Autophagy : Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging: Volume 8- Human Diseases

Language: English

Published by Elsevier Inc Jan 2016, 2016

0128029374 / 9780128029374

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Seller: AHA-BUCH GmbH, Einbeck, GermanyAHA-BUCH GmbH

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Neuware - Volume 8 Autophagy and Human Diseases, concentrates on the role of Autophagy in human diseases, including tumorigenesis. The diseases discussed include melanoma, liver cancer, pancreatic cancer, and neurodegenerative disorders. Loss of autophagy in the central nervous system causes neurodegeneration (Alzheimers disease, Huntington's disease, Parkin's disease, and Amyotrophic Lateral Sclerosis). Melanoma is one of the most serious diseases in humans. Autophagy plays a key role in the anticancer response to Chemotherapy. However, autophagy can increase or decrease the effectiveness of chemotherapy. The reasons for these contradictory effects are explained. Autophagy also plays a role in idiopathic inflammatory diseases, infection, and immunity. An explanation is given how autophagy is closely linked to control of innate and adaptive immune responses in host defense in part by regulating cytokine production. The role of autophagy in cutaneous malignant melanoma is discussed in detail and expression of Beclin 1 and LC3 autophagic genes in melanoma is included to explain the molecular mechanisms underlying this very serious disease, which tends to metastasize to the brain. The effect of the treatment of this disease using Terfenadine through the induction of autophagy and apoptosis is also included. Autophagy and apoptosis are two main mechanisms involved in programmed cell death.

Seller Inventory # 9780128029374

Title
Autophagy : Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging: Volume 8- Human Diseases
Author
M. A. Hayat
Publisher
Elsevier Inc Jan 2016
Publication year
2016
Condition
Neu
Binding
Buch
Language
English
ISBN 10
0128029374
ISBN 13
9780128029374
Item weight
934 grams
Dimensions
235x191x24 mm

AHA-BUCH GmbH

Einbeck, Germany

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