Cell cycle dysregulation is a hallmark of all cancers, resulting in uncontrolled proliferation. Cyclin dependent kinases (CDKs), a family of proteins that are involved in the regulation of …
A Fassl, Y Geng, P Sicinski - Science, 2022 - science.org
BACKGROUND Cyclins and cyclin-dependent kinases (CDKs) drive cell division. Of particular importance to the cancer field are D-cyclins, which activate CDK4 and CDK6. In …
GL Rampioni Vinciguerra, M Sonego, I Segatto… - Frontiers in …, 2022 - frontiersin.org
The cyclin D-CDK4/6 complexes play a pivotal role in controlling the cell cycle. Deregulation in cyclin D-CDK4/6 pathway has been described in many types of cancer and it invariably …
S Goel, MJ DeCristo, SS McAllister, JJ Zhao - Trends in cell biology, 2018 - cell.com
Pharmacologic inhibitors of cyclin-dependent kinases 4 and 6 (CDK4/6) have recently entered the therapeutic armamentarium of clinical oncologists, and show promising activity …
Breast Cancer (BC) is the second most common type of cancer worldwide and displays the highest cancer-related mortality among women worldwide. Targeted therapies have …
PJ Roberts, V Kumarasamy, AK Witkiewicz… - Molecular cancer …, 2020 - AACR
Abstract Cyclin-dependent kinases 4 and 6 (CDK4/6) have emerged as important therapeutic targets. Pharmacologic inhibitors of these kinases function to inhibit cell-cycle …
M Álvarez-Fernández, M Malumbres - Cancer cell, 2020 - cell.com
Inhibiting the cell-cycle kinases CDK4 and CDK6 results in significant therapeutic effect in patients with advanced hormone-positive breast cancer. The efficacy of this strategy is …
S Pernas, SM Tolaney, EP Winer… - … advances in medical …, 2018 - journals.sagepub.com
The cyclin D/cyclin-dependent kinases 4 and 6 (CDK4/6)–retinoblastoma protein (RB) pathway plays a key role in the proliferation of both normal breast epithelium and breast …
Control of the cell cycle through selective pharmacological inhibition of CDK4/6 has proven beneficial in the treatment of breast cancer. Extending this level of control to additional cell …