GSE132759 The contribution of FGFR1 to the development of SCLC is dictated by the cell-of-origin
Contributors : Giustina Ferone ; Oscar Krijgsman ; Ton BernsSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusEnhanced RAF/MEK/ERK signaling plays an obligatory role in many different types of cancer. Although genetic lesions promoting its aberrant activation are found in lung adenocarcinoma (LADC), the biological role of this pathway is not well documented in small cell lung cancer (SCLC). Here we explored the role of this pathway in SCLC and the broader class of tumors with neuroendocrine (NE) differentiation by introducing a constitutively active form of Fibroblast growth factor receptor 1 (Fgfr1) together with biallelic inactivation of Rb1 and Trp53 in mouse lung. Our data show that FGFR1 expression primarily results in LADC but also in NE tumors depending on the cell-of-origin. FGFR1 activation selectively promoted NE bronchial lesions in a novel lung cell subpopulation, whereas it impaired progression of typical central SCLC initiated from CGRP-expressing NE cells, which is believed to be the most prominent cell-of-origin of SCLC. Strikingly, FGFR1 activation was well tolerated by K14-expressing cells that were efficiently transformed into SCLC and other NE lesions. Taken together, our results indicate that FGFR1 can serve either as driver or suppressor of distinct lung cancer subtypes depending on the cell-of-origin, which should be taken into account when considering FGFR1 as a therapeutic target.
Authors: Chang C, Wu H, Lu Q Abstract Food allergy is a global health problem, particularly in developed countries. It is mainly mediated by Th2 cell and IgE produced by B cells. While the pathogenesis of IgE-mediated food allergy is quite straightforward, the factors that lead to the development of food allergies at any age in children and adults are unclear. Recent studies have revealed that genetics, epigenetics, and environmental exposures contribute to the development of atopy. In this chapter, we discuss the interplay between these three key elements, reveal how epigenetic modifications may mediate genetic su...
Authors: Ceribelli A, Selmi C Abstract Genomic predisposition fails to fully explain the onset of complex diseases, which is well illustrated by the largely incomplete concordance among monozygotic twins. Epigenetic mechanisms, including DNA methylation, chromatin remodeling, and non-coding RNA, are the link between environmental stimuli and disease onset on a permissive genetic background in autoimmune and chronic inflammatory diseases. Autoimmune diseases now include almost 100 conditions and are estimated to cumulatively affect up to 5% of the world population with a healthcare expenditure superior to cancer wor...
Authors: Zhang L, Lu Q, Chang C Abstract Epigenetic mechanisms, which include DNA methylation, histone modification, and microRNA (miRNA), can produce heritable phenotypic changes without a change in DNA sequence. Disruption of gene expression patterns which are governed by epigenetics can result in autoimmune diseases, cancers, and various other maladies. Mechanisms of epigenetics include DNA methylation (and demethylation), histone modifications, and non-coding RNAs such as microRNAs. Compared to numerous studies that have focused on the field of genetics, research on epigenetics is fairly recent. In contrast to ...
CONCLUSION: Radiological imaging is essential for the management of patients affected by lung cancer. PMID: 32445458 [PubMed - as supplied by publisher]
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