**Introduction**

**Chapter 1**

**Provisional chapter**

**Introductory Chapter: Genes Expression in the Control**

**Introductory Chapter: Genes Expression in the Control** 

The human body is made of up to trillions of cells. Those cells respond to three characteristics: the differentiation into up to 200 different cellular types which acquire specific functions, the cooperation between those cells using various signaling pathways to sustain the body's physiological unity, and the genetic programming of cell death (the apoptosis). The programmed cell death goes hand in hand with the sustainability of life highlighted at the cell level by the "immortality" of cancer cells, the permanent renewal process of certain tissues such as those

The cancer is a genomic disease in which the early stage is represented by activation of oncogene and inactivation of suppressor genes, which result in transformed cells that grow out of cell cycle control. Two families of genes, the oncogenes and antioncogenes (also called tumor suppressor genes), cause and accelerate the carcinogenesis process when their structure or the regulation of their expression is altered. These genes are equivalent in cancer etiology but differ themselves by their functions and by the mechanisms of their activation. The expression of oncogenes and antioncogenes, respectively, controls in a positive and negative way the cell

Among the oncogenes, HER2 is involved in the early stages of carcinogenesis. HER2 is located on chromosome 17 [2] and codes for a transmembrane tyrosine kinase receptor that belongs to a family of four members: human epidermal growth factor receptor (HER) [3]. HER is activated after the binding of its ligand which allows the phosphorylation of tyrosine residues in the intracellular domain of the receptor. This activation leads to signaling pathways promoting cell proliferation, survival, migration, adhesion, angiogenesis, or differentiation

of the intestine and blood, as well as the sustainability of the species.

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

distribution, and reproduction in any medium, provided the original work is properly cited.

DOI: 10.5772/intechopen.81917

**of Cell Cycle and Their Potential Value in Cancer**

**of Cell Cycle and Their Potential Value in Cancer** 

**Prognosis**

**Prognosis**

Guy Joseph Lemamy

Guy Joseph Lemamy

**1. Introduction**

cycle progression [1] (**Figure 1**).

Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.81917
