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====Treatments==== {{Further|topic=a clinical pathology test that measures apoptosis|MiCK assay}} The main method of treatment for potential death from signaling-related diseases involves either increasing or decreasing the susceptibility of apoptosis in diseased cells, depending on whether the disease is caused by either the inhibition of or excess apoptosis. For instance, treatments aim to restore apoptosis to treat diseases with deficient cell death and to increase the apoptotic threshold to treat diseases involved with excessive cell death. To stimulate apoptosis, one can increase the number of death receptor ligands (such as TNF or TRAIL), antagonize the anti-apoptotic Bcl-2 pathway, or introduce Smac mimetics to inhibit the inhibitor (IAPs).<ref name="pmid31380246">{{cite journal | vauthors = Jan R, Chaudhry GE | title = Understanding Apoptosis and Apoptotic Pathways Targeted Cancer Therapeutics | journal = Advanced Pharmaceutical Bulletin | volume = 9 | issue = 2 | pages = 205β218 | date = June 2019 | pmid = 31380246 | pmc = 6664112 | doi = 10.15171/apb.2019.024 }}</ref> The addition of agents such as Herceptin, Iressa, or Gleevec works to stop cells from cycling and causes apoptosis activation by blocking growth and survival signaling further upstream. Finally, adding p53-[[MDM2]] complexes displaces p53 and activates the p53 pathway, leading to cell cycle arrest and apoptosis. Many different methods can be used either to stimulate or to inhibit apoptosis in various places along the death signaling pathway.<ref>{{cite journal | vauthors = Boehm I | title = Apoptosis in physiological and pathological skin: implications for therapy | journal = Current Molecular Medicine | volume = 6 | issue = 4 | pages = 375β394 | date = June 2006 | pmid = 16900661 | doi = 10.2174/156652406777435390 }}</ref> Apoptosis is a multi-step, multi-pathway cell-death programme that is inherent in every cell of the body. In cancer, the apoptosis cell-division ratio is altered. Cancer treatment by chemotherapy and irradiation kills target cells primarily by inducing apoptosis.<ref>{{cite journal |last1=Lowe |first1=Scott W. |last2=Lin |first2=Albert W. |title=Apoptosis in cancer |journal=Carcinogenesis |date=2000-03-01 |volume=21 |issue=3 |pages=485β495 |doi=10.1093/carcin/21.3.485 |pmid=10688869 |url=https://www.nature.com/articles/4401986 |access-date=2025-01-22}}</ref>
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