A pathophysiological response or cause of many diseases is inflammation. Inflammation is triggered by the immune system and stimulated by a variety of factors including pathogens, damaged cells, cytokines & stress. These factors may lead to acute or chronic inflammatory responses in various organs, including the lungs, liver, intestine, heart, and brain. In fact, it can culminate into tissue/organ damage or disease. Various agents - both infectious and non-infectious - can lead to cell damage and activation of transcription factors (eg. NF-kB, beta-catenin, HiF1a, Notch1, BiP) which trigger further activation of inflammatory signaling pathways, such as NF-kB, Wnt, S1P-S1PR1, VEGF-VEGFR2, among others.
Inflammation can lead to various diseases, including cancer. Cancer is a multifaceted disease which is therapeutically challenging. Insights from almost four decades of research clearly point to the critical role of spatio-temporally deregulated signaling pathways in the development and advancement of cancer. In the last few years, high-throughput technologies - including the advent of next generation sequencing and other array-based technologies - have deepened our understanding of the various signal transduction pathways that contribute to the development of drug resistance and to the final stages of metastatic disease.
Understanding the signaling mechanisms under health and disease conditions is key to develop potential therapeutics. In this Research Topic, we would like to focus on the role of various signaling pathways including NF-kB, Wnt/b-catenin, S1P-S1PR1, VEGF-VEGFR2, HiF1a, and BiP in chronic inflammation and cancer. Specific role of various immune cells and inflammatory mediators are also of interest. Studies focusing on immune-inflammatory suppressor cell types such as Treg, Breg, MDSC, Th2, macrophage subtypes are also of high interest. The aim is to highlight the advances in our understanding of the etiology, signaling cascades and mechanisms, and the resolution of inflammatory diseases with a special emphasis on its relation to cancer research.
This Research Topic aims to explore our current understanding of various molecular signaling pathways in homeostatic condition and when perturbed in various pathophysiological conditions. Submissions may include original research and review articles, but also more clinical/translational studies are welcome.
We welcome submissions on (but not limited to) the following topics:
1. S1P-S1PR1-mediated cell signaling pathways related to inflammation and lung vascular disorders with a special emphasis on cancer.
2. The role of VEGF-VEGFR2 mediated signaling in the context of inflammation and cancer.
3. Epigenetic modulation of various transcription factors viz; NF-kB, beta-catenin and BiP in regulating the fate of S1P-S1PR1 signaling axis.
4. Transcriptional regulation of HiF1a, Notch1, ERG, NF-kB mediated through the VEGF-VEGFR2 signaling axis.
5. Post-translation regulation of the S1PR1- and VEGFR2-mediated signaling involved in inflammation and cancer.
A pathophysiological response or cause of many diseases is inflammation. Inflammation is triggered by the immune system and stimulated by a variety of factors including pathogens, damaged cells, cytokines & stress. These factors may lead to acute or chronic inflammatory responses in various organs, including the lungs, liver, intestine, heart, and brain. In fact, it can culminate into tissue/organ damage or disease. Various agents - both infectious and non-infectious - can lead to cell damage and activation of transcription factors (eg. NF-kB, beta-catenin, HiF1a, Notch1, BiP) which trigger further activation of inflammatory signaling pathways, such as NF-kB, Wnt, S1P-S1PR1, VEGF-VEGFR2, among others.
Inflammation can lead to various diseases, including cancer. Cancer is a multifaceted disease which is therapeutically challenging. Insights from almost four decades of research clearly point to the critical role of spatio-temporally deregulated signaling pathways in the development and advancement of cancer. In the last few years, high-throughput technologies - including the advent of next generation sequencing and other array-based technologies - have deepened our understanding of the various signal transduction pathways that contribute to the development of drug resistance and to the final stages of metastatic disease.
Understanding the signaling mechanisms under health and disease conditions is key to develop potential therapeutics. In this Research Topic, we would like to focus on the role of various signaling pathways including NF-kB, Wnt/b-catenin, S1P-S1PR1, VEGF-VEGFR2, HiF1a, and BiP in chronic inflammation and cancer. Specific role of various immune cells and inflammatory mediators are also of interest. Studies focusing on immune-inflammatory suppressor cell types such as Treg, Breg, MDSC, Th2, macrophage subtypes are also of high interest. The aim is to highlight the advances in our understanding of the etiology, signaling cascades and mechanisms, and the resolution of inflammatory diseases with a special emphasis on its relation to cancer research.
This Research Topic aims to explore our current understanding of various molecular signaling pathways in homeostatic condition and when perturbed in various pathophysiological conditions. Submissions may include original research and review articles, but also more clinical/translational studies are welcome.
We welcome submissions on (but not limited to) the following topics:
1. S1P-S1PR1-mediated cell signaling pathways related to inflammation and lung vascular disorders with a special emphasis on cancer.
2. The role of VEGF-VEGFR2 mediated signaling in the context of inflammation and cancer.
3. Epigenetic modulation of various transcription factors viz; NF-kB, beta-catenin and BiP in regulating the fate of S1P-S1PR1 signaling axis.
4. Transcriptional regulation of HiF1a, Notch1, ERG, NF-kB mediated through the VEGF-VEGFR2 signaling axis.
5. Post-translation regulation of the S1PR1- and VEGFR2-mediated signaling involved in inflammation and cancer.
