Editorial: Cell Death and Targeted Cancer Therapies.

Bagci-Onder, Tugba; Kutuk, Ozgur; Chonghaile, Triona Ni; Knippschild, Uwe

dc.contributor.author	Bagci-Onder, Tugba
dc.contributor.author	Kutuk, Ozgur
dc.contributor.author	Chonghaile, Triona Ni
dc.contributor.author	Knippschild, Uwe
dc.date.accessioned	2024-07-16T11:09:03Z
dc.date.available	2024-07-16T11:09:03Z
dc.date.issued	2022-07-06
dc.identifier.issn	2296-634X
dc.identifier.pmid	35874828
dc.identifier.doi	10.3389/fcell.2022.967720
dc.identifier.uri	http://hdl.handle.net/10147/642255
dc.description	Cell death is critical for organismal development, maintenance of tissue homeostasis and the prevention of diseases, such as cancer. The most well-established mechanism of cell death is apoptosis, and cancer cells are known to adopt mechanisms to evade it. However, the roles of non-apoptotic cell death mechanisms, such as pyroptosis, necroptosis, and ferroptosis, in regulating cancer progression and therapy response are emerging. Development of therapy resistance involves the de-regulation of these cell death programs as well as tumor cell-microenvironment interactions. Our understanding of the precise mechanisms of cell death signaling networks in response to cancer therapies continue to evolve. Resistance to therapy poses a prominent problem for the successful treatment of cancer, and there is a vast amount of information emerging in the field of therapy resistance. One of the important players in regulating resistance to therapies is the tumor microenvironment. For example, the bone marrow microenvironment can provide survival signals to leukemic stem cells, enabling survival of cells leading eventually to relapse of the disease. O’Reilly et al. developed an in vitro model system to study quiescent acute myelogenous leukemia (AML) cells in the bone marrow microenvironment. Using a hydrogel co-culture system, they induced quiescence in AML cells, which was enhanced in hypoxic conditions. Next, they screened a total of 1,600 drugs to identify therapeutics that could activate quiescent AML cells. Sequential treatments with hedgehog inhibitors, adipocyte peptides and tyrosine kinase inhibitors could move a proportion of cells into a cycling state. It was not clear from the studies if this also enhanced apoptosis within cells. Potentially, this could be a useful strategy to target residual quiescent cells in the bone marrow to prevent disease relapse.	en_US
dc.language.iso	en	en_US
dc.rights	Attribution 4.0 International	*
dc.rights.uri	http://creativecommons.org/licenses/by/4.0/	*
dc.subject	apoptosis	en_US
dc.subject	Cancer	en_US
dc.subject	cell death	en_US
dc.subject	ferroptosis	en_US
dc.subject	pyroptosis	en_US
dc.subject	therapy resistance	en_US
dc.title	Editorial: Cell Death and Targeted Cancer Therapies.	en_US
dc.type	Other	en_US
dc.identifier.journal	Frontiers in cell and developmental biology	en_US
dc.source.journaltitle	Frontiers in cell and developmental biology
dc.source.volume	10
dc.source.beginpage	967720
dc.source.endpage
refterms.dateFOA	2024-07-16T11:09:05Z
dc.source.country	Switzerland