be necessary to facilitate access to, and utilisation of, health services to all individuals, and to address structural inequities, including racism, that disproportionally affect racial/ethnic minorities in the USA.

383 citations

Journal ArticleDOI
TL;DR: It is shown that expression of the viral accessory protein PB1-F2 enhances inflammation during primary viral infection of mice and increases both the frequency and severity of secondary bacterial pneumonia.

383 citations

Journal ArticleDOI
01 Dec 2000-Immunity
TL;DR: A novel function of IL-6 is described: the negative regulation of CD4+ Th1 cell differentiation, which promotes CD 4+ Th2 differentiation and inhibits Th1 differentiation by two independent molecular mechanisms.

383 citations

Journal ArticleDOI
TL;DR: In this paper, the efficacy and safety of tricyclic antidepressants were evaluated using genotype-directed dosing of CYP2D6 and C19 polymorphic enzymes.
Abstract: Polymorphisms in CYP2D6 and CYP2C19 affect the efficacy and safety of tricyclics, with some drugs being affected by CYP2D6 only, and others by both polymorphic enzymes. Amitriptyline, clomipramine, doxepin, imipramine, and trimipramine are demethylated by CYP2C19 to pharmacologically active metabolites. These drugs and their metabolites, along with desipramine and nortriptyline, undergo hydroxylation by CYP2D6 to less active metabolites. Evidence from published literature is presented for CYP2D6 and CYP2C19 genotype-directed dosing of tricyclic antidepressants.

383 citations


Authors

Showing all 9410 results

NameH-indexPapersCitations
Richard A. Flavell2311328205119
David Baltimore203876162955
John C. Reed190891164382
Joan Massagué189408149951
Stuart H. Orkin186715112182
Douglas R. Green182661145944
Richard K. Wilson173463260000
Todd R. Golub164422201457
Robert G. Webster15884390776
Elaine R. Mardis156485226700
David Cella1561258106402
Rafi Ahmed14663393190
Ching-Hon Pui14580572146
Yoshihiro Kawaoka13988375087
Seth M. Steinberg13793680148
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202333
2022108
20211,277
20201,136
2019965
2018877