CDK4 and CDK6 are cyclin-dependent kinases that control the transition between the G1 and S phases of the cell cycle. CDK4/6 activity is typically deregulated and overactive in cancer cells. There can be amplification or overexpression of the genes encoding cyclins or of the genes encoding the CDKs themselves. Additionally, loss of endogenous INK4 inhibitors, by gene deletion, mutation, or promoter hypermethylation, can also lead to overactivity of CDK4 and CDK6. 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. 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 these drugs with endocrine therapy alone. Besides abemaciclib demonstrated an important activity in endocrine-resistant patients thus determining a survival prolongation delaying the time to chemotherapy. These results had never been seen in these setting of patients. 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 breast cancer with special point of view in their future development in every setting.

ASTONE Antonio       Fondazione Policlinico Universitario A. Gemelli IRCCS,  Roma

BOTTICELLI Andrea   Ospedale Sant’Andrea Roma

BRIA Emilio                 Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma

D’AURIA GIULIANA    Ospedale Sandro Pertini, Roma

FABBRI Agnese          Ospedale Belcolle, Viterbo

FABI Alessandra         Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma

GAMUCCI Teresa       Ospedale Sandro Pertini, Roma

GENERALI Daniele     ASST di Cremona, Università di Trieste

MASETTI Riccardo     Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma

MINELLI Mauro          Azienda Ospedaliera San Giovanni Addolorata, Roma

ORLANDI Armando   Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma

PARIS Ida                   Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma

PIZZUTI Laura           Istituto Regina Elena, Roma

SCAMBIA Giovanni  Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma

VICI patrizia               Istituto Regina Elena, Roma

Vigneri Paolo            Policlinico “G. Rodolico – S. Marco, Catania

Sono stati assegnati nr 2 crediti ECM per le seguenti categorie: Medico Chirurgo (specializzazioni: anatomopatologi, ginecologi, oncologi, chirurgia generale, radioterapisti) e Infermieri.

PROVIDER

Università Cattolica del Sacro Cuore

Formazione Permanente ECM, convegni e manifestazioni

Accreditato dalla Commissione Nazionale ECM n° 2463

E-mail:  Daniele.Petricca@unicatt.it

Tel  +39 06 3015 4074

fax +39 06 3051 732

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