Breast cancer is the most frequently diagnosed cancer in women with a high incidence and mortality worldwide. Nearly 70% of breast carcinomas are steroid hormone receptors positive luminal carcinomas and the patients are treated with endocrine therapy. The treatment is principally targeted to block estrogen receptor or the synthesis of the ligand. Increase evidences also suggest that progesterone receptor may be a target for therapy. Deregulation of cell cycle is a hallmark of cancer and participates in breast tumorigenesis. Thus the use of CDK4/6 inhibitors has been recently approved in combination with endocrine therapy for the treatment of luminal carcinomas. There is an interaction between hormone receptors and cell cycle proteins that participates in the progression of breast cancer and may play a role in the mechanism of resistance to endocrine therapy. Steroid receptors are involved in the transcriptional regulation of the cyclins that control the G1 phase of the cell cycle. In addition, it has been reported that some cyclin/CDK complexes may activate the hormone receptors by phosphorylation of the receptor or their coactivators. This activation of the receptor may occur in a ligand independent manner, conferring the ability to bypass the endocrine treatment. On the other hand, the alteration of the expression or activity of cell cycle regulators may also be part of the mechanism of endocrine resistance by an uncontrolled cell proliferation.
The aim of this special issue is to explore the role of the signaling pathways of hormone receptors and cell cycle proteins in breast cancer and how their interplay could modulate the response to endocrine therapy and to cell cycle inhibitors treatment. This knowledge will provide tools to improve breast cancer therapies.
All article types are welcome.
Breast cancer is the most frequently diagnosed cancer in women with a high incidence and mortality worldwide. Nearly 70% of breast carcinomas are steroid hormone receptors positive luminal carcinomas and the patients are treated with endocrine therapy. The treatment is principally targeted to block estrogen receptor or the synthesis of the ligand. Increase evidences also suggest that progesterone receptor may be a target for therapy. Deregulation of cell cycle is a hallmark of cancer and participates in breast tumorigenesis. Thus the use of CDK4/6 inhibitors has been recently approved in combination with endocrine therapy for the treatment of luminal carcinomas. There is an interaction between hormone receptors and cell cycle proteins that participates in the progression of breast cancer and may play a role in the mechanism of resistance to endocrine therapy. Steroid receptors are involved in the transcriptional regulation of the cyclins that control the G1 phase of the cell cycle. In addition, it has been reported that some cyclin/CDK complexes may activate the hormone receptors by phosphorylation of the receptor or their coactivators. This activation of the receptor may occur in a ligand independent manner, conferring the ability to bypass the endocrine treatment. On the other hand, the alteration of the expression or activity of cell cycle regulators may also be part of the mechanism of endocrine resistance by an uncontrolled cell proliferation.
The aim of this special issue is to explore the role of the signaling pathways of hormone receptors and cell cycle proteins in breast cancer and how their interplay could modulate the response to endocrine therapy and to cell cycle inhibitors treatment. This knowledge will provide tools to improve breast cancer therapies.
All article types are welcome.
