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Cyclin-dependent kinases in breast cancer: expression pattern and therapeutic implications

Journal

MEDICAL ONCOLOGY
Volume 39, Issue 6, Pages -

Publisher

HUMANA PRESS INC
DOI: 10.1007/s12032-022-01731-x

Keywords

Cyclin-dependent kinases; Cyclins; Breast cancer; Cell cycle; CDK inhibitors; Prognosis

Categories

Funding

  1. Jammu Kashmir Science Technology and Innovation Council (JKST&IC), Department of Science and Technology, Govt of JK [JKSTIC/SRE/885-87]
  2. Almaarefa University Riyadh, Saudi Arabia [TUMA-2021-1]

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Breast cancer is one of the most common malignancies worldwide, and dysregulation of the cell cycle is an important factor in its development. Cyclin-dependent kinases (CDKs) play a crucial role in the progression and treatment of breast cancer.
Presently, breast cancer (BC) is one of the most common malignancies diagnosed and the leading cause of tumor-related deaths among women worldwide. Cell cycle dysregulation is one of the hallmarks of cancer, resulting in uncontrolled cell proliferation. Cyclin-dependent kinases (CDKs) are central to the cell cycle control system, and deregulation of these kinases leads to the development of malignancies, including breast cancer. CDKs and cyclins have been reported as crucial components involved in tumor cell proliferation and metastasis. Given the aggressive nature, tumor heterogeneity, and chemoresistance, there is an urgent need to explore novel targets and therapeutics to manage breast cancer effectively. Inhibitors targeting CDKs modulate the cell cycle, thus throwing light upon their therapeutic aspect where the progression of tumor cells could be inhibited. This article gives a comprehensive account of CDKs in breast cancer progression and metastasis and recent developments in the modulation of CDKs in treating malignancies. We have also explored the expression pattern and prognostic significance of CDKs in breast cancer patients. The article will also shed light on the Implications of CDK inhibition and TGF-beta signaling in breast cancer. [GRAPHICS] .

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