Molecular Mechanisms Underlying Pituitary Pathogenesis
During the last years, progress has been made on the identification of mechanisms involved in anterior pituitary cell transformation and tumorigenesis. Oncogene activation, tumor suppressor gene inactivation, epigenetic changes, and microRNAs deregulation contribute to the initiation of pituitary tu...
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todo:paper_00062928_v54_n2_p107_Sapochnik2023-10-03T14:04:12Z Molecular Mechanisms Underlying Pituitary Pathogenesis Sapochnik, M. Nieto, L.E. Fuertes, M. Arzt, E. IL-6 OIS Pituitary tumors PTTG Senescence interleukin 6 microRNA IL6 protein, human interleukin 6 microRNA pituitary tumor-transforming protein 1, human securin carcinogenesis cell cycle cell proliferation human hypophysis adenoma hypophysis tumor oncogene Review senescence signal transduction adenoma cell aging DNA damage genetic epigenesis genetics hypophysis hypophysis tumor metabolism pathology tumor suppressor gene Adenoma Cell Aging Cell Cycle DNA Damage Epigenesis, Genetic Genes, Tumor Suppressor Humans Interleukin-6 MicroRNAs Oncogenes Pituitary Gland Pituitary Neoplasms Securin Signal Transduction During the last years, progress has been made on the identification of mechanisms involved in anterior pituitary cell transformation and tumorigenesis. Oncogene activation, tumor suppressor gene inactivation, epigenetic changes, and microRNAs deregulation contribute to the initiation of pituitary tumors. Despite the high prevalence of pituitary adenomas, they are mostly benign, indicating that intrinsic mechanisms may regulate pituitary cell expansion. Senescence is characterized by an irreversible cell cycle arrest and represents an important protective mechanism against malignancy. Pituitary tumor transforming gene (PTTG) is an oncogene involved in early stages of pituitary tumor development, and also triggers a senescence response by activating DNA-damage signaling pathway. Cytokines, as well as many other factors, play an important role in pituitary physiology, affecting not only cell proliferation but also hormone secretion. Special interest is focused on interleukin-6 (IL-6) because its dual function of stimulating pituitary tumor cell growth but inhibiting normal pituitary cells proliferation. It has been demonstrated that IL-6 has a key role in promoting and maintenance of the senescence program in tumors. Senescence, triggered by PTTG activation and mediated by IL-6, may be a mechanism for explaining the benign nature of pituitary tumors. © 2015, Springer Science+Business Media New York. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00062928_v54_n2_p107_Sapochnik |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
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R-134 |
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Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
IL-6 OIS Pituitary tumors PTTG Senescence interleukin 6 microRNA IL6 protein, human interleukin 6 microRNA pituitary tumor-transforming protein 1, human securin carcinogenesis cell cycle cell proliferation human hypophysis adenoma hypophysis tumor oncogene Review senescence signal transduction adenoma cell aging DNA damage genetic epigenesis genetics hypophysis hypophysis tumor metabolism pathology tumor suppressor gene Adenoma Cell Aging Cell Cycle DNA Damage Epigenesis, Genetic Genes, Tumor Suppressor Humans Interleukin-6 MicroRNAs Oncogenes Pituitary Gland Pituitary Neoplasms Securin Signal Transduction |
| spellingShingle |
IL-6 OIS Pituitary tumors PTTG Senescence interleukin 6 microRNA IL6 protein, human interleukin 6 microRNA pituitary tumor-transforming protein 1, human securin carcinogenesis cell cycle cell proliferation human hypophysis adenoma hypophysis tumor oncogene Review senescence signal transduction adenoma cell aging DNA damage genetic epigenesis genetics hypophysis hypophysis tumor metabolism pathology tumor suppressor gene Adenoma Cell Aging Cell Cycle DNA Damage Epigenesis, Genetic Genes, Tumor Suppressor Humans Interleukin-6 MicroRNAs Oncogenes Pituitary Gland Pituitary Neoplasms Securin Signal Transduction Sapochnik, M. Nieto, L.E. Fuertes, M. Arzt, E. Molecular Mechanisms Underlying Pituitary Pathogenesis |
| topic_facet |
IL-6 OIS Pituitary tumors PTTG Senescence interleukin 6 microRNA IL6 protein, human interleukin 6 microRNA pituitary tumor-transforming protein 1, human securin carcinogenesis cell cycle cell proliferation human hypophysis adenoma hypophysis tumor oncogene Review senescence signal transduction adenoma cell aging DNA damage genetic epigenesis genetics hypophysis hypophysis tumor metabolism pathology tumor suppressor gene Adenoma Cell Aging Cell Cycle DNA Damage Epigenesis, Genetic Genes, Tumor Suppressor Humans Interleukin-6 MicroRNAs Oncogenes Pituitary Gland Pituitary Neoplasms Securin Signal Transduction |
| description |
During the last years, progress has been made on the identification of mechanisms involved in anterior pituitary cell transformation and tumorigenesis. Oncogene activation, tumor suppressor gene inactivation, epigenetic changes, and microRNAs deregulation contribute to the initiation of pituitary tumors. Despite the high prevalence of pituitary adenomas, they are mostly benign, indicating that intrinsic mechanisms may regulate pituitary cell expansion. Senescence is characterized by an irreversible cell cycle arrest and represents an important protective mechanism against malignancy. Pituitary tumor transforming gene (PTTG) is an oncogene involved in early stages of pituitary tumor development, and also triggers a senescence response by activating DNA-damage signaling pathway. Cytokines, as well as many other factors, play an important role in pituitary physiology, affecting not only cell proliferation but also hormone secretion. Special interest is focused on interleukin-6 (IL-6) because its dual function of stimulating pituitary tumor cell growth but inhibiting normal pituitary cells proliferation. It has been demonstrated that IL-6 has a key role in promoting and maintenance of the senescence program in tumors. Senescence, triggered by PTTG activation and mediated by IL-6, may be a mechanism for explaining the benign nature of pituitary tumors. © 2015, Springer Science+Business Media New York. |
| format |
JOUR |
| author |
Sapochnik, M. Nieto, L.E. Fuertes, M. Arzt, E. |
| author_facet |
Sapochnik, M. Nieto, L.E. Fuertes, M. Arzt, E. |
| author_sort |
Sapochnik, M. |
| title |
Molecular Mechanisms Underlying Pituitary Pathogenesis |
| title_short |
Molecular Mechanisms Underlying Pituitary Pathogenesis |
| title_full |
Molecular Mechanisms Underlying Pituitary Pathogenesis |
| title_fullStr |
Molecular Mechanisms Underlying Pituitary Pathogenesis |
| title_full_unstemmed |
Molecular Mechanisms Underlying Pituitary Pathogenesis |
| title_sort |
molecular mechanisms underlying pituitary pathogenesis |
| url |
http://hdl.handle.net/20.500.12110/paper_00062928_v54_n2_p107_Sapochnik |
| work_keys_str_mv |
AT sapochnikm molecularmechanismsunderlyingpituitarypathogenesis AT nietole molecularmechanismsunderlyingpituitarypathogenesis AT fuertesm molecularmechanismsunderlyingpituitarypathogenesis AT arzte molecularmechanismsunderlyingpituitarypathogenesis |
| _version_ |
1807317752555241472 |