par Pita, Jaime Miguel ;Raspé, Eric ;Coulonval, Katia ;Decaussin-Petrucci, Myriam;Tarabichi, Maxime ;Dom, Geneviève ;Libert, Frédérick ;Ruscas-Craciun, Ligia Ioana ;Andry, Guy ;Wicquart, Laurence;Leteurtre, Emmanuelle;Tresallet, Christophe;Marlow, Laura A;Copland, John A;Durante, Cosimo;Maenhaut, Carine ;Cavaco, Branca Maria;Dumont, Jacques Emile ;Costante, Giuseppe ;Roger, Pierre P.
Référence Frontiers in endocrinology, 14, page (1247542)
Publication Publié, 2023-10-26
Référence Frontiers in endocrinology, 14, page (1247542)
Publication Publié, 2023-10-26
Article révisé par les pairs
Résumé : | CDK4/6 inhibitors (CDK4/6i) have been established as standard treatment against advanced Estrogen Receptor-positive breast cancers. These drugs are being tested against several cancers, including in combinations with other therapies. We identified the T172-phosphorylation of CDK4 as the step determining its activity, retinoblastoma protein (RB) inactivation, cell cycle commitment and sensitivity to CDK4/6i. Poorly differentiated (PDTC) and anaplastic (ATC) thyroid carcinomas, the latter considered one of the most lethal human malignancies, represent major clinical challenges. Several molecular evidence suggest that CDK4/6i could be considered for treating these advanced thyroid cancers. |