Τίτλος:
The relevance of notch signaling in cancer progression
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
The Notch signaling pathway controls normal embryonic development and tissue homeostasis of many cell types. It regulates cell proliferation, fate, differentiation, and cell death by short-range signaling between nearby cells that come in contact. The Notch pathway has also been critically involved in the pathobiology of a variety of malignancies, regulating cancer initiation and development, as well as early stages of cancer progression, by adjusting conserved cellular programs. Fibroblasts, an essential for tumor growth component of stroma, have also been affected by Notch regulation. Sequencing Notch gene mutations have been identified in a number of human tumors, revealing information on the progression of specific cancer types, such as ovarian cancer and melanoma, immune-associated tumors such as myeloid neoplasms, but especially in lymphocytic leukemia. Activation of the Notch can be either oncogenic or it may contain growth-suppressive functions, acting as a tumor suppressor in other hematopoietic cells, hepatocytes, skin, and pancreatic epithelium. © 2021, Springer Nature Switzerland AG.
Συγγραφείς:
Fasoulakis, Z.
Daskalakis, G.
Theodora, M.
Antsaklis, P.
Sindos, M.
Diakosavvas, M.
Angelou, K.
Loutradis, D.
Kontomanolis, E.N.
Περιοδικό:
Advances in Experimental Medicine and Biology
Λέξεις-κλειδιά:
Notch receptor; Notch3 receptor; protein Jagged 1; Notch receptor, angiogenesis; apoptosis; carcinogenesis; cell activation; cell cycle regulation; cell differentiation; cell proliferation; enzyme activation; enzyme mechanism; enzyme regulation; fibroblast; gene targeting; genetic transcription; human; immunoregulation; nervous system development; nonhuman; Notch signaling; priority journal; tumor associated leukocyte; tumor promotion; tumor suppressor gene; disease exacerbation; genetics; metabolism; neoplasm; oncogene; pathology; signal transduction, Disease Progression; Genes, Tumor Suppressor; Humans; Neoplasms; Oncogenes; Receptors, Notch; Signal Transduction
DOI:
10.1007/978-3-030-55031-8_11
