Cell Cycle Dysregulation in Breast Cancer

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Therapeutic potential of Cell Cycle Kinases in Breast Cancer

Abstract

Cancer, a condition characterized by abnormal cell growth, is closely linked to the cell cycle. In reaction to mitogenic cues, all malignancies comprise an aberrant buildup of tumor tissues that are promoted toward uncontrollable cell multiplication and growth. Genetic or epigenetic alterations in cell cycle-regulating genes as well as other genes that govern the cell cycle are examples of oncogenic stimuli. This shows that cancer is caused by many, different paths of genetic changes. Oncogenes (such as CDKs and cyclins and CDKs) and tumor suppressor genes (such as CDK inhibitors) produce proteins that control cell cycle mechanism and stimulate or repress progression of cell cycle, respectively. The discovery of CDKs and cyclins aids in the explanation and comprehension of cell cycle system molecular pathways. Cyclins A, B, C, D1, and E, as well as CDKs and CDK-inhibitor molecules p21, p16, p53, and p27, are believed to have important functions in cell cycle management throughout breast cancer development and are strictly controlled in normal breast epithelium cells. These proteins are dysregulated in response to mitogenic stimulation, promoting neoplastic conversion of mammary epithelial cells. This chapter’s objective is to describe the functions of tumor-suppressive and oncogenic cell cycle elements in breast carcinoma growth and prognosis.

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Mir, M.A., Khan, S.U., Aisha, S. (2023). Cell Cycle Dysregulation in Breast Cancer. In: Mir, M. (eds) Therapeutic potential of Cell Cycle Kinases in Breast Cancer. Springer, Singapore. https://doi.org/10.1007/978-981-19-8911-7_5

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