**7. Conclusion**

Critical contribution of cell cycle regulating kinases Cdk to carcinogenesis provides a promising target for diagnostic characterization of malignancies and development of novel therapeutic interventions. Numerous compounds directly inhibiting Cdk and, as a consequence, cell proliferation have been developed, and 9 of them are currently under clinical evaluation (phase I and II) as antitumor agents. Most of the candidates are pan-Cdk inhibitors affecting several Cdk family members with advantages in efficiency of tumor treatment due to not only inhibition of cell proliferation but also apoptosis induction. Only one inhibitor – pyrido[2,3-*d*]pyrimidine PD 0332991 – has been comprehensible described with preferential selectivity for Cdk4 and Cdk6 applicable for Rb positive tumors with primarily defects in Cdk4/ Cdk6 pathway. Application of Cdk inhibitors to patients with advanced cancers resulted in stabilization of disease. Combination with classical chemotherapeutic agents and adjustment of therapeutic schedules may also cause tumor regression and contribute to prevention of drug resistance. More detailed preclinical evaluation using suitable tumor models and focused clinical trials will give valuable implications for new mechanism-based approaches and Cdk drug developments as well as tumor specific treatment.
