Uptodate cyclin inhibitors: how increase the bar
- 04 Mar 2019
|Numero crediti assegnati||5|
|Categorie con ECM||Medico Chirurgo (Anatomia patologica, Ginecologia e ostetricia, Oncologia, Radioterapia)|
|Presidente||Prof. Giovanni Scambia|
|Segreteria Scientifica||Dott.ssa Ida Paris|
|Segreteria organizzativa||Molipharma s.r.l.|
A major target of CDK4 and CDK6 during cell-cycle progression is the retinoblastoma protein (Rb). When Rb is phosphorylated, its growth-suppressive properties are inactivated. Selective CDK4/6 inhibitors “turn off” these kinases and dephosphorylate Rb, resulting in a block of cell-cycle progression in mid-G1.This causes cell-cycle arrest and prevents the proliferation of cancer cells. Although the initial response to a selective CDK4/6 inhibitor is typically cell-cycle arrest, in some cases arrested cells enter a state of senescence.
Understanding the determinants of whether a cell undergoes reversible G1 arrest or enters a senescent state is an important research area. Cancer cells entering senescence may undergo gradual regression over time; it is in such cancers that CDK4/6 inhibitors may produce the greatest clinical benefit. This mechanism of action is known in estrogen receptor– positive breast cancer and seems to be dependent upon CDK4 for proliferation.To date, estrogen receptor–positive breast cancer is the malignancy for which this class of drugs has proven most effective and for which we have the most mature data from randomized trials comparing endocrine therapy alone with endocrine therapy combined with CDK4/6 inhibition.
This meeting would like to review the mechanisms of action and efficacy of these drugs in order to evidence the best choice in clinical management of estrogen receptor–positive metastatic breast cancer with special point of view in their future development.
Le iscrizioni di questo corso sono chiuse dal 04 March 2019