Dear Colleagues,

The ability of cancer cells to maintain their continuous proliferation may be the most fundamental characteristic of these cells. To maintain the homeostasis of the cell population and consequently preserve the architecture and function of normal tissue, cancer cells carefully regulate growth-promoting signals that directly enter and advance through the cell growth and division cycle. By disabling these signals, cancer cells take control of their fate. Growth factors that bind to cell-surface receptors, which often include intracellular tyrosine kinase domains, constitute a major component of enabling signals. Growth factors that connect to cell-surface receptors, which typically include intracellular tyrosine kinase domains, transmit enabling signals in a significant part. The latter then proceed to emit signals via branched intracellular signaling pathways that frequently control progression via the cell cycle and cell growth; these signals also affect additional biological characteristics of the cell, such as cell survival and energy metabolism.

The growth factor signals affecting cell quantity and position within tissues are temporally and spatially regulated, which is one of several reasons why these mechanisms are difficult to understand. There are several different ways that cancer cells can obtain the ability to maintain proliferative signaling. They may create growth factor ligands on their own, which stimulate autocrine proliferative responses. Alternately, normal cells in the stroma that surround and support tumors may send signals to the cancer cells to stimulate them, and the cancer cells may respond by supplying normal cells with growth factors. Receptor signaling can also be deregulated by increasing the levels of receptor proteins displayed at the surface of the cancer cells, making such cells hyperresponsive to otherwise limited amounts of growth factor ligand; the same outcome can result from structural changes in the stroma.

This Special Issue on tumorigenesis and cell proliferation aims to bring academia together to address challenges and provide solutions for the development of tumorigenesis and to explore novel aspects of tumor progression. This Special Issue will investigate these new dimensions by providing comprehensive coverage of cutting-edge emergent concerns. Original research and review articles are welcome.

Prof. Dr. Xiaodong Zhang
Guest Editor

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• tumorigenesis
• cell proliferation
• protein modificatiion including protein ubiquitination and protein phosphorylation