Mechanisms of receptor tyrosine kinase activation in cancer

 

Re-written summaries by: Anuva Gajjar

Date Published: 12/10/2022

Original research links:

https://pubmed.ncbi.nlm.nih.gov/29455648/

Introduction:

The study "Mechanisms of receptor tyrosine kinase activation in cancer" by Du and Lovly aims to review and understand the various mechanisms by which receptor tyrosine kinases (RTKs) are activated in cancer. RTKs are a family of transmembrane proteins that are involved in cell growth, survival, and differentiation. Aberrant activation of RTKs is a common feature of cancer and is often associated with poor prognosis. The authors aim to review the current literature on the mechanisms of RTK activation in cancer and to understand the implications of these mechanisms for cancer therapy. RTKs play a crucial role in cell signaling, and their dysregulation is often associated with cancer development. The over-activation of these receptors results in uncontrolled cell proliferation, survival, and migration, which are hallmarks of cancer cells. The authors aim to investigate the different mechanisms by which RTKs are activated in cancer, and the implications of these mechanisms in cancer therapy.

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Methods:

The authors conducted a literature review of studies on the mechanisms of RTK activation in cancer. They searched for relevant articles in multiple databases such as Pubmed, Scopus, and Web of Science and analyzed the studies for their methods, results, and conclusions. They also analyzed the studies for the specific RTKs studied, the mechanisms of activation, and the implications for cancer therapy. They used various keywords such as "RTKs", "Receptor tyrosine kinases", "Cancer" and "Activation mechanisms" to search the literature. They also analyzed the studies for the specific RTKs studied, the mechanisms of activation, and the implications for cancer therapy.

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Results:

The authors found that there are several mechanisms by which RTKs can be activated in cancer, including mutations, gene amplifications, and overexpression of RTK ligands. They found that mutations in the coding regions of RTKs can lead to their over-activation, and this is often associated with poor prognosis in cancer patients. Gene amplification, on the other hand, leads to an increase in the copy number of RTKs, which also results in their over-activation. Overexpression of RTK ligands, such as growth factors, can also lead to the over-activation of RTKs. They also found that RTK activation can be caused by aberrant signaling through downstream signaling pathways, such as the RAS/RAF/MEK/ERK pathway. This can happen when mutations in these downstream signaling pathways lead to their over-activation, which in turn leads to the over-activation of RTKs. The study also found that RTK activation can lead to the development of resistance to targeted therapies and can be associated with poor prognosis in cancer patients.

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Conclusion:

The study concludes that there are several mechanisms by which RTKs can be activated in cancer and that these mechanisms have important implications for cancer therapy. The authors suggest that a better understanding of the mechanisms of RTK activation in cancer is necessary for the development of more effective targeted therapies. They also suggest that the identification of RTK activation mechanisms can be used as a biomarker for the identification of patients who are most likely to respond to targeted therapies.

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