<abstract xmlns="http://www.w3.org/1999/xhtml">

<p>According to scientific data, cancer is a very ancient disease, and along with the perfection of humanity it becomes more progressive. The development of technologies that detect molecular changes in the pathogenesis and subsequent development of carcinogenesis has led to the beginning of a new era in oncology. The cell cycle is tightly controlled by a group of protein kinases, including cyclin and cyclin-dependent kinases. These events occur in a strictly regulated time sequence supported by consistent restriction points. p53, p21, p16, retinoblastoma (and other proteins), cyclins and cyclin-related kinases repair DNA before the cell cycle enters the phase of synthesis and mitosis. Loss of regulatory activity of p53 and pRB, stable activation of E2F stimulates uncontrolled cell proliferation, leading to neoplastic cell growth. The Ras/Raf/MEK/ERK signalling pathway is also a complex network of sequentially activated proteins that play a major role in the onset and development of cancer. It can regulate not only the biological functions, such as cell proliferation, cycle regulation, cell differentiation, apoptosis and tissue formation, but it is also associated with tumor development. Stable mutations in the genome or defects in the epigenome lead to dysregulation in the normal biological cycle of the cell, underlying DNA chain damage or dysfunction in the control system, determined by various types of carcinogenic factors, both known and unknown.</p>
</abstract>

According to scientific data, cancer is a very ancient disease, and along with the perfection of humanity it becomes more progressive. The development of technologies that detect molecular changes in the pathogenesis and subsequent development of carcinogenesis has led to the beginning of a new era in oncology. The cell cycle is tightly controlled by a group of protein kinases, including cyclin and cyclin-dependent kinases. These events occur in a strictly regulated time sequence supported by consistent restriction points. p53, p21, p16, retinoblastoma (and other proteins), cyclins and cyclin-related kinases repair DNA before the cell cycle enters the phase of synthesis and mitosis. Loss of regulatory activity of p53 and pRB, stable activation of E2F stimulates uncontrolled cell proliferation, leading to neoplastic cell growth. The Ras/Raf/MEK/ERK signalling pathway is also a complex network of sequentially activated proteins that play a major role in the onset and development of cancer. It can regulate not only the biological functions, such as cell proliferation, cycle regulation, cell differentiation, apoptosis and tissue formation, but it is also associated with tumor development. Stable mutations in the genome or defects in the epigenome lead to dysregulation in the normal biological cycle of the cell, underlying DNA chain damage or dysfunction in the control system, determined by various types of carcinogenic factors, both known and unknown.

Cancer - dysregulation of the cell cycle and transduction of cascade signals

Romanian Journal of Rhinology

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

{"article-title":"Cancer - dysregulation of the cell cycle and transduction of cascade signals"}

According to scientific data, cancer is a very ancient disease, and along with the perfection of humanity it becomes more progressive. The development of...

Cancer - dysregulation of the cell cycle and transduction of cascade signals

Publié en ligne: 31 juil. 2021

Pages: 90 - 100

Reçu: 16 avr. 2021

Accepté: 20 mai 2021

DOI: https://doi.org/10.2478/rjr-2021-0017

Mots clés
carcinogenesis, gene mutation, cell cycle, cyclin, p53, signal transduction

© 2021 Akhmad Madaminov et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Cancer - dysregulation of the cell cycle and transduction of cascade signals

Publié en ligne: 31 juil. 2021

Pages: 90 - 100

Reçu: 16 avr. 2021

Accepté: 20 mai 2021

DOI: https://doi.org/10.2478/rjr-2021-0017

Mots cléscarcinogenesis, gene mutation, cell cycle, cyclin, p53, signal transduction

© 2021 Akhmad Madaminov et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Mots clés
carcinogenesis, gene mutation, cell cycle, cyclin, p53, signal transduction