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Sökning: WFRF:(Berglind A.)

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  • Schofield, James P. R., et al. (författare)
  • Stratification of asthma phenotypes by airway proteomic signatures
  • 2019
  • Ingår i: Journal of Allergy and Clinical Immunology. - Elsevier. - 0091-6749 .- 1097-6825. ; 144:1, s. 70-82
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Stratification by eosinophil and neutrophil counts increases our understanding of asthma and helps target therapy, but there is room for improvement in our accuracy in prediction of treatment responses and a need for better understanding of the underlying mechanisms. Objective: We sought to identify molecular subphenotypes of asthma defined by proteomic signatures for improved stratification. Methods: Unbiased label-free quantitative mass spectrometry and topological data analysis were used to analyze the proteomes of sputum supernatants from 246 participants (206 asthmatic patients) as a novel means of asthma stratification. Microarray analysis of sputum cells provided transcriptomics data additionally to inform on underlying mechanisms. Results: Analysis of the sputum proteome resulted in 10 clusters (ie, proteotypes) based on similarity in proteomic features, representing discrete molecular subphenotypes of asthma. Overlaying granulocyte counts onto the 10 clusters as metadata further defined 3 of these as highly eosinophilic, 3 as highly neutrophilic, and 2 as highly atopic with relatively low granulocytic inflammation. For each of these 3 phenotypes, logistic regression analysis identified candidate protein biomarkers, and matched transcriptomic data pointed to differentially activated underlying mechanisms. Conclusion: This study provides further stratification of asthma currently classified based on quantification of granulocytic inflammation and provided additional insight into their underlying mechanisms, which could become targets for novel therapies.
  • Gad, Helge, et al. (författare)
  • MTH1 inhibition eradicates cancer by preventing sanitation of the dNTP pool
  • 2014
  • Ingår i: Nature. - Nature Publishing Group. - 0028-0836. ; 508:7495, s. 215-221
  • Tidskriftsartikel (refereegranskat)abstract
    • Cancers have dysfunctional redox regulation resulting in reactive oxygen species production, damaging both DNA and free dNTPs. The MTH1 protein sanitizes oxidized dNTP pools to prevent incorporation of damaged bases during DNA replication. Although MTH1 is non-essential in normal cells, we show that cancer cells require MTH1 activity to avoid incorporation of oxidized dNTPs, resulting in DNA damage and cell death. We validate MTH1 as an anticancer target in vivo and describe small molecules TH287 and TH588 as first-in-class nudix hydrolase family inhibitors that potently and selectively engage and inhibit the MTH1 protein in cells. Protein co-crystal structures demonstrate that the inhibitors bindin the active site of MTH1. The inhibitors cause incorporation of oxidized dNTPs in cancer cells, leading to DNA damage, cytotoxicity and therapeutic responses in patient-derived mouse xenografts. This study exemplifies the non-oncogene addiction concept for anticancer treatment and validates MTH1 as being cancer phenotypic lethal.
  • Lunavat, Taral R, et al. (författare)
  • BRAF(V600) inhibition alters the microRNA cargo in the vesicular secretome of malignant melanoma cells
  • 2017
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - 0027-8424. ; 114:29, s. E5930-E5939
  • Tidskriftsartikel (refereegranskat)abstract
    • The BRAF inhibitors vemurafenib and dabrafenib can be used to treat patients with metastatic melanomas harboring BRAF(V600) mutations. Initial antitumoral responses are often seen, but drug-resistant clones with reactivation of the MEK-ERK pathway soon appear. Recently, the secretome of tumor-derived extracellular vesicles (EVs) has been ascribed important functions in cancers. To elucidate the possible functions of EVs in BRAF-mutant melanoma, we determined the RNA content of the EVs, including apoptotic bodies, microvesicles, and exosomes, released from such cancer cells after vemurafenib treatment. We found that vemurafenib significantly increased the total RNA and protein content of the released EVs and caused significant changes in the RNA profiles. RNA sequencing and quantitative PCR show that cells and EVs from vemurafenib-treated cell cultures and tumor tissues harvested from cell-derived and patient-derived xenografts harbor unique miRNAs, especially increased expression of miR-211-5p. Mechanistically, the expression of miR-211-5p as a result of BRAF inhibition was induced by increased expression of MITF that regulates the TRPM1 gene resulting in activation of the survival pathway. In addition, transfection of miR-211 in melanoma cells reduced the sensitivity to vemurafenib treatment, whereas miR-211-5p inhibition in a vemurafenib resistant cell line affected the proliferation negatively. Taken together, our results show that vemurafenib treatment induces miR-211-5p up-regulation in melanoma cells both in vitro and in vivo, as well as in subsets of EVs, suggesting that EVs may provide a tool to understand malignant melanoma progression.
  • Berglind, L, et al. (författare)
  • Delay and inequality in treatment of the elderly with suspected acute coronary syndrome.
  • 2014
  • Ingår i: International journal of cardiology. - 1874-1754. ; 176:3
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND/OBJECTIVES: The aim of this study is to determine differences between elderly patients (≥80 years) and younger patients with suspected acute coronary syndrome (ACS) regarding delay times before diagnostic tests and treatments. METHODS: All patients with chest pain who were admitted to a hospital in the Gothenburg area were included consecutively over a 3-month period. They were divided into an elderly group (≥80 years) and a reference group (<80 years). Previous medical history, ECG findings, treatments, diagnostic tests, and delay times were registered. RESULTS: Altogether, 2588 patients were included (478 elderly and 2110 reference). There were no significant differences in delay time to hospital ward admission, to first medical therapy with aspirin, or to investigation with coronary angiography (CA) between the two groups. The elderly patients had a significantly shorter median time from first medical contact to first ECG (12 vs. 14 min, p=0.002) but after adjustment for confounding factors, especially mode of transport, the opposite was found to be the case (p=0.002). Elderly hospitalized patients with ACS were less often investigated with CA (44% vs. 89%, p<0.0001) and received less medical treatment with P2Y12 antagonists and lipid lowering drugs. CONCLUSIONS: Elderly individuals with chest pain could not be shown to have a delay to hospital admission compared to their younger counterparts. Nevertheless, higher age was associated with a longer time to first ECG. The elderly patients received less active therapy, and fear of age-related side effects might explain this difference.
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