Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ongoing climatic changes induced by human activities increases in atmospheric carbon dioxide (CO2), which have considerable effects on the structure and function of ecosystems, including carbon (C) storage, plant functional traits and therefore on a wide set of ecosystem services. Plant functional diversity is benefit to improve plant photosynthesis and enhance C efficiency and therefore decrease CO2. Here, the focus of this article is on integrating of plant functional diversity and C storage, which aims to contribute to C sequestration for climate change mitigation following vegetation restoration in Loess Plateau, China. Firstly, the CWM (plant community-weighted mean) traits of the most abundant plant species can account for C storage in AGBC (above-ground biomass C), ALC (above-ground litter C), STC (soil total carbon) and TEC (total ecosystem carbon). Secondly, the CWM of plant height and LCC (leaf carbon concentration) had a positive effect C storage in different part (AGBC, ALC, STC and TEC), while the CWM of LNC (leaf nitrogen concentration) and SLA (specific leaf area) had a negative effect on C storage in different part. Further, the CWM of plant height, LCC, SLA and plant functional dispersion (FDis) can be used to predict C storage by multiple linear regression analysis. Finally, the positive association between FDis and C storage was found in SEM, shedding light on the key role of plant functional diversity driving C storage following vegetation restoration. The findings presented here highlight the importance of both plant traits of dominant species and plant functional diversity in regulating C storage, and show that favorable climate conditions, particularly vegetation restoration, tend to increase C storage and plant functional diversity, which have important implications for improving global C cycling and ecosystem services.
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PMID:Plant functional diversity drives carbon storage following vegetation restoration in Loess Plateau, China. 3121 12

Hepatocellular carcinoma (HCC), the most prevalent primary liver cancer, is a leading cause of cancer-related death worldwide because of rising incidence and limited therapy. Although treatment with sorafenib or lenvatinib is the standard of care in patients with advanced-stage HCC, the survival benefit from sorafenib is limited due to low response rate and drug resistance. Ibrutinib, an irreversible tyrosine kinase inhibitor (TKI) of the TEC (e.g., BTK) and ErbB (e.g., EGFR) families, is an approved treatment for B-cell malignancies. Here, we demonstrate that ibrutinib inhibits proliferation, spheroid formation, and clonogenic survival of HCC cells, including sorafenib-resistant cells. Mechanistically, ibrutinib inactivated EGFR and its downstream Akt and ERK signaling in HCC cells, and downregulated a set of critical genes involved in cell proliferation, migration, survival, and stemness, and upregulated genes promoting differentiation. Moreover, ibrutinib showed synergy with sorafenib or regorafenib, a sorafenib congener, by inducing apoptosis of HCC cells. In vivo, this TKI combination significantly inhibited HCC growth and prolonged survival of immune-deficient mice bearing human HCCLM3 xenograft tumors and immune-competent mice bearing orthotopic mouse Hepa tumors at a dose that did not exhibit systemic toxicity. In immune-competent mice, the ibrutinib-sorafenib combination reduced the numbers of BTK+ immune cells in the tumor microenvironment. Importantly, we found that the BTK+ immune cells were also enriched in the tumor microenvironment in a subset of primary human HCCs. Collectively, our findings implicate BTK signaling in hepatocarcinogenesis and support clinical trials of the sorafenib-ibrutinib combination for this deadly disease.
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PMID:Ibrutinib Potentiates Antihepatocarcinogenic Efficacy of Sorafenib by Targeting EGFR in Tumor Cells and BTK in Immune Cells in the Stroma. 3158 34