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Molecular mechanisms of cellular stress responses in cancer and their therapeutic implications

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194964 Year: Pages: 159 DOI: 10.3389/978-2-88919-496-4 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2015-11-16 15:44:59
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Abstract

In response to stress, cells can activate a myriad of signalling pathways to bring about a specific cellular outcome, including cell cycle arrest, DNA repair, senescence and apoptosis. This response is pivotal for tumour suppression as all of these outcomes result in restriction of the growth and/or elimination of damaged and pre-malignant cells. Thus, a large number of anti-cancer agents target specific components of stress response signalling pathways with the aim of causing tumour regression by stimulating cell death. However, the efficacy of these agents is often impaired due to mutations in genes that are involved in these stress-responsive signalling pathways and instead the oncogenic potential of a cell is increased leading to the initiation and/or progression of tumourigenesis. Moreover, these genetic defects can increase or contribute to resistance to chemotherapeutic agents and/or radiotherapy. Modulating the outcome of cellular stress responses towards cell death in tumour cells without affecting surrounding normal cells is thus one of the ultimate aims in the development of new cancer therapeutics. To achieve this aim, a detailed understanding of cellular stress response pathways and their aberrations in cancer is required.This Research topic aims to reflect the broadness and complexity of this important area of cancer research.

Cellular and Phenotypic Plasticity in Cancer

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196623 Year: Pages: 77 DOI: 10.3389/978-2-88919-662-3 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2016-08-16 10:34:25
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The process of Epithelial-Mesenchymal-Transition (EMT) is known to result in a phenotype change in cells from a proliferative state to a more invasive state. EMT has been reported to drive the metastatic spread of various cancers and has also been associated with drug resistance to cytotoxics and targeted therapeutics. Recently phenotype switching akin to EMT has been reported in non-epithelial cancers such as metastatic melanoma. This process involves changes in EMT-Transcription Factors (EMT-TFs), suggesting that phenotype-switching may be common to several tumour types. It remains unclear as to whether the presence of both Epilthelial-like and Mesenchymal-like cells are a pre-requisite for phenotype switching within a tumour, how this heterogeneity is regulated, and if alteration of cell phenotype is sufficient to mediate migratory changes, or whether drivers of cell migration result in an associated phenotype switch in cancer cells. Similarly it has yet to be clarified if cells in an altered phenotype can be refractory to drug therapy or whether mediators of drug resistance induce a concurrent phenotypic change. Little is known today about the underlying genetic, epigenetic and transient changes that accompany this phenotypic switch and about the role for the tumor micro-environment in influencing it. Hence this is currently an area of speculation and keen interest in the Oncology field with wide-ranging translational implications. In this Frontiers Research Topic, we discuss our current understanding of these concepts in various cancer types including breast cancer, colorectal cancer and metastatic melanoma. This topic covers how these processes of cellular and phenotypic plasticity are regulated and how they relate to cancer initiation, progression, dormancy, metastases and response to cytotoxics or targeted therapies.

Pheochromocytoma (PHEO) and Paraganglioma (PGL)

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ISBN: 9783039216543 / 9783039216550 Year: Pages: 380 DOI: 10.3390/books978-3-03921-655-0 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2019-12-09 11:49:16
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Abstract

This book outlines some new advances in genetics, clinical evaluation, localization, therapy (newly including immunotherapy) of pheochromocytoma and paraganglioma including their metastatic counterparts. Well-known and experienced clinicians and scientists contributed to this book to include some novel approaches to these tumors. This book will serve to various health care professionals from different subspecialties, but mainly oncologists, endocrinologists, endocrine surgeons, pediatricians, and radiologists. This book shows that the field of pheochromocytoma/paraganglioma is evolving and a significant progress has been made in last 5 years requiring that health care professionals and scientists will learns new information and implement it in their clinical practice or scientific work, respectively. This book should not be missed by anybody who is focusing on neuroendocrine tumors, their newest evaluation and treatment.

Keywords

pheochromocytoma --- paraganglioma --- adrenocortical carcinoma --- adrenal tumor --- pan-cancer analysis --- neural crest --- neuroendocrine --- paraganglioma --- head and neck --- radiotherapy --- 18F-FDOPA --- PET --- GTV --- SDHB --- SDHD --- mortality --- paraganglioma --- pheochromocytoma --- radiofrequency ablation --- cryoablation --- percutaneous ethanol injection --- neuroendocrine tumor --- minimally invasive procedure --- percutaneous ablation --- PASS --- GAPP --- histology --- meta-analysis --- paraganglioma --- pheochromocytoma --- carotid body --- angiogenesis --- mitochondria --- neural crest --- neurogenesis --- paraganglioma --- stem-like tumor cells --- vasculogenesis --- xenograft --- pheochromocytoma --- catecholamine --- global longitudinal strain --- speckle-tracking echocardiography --- subclinical systolic dysfunction --- pheochromocytoma --- paraganglioma --- neuroendocrine tumor --- targeted therapy --- therapy resistance --- FGF21 --- pheochromocytoma --- paraganglioma --- diabetes mellitus --- obesity --- energy metabolism --- calorimetry --- chromogranin A --- metanephrines --- pheochromocytoma --- paraganglioma --- hypoxia --- pseudohypoxia --- spheroids --- HIF --- EPAS1 --- catecholamine --- pheochromocytoma and paraganglioma --- phosphorylation tyrosine hydroxylase --- dog --- pheochromocytoma --- paraganglioma --- SDHB --- SDHD --- mutation --- chromosomal alteration --- comparative genomics --- pheochromocytoma --- paraganglioma --- metastatic --- immunotherapy --- innate immunity --- adaptive immunity --- toll-like receptor --- pathogen-associated molecular patterns --- neutrophil --- T cell --- pheochromocytoma --- paraganglioma --- hypertension --- blood pressure variability --- average real variability --- weighted standard deviation --- paraganglioma --- somatostatinoma --- polycythemia --- EPAS1 --- transgenic mice --- erythropoietin --- pheochromocytoma --- paraganglioma --- TCA cycle --- germline mutation --- metastatic OR malignant pheochromocytoma --- paraganglioma --- ectopic secretion --- lL-6 --- normetanephrines --- VHL --- NF1 --- EPAS1 --- hypoxia-inducible factor --- inflammation --- radiosensitization --- succinate dehydrogenase --- mouse pheochromocytoma cells --- immunohistochemistry --- fluorescence imaging --- pheochromocytoma --- paraganglioma --- next-generation sequencing --- sporadic --- hereditary --- CNV detection --- pheochromocytoma --- paraganglioma --- PET-CT --- 11C-hydroxy-ephedrine --- adrenal incidentaloma --- pheochromocytoma --- paraganglioma --- 177Lu-DOTATATE --- peptide receptor radiotherapy --- PRRT --- neuroendocrine tumor --- NET --- PCC --- PGL --- postoperative --- pheochromocytoma --- hypertension --- hypotension --- arrhythmia --- PPGL --- catecholamines --- adrenomedullary function --- n/a

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