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dc.contributor.author
Vaccaro, Maria Ines
dc.contributor.author
González, Claudio Daniel
dc.contributor.other
Chaudhary, M. Iqbal
dc.date.available
2021-04-26T12:59:32Z
dc.date.issued
2018
dc.identifier.citation
Vaccaro, Maria Ines; González, Claudio Daniel; Targeting Autophagy In Cancer Therapy; Bentham Science Publishers; 9; 2018; 91-110
dc.identifier.isbn
978-1-68108-702-3
dc.identifier.uri
http://hdl.handle.net/11336/130830
dc.description.abstract
Macroautophagy is a physiological cellular process that sequesters senescent or damaged organelles and proteins in autophagosomes for recycling of their products. Autophagy is also involved in the removal of cells that have undergone classical type 1 apoptosis. Hence, autophagy can be generally considered as a protector of cells against various stressors and a cellular response to routine wear-and-tear. On the other hand, autophagy may also lead to a form of non-apoptotic cell death, which is called type 2 programmed cell death. Thus, autophagy can either protect cells or promote cell death, depending on the cellular and environmental context. So far, contradictory data are available regarding the activity of autophagy and its regulation in cancer cells. In nonmalignant healthy tissues, autophagy seems to suppress the transition of normal to cancer cells. In addition, an exaggerated autophagy rate might drive neoplastic cells to death through several mechanisms, many of which are still not elucidated. Nevertheless, experimental evidence pointed at autophagy as a cancer cell mechanism to survive under adverse environmental conditions, or as a defective programmed cell death mechanism that favors cancer cell resistance to treatment. In the end, the role of autophagy in cancer is complex and it seems to depend on histology, stage, and multiple genetic variations and epigenetic changes. The tumor surrounding microenvironment exhibits a very complex set of interactions with autophagy at cancer tissues and represents another factor that is able to regulate tumor cell-kinetics and growth, as well as the response to therapies. In summary, while there is certain evidence that autophagy may act as a barrier to tumor initiation in some specific tissues, there is mounting evidence that autophagy has a significant pro-tumorigenic role in established cancers. Cancer therapies, including chemotherapy, radiotherapy and immunotherapy, are also associated with relevant changes into the autophagy intensity and flow. Some antineoplastic agents increase the autophagy rate; some other are associated with a reduction of the autophagy rate. Autophagy may modulate anticancer immunity by affecting several cellular and humoral mechanisms involved at these critical processes. Immunotherapeutic agents recently introduced in oncology clearly induce relevant modifications on autophagy flow in several tumor types. In addition, it has been demonstrated that certain non-antineoplastic drugs may exert some autophagy inducing effect on cancer cells. On the other hand, other agents block autophagy flow synergizing with the effect of some antineoplastic agents. Autophagy modulation is at this moment, a clear target for further development of cancer therapy. A description of the mechanisms that regulate autophagy in cancer cells and their surrounding micro-environment and the potential consequences of the pharmacologically induced modifications of these processes, constitute the main objective of this chapter.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Bentham Science Publishers
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Cancer
dc.subject
therapy
dc.subject
autophagy
dc.subject
drug-discovery
dc.subject.classification
Oncología
dc.subject.classification
Medicina Clínica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Targeting Autophagy In Cancer Therapy
dc.type
info:eu-repo/semantics/publishedVersion
dc.type
info:eu-repo/semantics/bookPart
dc.type
info:ar-repo/semantics/parte de libro
dc.date.updated
2021-03-26T19:59:05Z
dc.journal.volume
9
dc.journal.pagination
91-110
dc.journal.pais
Reino Unido
dc.description.fil
Fil: Vaccaro, Maria Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
dc.description.fil
Fil: González, Claudio Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas "Norberto Quirno". CEMIC-CONICET; Argentina
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.eurekaselect.com/52946/volume/1
dc.conicet.paginas
315
dc.source.titulo
Frontiers in Anti-Cancer Drug Discovery
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