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Comprehensive advances in HER2-positive and HER2-negative breast cancer: unveiling molecular mechanisms and exploring cutting-edge targeted therapies for enhanced patient outcomes | Naunyn-Schmiedeberg's Archives of Pharmacology
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The human epidermal growth factor receptor (HER2), part of the tyrosine kinase family, serves as a key therapeutic target for patients with breast cancer, particularly those with HER2 overexpression. HER2 is overexpressed or amplified in approximately 15–20% of breast cancers. It includes HER1, HER2, HER3, and HER4, which progress the growth of cancerous cells. Key signaling pathways involved in HER2-driven breast cancer progression include the MAPK and mTOR pathways, which activate a cascade of factors that promote DNA synthesis and cell growth. A crucial process in HER2 cancer development is HER2 dimerization, which forms a functional oncogenic unit and is followed crucially by HER2:HER3 heterodimerization that leads to downstream signaling pathways. Alterations in the HER2 in solid tumors and ERBB2 gene mutations have led to advancements and implantation of precision-targeted approaches, as well as to combat the issues from the traditional approaches of targeting. In this review, we have thoroughly discussed different HER2-targeting therapies, which include monoclonal antibodies, antibody–drug conjugates, tyrosine kinase inhibitors, poly (ADP-ribose) polymerase inhibitors, CDK4/6 inhibitors, molecular probes targeting by PET/CT imaging, cancer vaccines, and cell therapies like CART-T and CAR-M cell therapy. Some of these targeted therapies have shown effectiveness in managing HER2-positive breast cancer and promoting tumor regression, while some remain under investigation for their potential benefits. Graphical abstract Representation of the different targeted therapies in HER2-positive and negative breast cancer, spotlighting the lesions in overexpressed HER2 receptor. Different new and emerging targeting therapies for targeting HER2 receptor is highlighted, and all these therapies have been found very useful in combating the uncontrolled cell growth.
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- Chiodo C et al (2021) The other side of the coin: may androgens have a role in breast cancer risk?
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headline:Comprehensive advances in HER2-positive and HER2-negative breast cancer: unveiling molecular mechanisms and exploring cutting-edge targeted therapies for enhanced patient outcomes
description:The human epidermal growth factor receptor (HER2), part of the tyrosine kinase family, serves as a key therapeutic target for patients with breast cancer, particularly those with HER2 overexpression. HER2 is overexpressed or amplified in approximately 15–20% of breast cancers. It includes HER1, HER2, HER3, and HER4, which progress the growth of cancerous cells. Key signaling pathways involved in HER2-driven breast cancer progression include the MAPK and mTOR pathways, which activate a cascade of factors that promote DNA synthesis and cell growth. A crucial process in HER2 cancer development is HER2 dimerization, which forms a functional oncogenic unit and is followed crucially by HER2:HER3 heterodimerization that leads to downstream signaling pathways. Alterations in the HER2 in solid tumors and ERBB2 gene mutations have led to advancements and implantation of precision-targeted approaches, as well as to combat the issues from the traditional approaches of targeting. In this review, we have thoroughly discussed different HER2-targeting therapies, which include monoclonal antibodies, antibody–drug conjugates, tyrosine kinase inhibitors, poly (ADP-ribose) polymerase inhibitors, CDK4/6 inhibitors, molecular probes targeting by PET/CT imaging, cancer vaccines, and cell therapies like CART-T and CAR-M cell therapy. Some of these targeted therapies have shown effectiveness in managing HER2-positive breast cancer and promoting tumor regression, while some remain under investigation for their potential benefits. Representation of the different targeted therapies in HER2-positive and negative breast cancer, spotlighting the lesions in overexpressed HER2 receptor. Different new and emerging targeting therapies for targeting HER2 receptor is highlighted, and all these therapies have been found very useful in combating the uncontrolled cell growth.
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description:The human epidermal growth factor receptor (HER2), part of the tyrosine kinase family, serves as a key therapeutic target for patients with breast cancer, particularly those with HER2 overexpression. HER2 is overexpressed or amplified in approximately 15–20% of breast cancers. It includes HER1, HER2, HER3, and HER4, which progress the growth of cancerous cells. Key signaling pathways involved in HER2-driven breast cancer progression include the MAPK and mTOR pathways, which activate a cascade of factors that promote DNA synthesis and cell growth. A crucial process in HER2 cancer development is HER2 dimerization, which forms a functional oncogenic unit and is followed crucially by HER2:HER3 heterodimerization that leads to downstream signaling pathways. Alterations in the HER2 in solid tumors and ERBB2 gene mutations have led to advancements and implantation of precision-targeted approaches, as well as to combat the issues from the traditional approaches of targeting. In this review, we have thoroughly discussed different HER2-targeting therapies, which include monoclonal antibodies, antibody–drug conjugates, tyrosine kinase inhibitors, poly (ADP-ribose) polymerase inhibitors, CDK4/6 inhibitors, molecular probes targeting by PET/CT imaging, cancer vaccines, and cell therapies like CART-T and CAR-M cell therapy. Some of these targeted therapies have shown effectiveness in managing HER2-positive breast cancer and promoting tumor regression, while some remain under investigation for their potential benefits. Representation of the different targeted therapies in HER2-positive and negative breast cancer, spotlighting the lesions in overexpressed HER2 receptor. Different new and emerging targeting therapies for targeting HER2 receptor is highlighted, and all these therapies have been found very useful in combating the uncontrolled cell growth.
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