Prenatal Smoke Exposure, Tyrosine Receptor Kinase Methylation, and Childhood Respiratory Health

2013 ◽  
Vol 2013 (1) ◽  
pp. 3977
Author(s):  
Carrie V. Breton ◽  
Xinhui Wang ◽  
Kim Siegmund ◽  
Frank Gilliland
2016 ◽  
Vol 2016 (1) ◽  
Author(s):  
Lu Gao ◽  
Joshua Millstein ◽  
Kimberly Siegmund ◽  
Carrie Breton*

2020 ◽  
Vol 124 (2) ◽  
pp. 536-543 ◽  
Author(s):  
Mariam Charkviani ◽  
Nino Muradashvili ◽  
Nurul Sulimai ◽  
David Lominadze

For the first time we showed that fibrinogen (Fg) can associate with cellular prion protein (PrPC) on the surface of cultured mouse brain astrocytes. At high levels, Fg causes upregulation of astrocyte PrPC and astrocyte activation accompanied with overexpression of tyrosine receptor kinase B (TrkB), which results in nitric oxide (NO) production and generation of reactive oxygen species (ROS). Fg/PrPC interaction can be a triggering mechanism for TrkB-NO-ROS axis activation and the resultant astrocyte-mediated neurodegeneration.


Author(s):  
Amanda L. Johnson ◽  
Caroline X. Gao ◽  
Martine Dennekamp ◽  
Grant J. Williamson ◽  
David Brown ◽  
...  

In 2014, wildfires ignited a fire in the Morwell open cut coal mine, Australia, which burned for six weeks. This study examined associations between self-reported respiratory outcomes in adults and mine fire-related PM2.5 smoke exposure. Self-reported data were collected as part of the Hazelwood Health Study Adult Survey. Eligible participants were adult residents of Morwell. Mine fire-related PM2.5 concentrations were provided by the Commonwealth Scientific and Industrial Research Organisation Oceans & Atmosphere Flagship. Personalised mean 24-h and peak 12-h mine fire-related PM2.5 exposures were estimated for each participant. Data were analysed by multivariate logistic regression. There was some evidence of an association between respiratory outcomes and mine fire PM2.5 exposure. Chronic cough was associated with an odds ratio (OR) of 1.13 (95% confidence interval 1.03 to 1.23) per 10 μg/m3 increment in mean PM2.5 and 1.07 (1.02 to 1.12) per 100 μg/m3 increment in peak PM2.5. Current wheeze was associated with peak PM2.5, OR = 1.06 (1.02 to 1.11) and chronic phlegm with mean PM2.5 OR = 1.10 (1.00 to 1.20). Coal mine PM2.5 smoke exposure was associated with increased odds of experiencing cough, phlegm and wheeze. Males, participants 18–64 years, and those residing in homes constructed from non-brick/concrete materials or homes with tin/metal roofs had higher estimated ORs. These findings contribute to the formation of public health policy responses.


2018 ◽  
Vol 32 (3) ◽  
pp. 367-372 ◽  
Author(s):  
Munir Gunes Kutlu ◽  
Robert D Cole ◽  
David A Connor ◽  
Brendan Natwora ◽  
Thomas J Gould

2017 ◽  
Vol 66 ◽  
pp. S29
Author(s):  
Aditi Dubey ◽  
Ritu Sehgal ◽  
Ashutosh Kumar ◽  
T.C. Nag ◽  
S. Anurag ◽  
...  

2016 ◽  
Vol 19 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Jing Ni ◽  
Shaozhen Xie ◽  
Shakti H. Ramkissoon ◽  
Victor Luu ◽  
Yu Sun ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6194
Author(s):  
Prachi Mishra ◽  
Dipranjan Laha ◽  
Robert Grant ◽  
Naris Nilubol

Thyroid cancer is the most common type of endocrine malignancy comprising 2–3% of all cancers, with a constant rise in the incidence rate. The standard first-line treatments for thyroid cancer include surgery and radioactive iodine ablation, and a majority of patients show a good response to these therapies. Despite a better response and outcome, approximately twenty percent of patients develop disease recurrence and distant metastasis. With improved knowledge of molecular dysregulation and biological characteristics of thyroid cancer, the development of new treatment strategies comprising novel targets has accelerated. Biomarker-driven targeted therapies have now emerged as a trend for personalized treatments in patients with advanced cancers, and several multiple receptor kinase inhibitors have entered clinical trials (phase I/II/III) to evaluate their safety and efficacy. Most extensively investigated and clinically approved targeted therapies in thyroid cancer include the tyrosine receptor kinase inhibitors that target antiangiogenic markers, BRAF mutation, PI3K/AKT, and MAPK pathway components. In this review, we focus on the current advances in targeted mono- and combination therapies for various types of thyroid cancer.


2021 ◽  
Author(s):  
Brittany M. Smith ◽  
Jake VanCampen ◽  
Garth L. Kong ◽  
William Yashar ◽  
Yiu H. Tsang ◽  
...  

AbstractActivating mutations in the KIT tyrosine receptor kinase confer an adverse prognosis for patients with acute myeloid leukemia (AML). Outside of bone marrow transplantation, treatment options are limited. Here we demonstrate combined KIT and LSD1 inhibition produces synergistic cell death against KIT mutant AML cells. This combination suppresses MYC expression to drive cell cycle exit and apoptosis. This decreased MYC expression results from a loss of PU.1 binding at downstream MYC enhancers. The drug combination also inactivates PI3K/AKT/GSK3a/b signaling to decrease MYC protein abundance. KIT-mutant AML cells rapidly adapt to KIT inhibitor monotherapy by restoring PI3K/AKT activity, but cannot when treated with combined KIT and LSD1 inhibitor. In addition, we validate MYC suppression as a mechanism of synergy in KIT-mutant AML patient samples. Collectively, this work provides rational for a clinical trial to assess the efficacy of KIT and LSD1 inhibition in patients with KIT-mutant AML.Statement of significanceEffective treatment options for AML are limited. We describe the synergistic response to combined KIT and LSD1 inhibition in KIT-mutant AML and identify key biomarkers of drug response. The specificity and efficacy of this combination in cell lines and patient samples provides rationale for investigation in early phase clinical trials.


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