000153135 001__ 153135
000153135 005__ 20251017144642.0
000153135 0247_ $$2doi$$a10.3390/cancers17050760
000153135 0248_ $$2sideral$$a143563
000153135 037__ $$aART-2025-143563
000153135 041__ $$aeng
000153135 100__ $$0(orcid)0000-0002-1275-2600$$aSantander Ballestín, Sonia$$uUniversidad de Zaragoza
000153135 245__ $$aAdvances in CDK4 and 6 inhibitors: transforming breast cancer treatment
000153135 260__ $$c2025
000153135 5060_ $$aAccess copy available to the general public$$fUnrestricted
000153135 5203_ $$aBackground and Objectives: Breast cancer is the most common malignant neoplasm worldwide and the most prevalent one among women. It represents the leading cause of cancer-related death among females. Cyclin-dependent kinase 4 and 6 inhibitors disrupt the cell cycle, inducing cellular senescence and, ultimately, apoptosis. Consequently, they have become a novel type of adjuvant therapy for the treatment of advanced or metastatic breast cancer characterised by positive hormone receptors and human epidermal growth factor receptor 2 (HER-2) negative. Methods: A systematic review was conducted, analysing the available literature on cyclin-dependent kinase 4 and 6 inhibitors published over the last five years. The aim was to evaluate the efficacy and safety of adding these drugs to the standard endocrine therapy for this pathology. Results: The combination of cyclin-dependent kinase 4 and 6 inhibitors with endocrine therapy was shown to improve progression-free survival, overall survival, and chemotherapy-free intervals in patients who received this combination therapy. Conclusions: The addition of CDK4/6 inhibitors to endocrine therapy in the treatment of advanced or metastatic breast cancer with positive hormone receptors and HER-2 negative significantly improved PFS, median survival, and chemotherapy-free intervals compared with the use of hormonal treatments alone or in combination with a placebo. Currently, CDK4/6 inhibitors are becoming established as a new standard treatment for this pathology, offering lower toxicity than chemotherapy. However, it is necessary to deeply investigate the mechanisms of treatment resistance and develop effective therapies to overcome them.
000153135 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttps://creativecommons.org/licenses/by/4.0/deed.es
000153135 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000153135 700__ $$aAbadía Labena, María
000153135 700__ $$0(orcid)0000-0003-2153-0417$$aAvedillo-Salas, Ana$$uUniversidad de Zaragoza
000153135 700__ $$aMarco Continente, Cristina
000153135 700__ $$aArribas Blázquez, Marina
000153135 700__ $$0(orcid)0000-0003-4071-1467$$aLuesma Bartolomé, María José$$uUniversidad de Zaragoza
000153135 7102_ $$11003$$2027$$aUniversidad de Zaragoza$$bDpto. Anatom.Histolog.Humanas$$cArea Anatom.Embriol.Humana
000153135 7102_ $$11012$$2315$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Farmacología
000153135 773__ $$g17, 5 (2025), 760 [20 pp.]$$pCancers$$tCancers$$x2072-6694
000153135 8564_ $$s831630$$uhttps://zaguan.unizar.es/record/153135/files/texto_completo.pdf$$yVersión publicada
000153135 8564_ $$s2588718$$uhttps://zaguan.unizar.es/record/153135/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000153135 909CO $$ooai:zaguan.unizar.es:153135$$particulos$$pdriver
000153135 951__ $$a2025-10-17-14:32:39
000153135 980__ $$aARTICLE