Ribociclib
From Proteopedia
(Difference between revisions)
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[[Cyclin-dependent kinases]] (CDKs) 4 and 6 are enzymes that have been shown to promote cell division and multiplication in both normal and cancer cells. Many cancer cells have shown abnormalities that increase the activity of CDK, leading to the inactivation of certain [[Oncogenes & Tumor Suppressor Genes|tumor suppressor genes]].<ref name="a13">doi:10.1097/01.COT.0000444043.33304.c1</ref><ref name="a14">doi:10.1158/1535-7163.TARG-13-PR02</ref> | [[Cyclin-dependent kinases]] (CDKs) 4 and 6 are enzymes that have been shown to promote cell division and multiplication in both normal and cancer cells. Many cancer cells have shown abnormalities that increase the activity of CDK, leading to the inactivation of certain [[Oncogenes & Tumor Suppressor Genes|tumor suppressor genes]].<ref name="a13">doi:10.1097/01.COT.0000444043.33304.c1</ref><ref name="a14">doi:10.1158/1535-7163.TARG-13-PR02</ref> | ||
| - | When used in combination with other drugs such as an ALK or an MEK inhibitor, ribociclib has been shown to have a synergistic effect, resulting in improved responses.<ref name="a15">doi:10.1200/jco.2014.32.15_suppl.9009</ref><ref name="a16">doi:10.1158/1538-7445.AM2014-1000</ref> Again, this is likely a result of "crosstalk" between signaling pathways. Simply blocking one pathway in cancer tumorigenesis can sometimes result in "tumor compensation", where the tumor compensates for the blocked signaling pathway by utilizing other pathways to survive. By blocking several pathways at once, it is thought that the tumor is less able to compensate, and a greater anti-tumor response is often observed. Utilizing ribociclib in combination with other agents has been shown to reduce the development of resistance to these agents.<ref name="a13">doi:10.1097/01.COT.0000444043.33304.c1</ref> | + | When used in combination with other drugs such as an [[anaplastic lymphoma kinase]] ALK or an MEK inhibitor, ribociclib has been shown to have a synergistic effect, resulting in improved responses.<ref name="a15">doi:10.1200/jco.2014.32.15_suppl.9009</ref><ref name="a16">doi:10.1158/1538-7445.AM2014-1000</ref> Again, this is likely a result of "crosstalk" between signaling pathways. Simply blocking one pathway in cancer tumorigenesis can sometimes result in "tumor compensation", where the tumor compensates for the blocked signaling pathway by utilizing other pathways to survive. By blocking several pathways at once, it is thought that the tumor is less able to compensate, and a greater anti-tumor response is often observed. Utilizing ribociclib in combination with other agents has been shown to reduce the development of resistance to these agents.<ref name="a13">doi:10.1097/01.COT.0000444043.33304.c1</ref> |
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||
Revision as of 11:29, 31 October 2023
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References
- ↑ "Kisqali (ribociclib) Treatment: HR+/HER2- mBC". Novartis. Retrieved 24 August 2021.
- ↑ 2.0 2.1 doi: https://dx.doi.org/10.1097/01.COT.0000444043.33304.c1
- ↑ doi: https://dx.doi.org/10.1158/1535-7163.TARG-13-PR02
- ↑ doi: https://dx.doi.org/10.1200/jco.2014.32.15_suppl.9009
- ↑ doi: https://dx.doi.org/10.1158/1538-7445.AM2014-1000
