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Ionising radiation remains one of the most effective tools in the therapy of cancer. It combines the properties of an extremely efficient DNA-damaging agent with a high degree of spatial specificity. Nonetheless, there remain considerable differences in the outcome for treatment of tumours of differing histological type treated by radiotherapy. Tumours arising from lymphoid or germ cells are significantly more radiocurable than most solid tumours of epithelial origin. The molecular mechanisms underlying such differences in cellular radiosensitivity are the subject of current research. When normal mammalian cells are subjected to stress signals--e.g. radiation, chemotherapeutic drugs, oxygen deficiency--a range of gene products involved in the sensing and signalling of such stresses are activated. The response of eukaryotic cells to ionising radiation includes activation of DNA repair pathways and cell cycle checkpoints, with subsequent full 'biological' recovery or cell death. Radiation induces two different modes of cell death termed mitotic or clonogenic cell death, and apoptosis. Until recent years, there was surprisingly little mechanistic understanding of the events following induction of physical damage by radiation and biological outcome for the cell. There have been recent major advances in our understanding of the signal transduction pathways involved in determining the fate of cells after irradiation.
Departamento de Tecnología Médica, Facultad de Medicina, Universidad de Chile, Santiago, Chile
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Department of Chemistry and Biochemistry, Ohio University, Athens, Ohio, USA
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hormone, and how this hormone induces radioresistance due to an increase in the capacity of cellular DNA repair. Radiation therapy of the hypothalamic–pituitary area and growth hormone deficiency Radiotherapy and growth hormone deficiency The
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characteristics were included in the PI: acute symptoms, tumor size >5 cm, distant metastasis and WBC > 10.000/mm³ (max. 4 points). ATC patients with low PI (≤1) were treated more aggressively with multimodal treatment (surgery, radiotherapy and chemotherapy
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. Identifier and trial name Patient group Estimated patient enrollment Standard arm Experimental arm Primary end point Estimated completion date Locally advanced Pca Leuprorelin associated with radiotherapy vs
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: location and type of cancer CNS tumours at the hypothalamic–pituitary (HP) region Adrenal tumours Treatment modality Radiotherapy Accumulative dose and fractionation schedule Location – cranial irradiation to tumours
Baylor College of Medicine, Departments of Molecular and Cellular Biology, Radiology, Lester and Sue Smith Breast Center, Houston, Texas, USA
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Baylor College of Medicine, Departments of Molecular and Cellular Biology, Radiology, Lester and Sue Smith Breast Center, Houston, Texas, USA
Baylor College of Medicine, Departments of Molecular and Cellular Biology, Radiology, Lester and Sue Smith Breast Center, Houston, Texas, USA
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properties in conferring drug resistance. Resistance to radiotherapy Malignant cells are usually rapidly dividing, and their DNA damage repair systems frequently fail to perform dependably ( Nie 2012 ). Therefore, malignant cell growth can be effectively
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and possible misdiagnosis or unrecognised malignant potential should be borne in mind. Management The main treatment modalities for PGLs include surgery and radiotherapy (external-beam radiotherapy (EBRT) or stereotactic radiosurgery (SRS)). The
Department of Oncology and Hemato-Oncology (DIPO), University of Milan, Milan, Italy
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Department of Oncology and Hemato-Oncology (DIPO), University of Milan, Milan, Italy
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Division of Gynecologic Surgery, European Institute of Oncology, IRCCS, Via Ripamonti, Milan, Italy
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Department of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy
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, NCCN 2023 ). Generally, these patients undergo a multimodal treatment, including radical hysterectomy plus pelvic and para-aortic lymphadenectomy, chemotherapy with platinum salts and etoposide, and radiotherapy ( Gardner et al. 2011 , Satoh et al
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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. 2007 ). Others studies found radiation-induced signatures in post-Chernobyl PTC ( Port et al . 2007 , Stein et al . 2010 ), but without blind validation of the signature. A recent study compared cell cycle protein expression in sporadic and post-radiotherapy
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Overview External beam radiotherapy (EBRT) for papillary thyroid cancer (PTC) has been a controversial topic in the field of endocrinology, head and neck surgery, as well as radiation oncology. There is no consensus on who is a