proteins causes a disposal of drugs specially designed to target these proteins as therapeutic options. The retinoblastoma (Rb) protein, a tumor suppressor, regulates RNA transcription during the G1 cell growth phase to stop the proliferation of malignant cells [6]. Cyclin D1 proteins bind to cyclin-dependent kinase (CDK) enzymes 4 and 6 thereby inhibiting the regulatory function of the Rb protein. The National Comprehensive Cancer Network (NCCN) recognized CDK 4/6 inhibitors are palbociclib, abemaciclib and ribociclib in combination with aromatase inhibitors. Combination therapy provides treatment for HR positive/HER2 negative advanced or metastatic breast cancer by lowering estrogen levels to inhibit cell growth and cyclin-dependent kinase to block malignant cell division and proliferation [7; 8]. Abemaciclib and ribociclib showed a relative reduction in the risk of death of 25-30% [9]. By combining an aromatase inhibitor with palbociclib, progression free survival (PFS) is increased by 10 months, compared with hormone monotherapy [10]. Likewise, adding palbociclib to fulvestrant resulted in a double increase in PFS compared to those taking fulvestrant alone [11]. There is currently limited evidence to support the use of CDK 4/6 inhibitors as monotherapy. Increased data on the safety and tolerability of CDK 4/6 inhibitors in patients may help clinicians in the selection of initial therapy for patients with HR positive/HER2 negative breast cancer [12]. Platinum-based anticancer drugs such as _cis_platin, carboplatin and oxaliplatin have been widely employed in the treatment of several types of cancer, such as lung, colorectal, ovarian and breast cancers [13]. However, the efficacy and, therefore, the use of such platinum-based drugs have decreased due to the high risk of serious toxicity, such as neurotoxicity [14; 15]. Major advances have recently been made in drug delivery systems, due to miniaturization technologies that have improved the performance of existing drugs to provide new, more effective therapies [16]. The use of biomolecules such as peptides, nucleic acids and others reduced the amount of drug required by improving its targeted action [17]. The reduction in size at the nanometer level (<100 nm) has led to dramatic improvements in the way drugs are delivered [18]. All particles <100 nm in size could be formed via nanocrystals, drug-polymer complexation or using nanoscale shells that could trap drugs [19]. The fine size of nanoparticles or metal complexes allows for a loading of small molecules, peptides, proteins and nucleic acids that escape immunological detection unlike larger particles, which are easily excluded from the body. Recently, innovative research has developed towards metal-based anticancer drugs, such as gold derivatives, with the aim of improving the effectiveness, expanding the activity field and, above all, reducing the general toxicity [20; 21]. The pharmacological activity of gold compounds has been tested since ancient times; these compounds have been used in a series of treatments, including that for the rheumatoid arthritis and as an antibacterial and antitumor. Different studies have shown that gold derivatives act differently from platinum anticancer drugs, since their primary target is the proteasome; in this regards future approaches will bring to the development gold complexes selective for specific cancer cells and tumor targets in order to increase their effectiveness and better control of undesired side effects [22; 23]. The purpose of this review is to summarize the state of the art of the antitumor activity of gold compounds, complexes and nanoconjugates, providing a brief overview of their use against breast cancer. In particular, the following aspects will be treated:  
1. Drug delivery systems;
2. Gold nanosystems;
3. Gold complexes. The antiproliferative activity of these systems has been studied in several human breast cancer cell lines.