**3. Conclusions**

Endometriosis, even when in essence it is not a mortal disease, is a major health problem in general due to the disability it causes in young and fertile women, in full reproductive stage.

Genetic factors play a predominant role in approximately one-third of chronic disorders in adulthood; so, it is logical to think that endometriosis in turn presents a genetic etiology. Genetic diseases in general can be chromosomal, monogenic, or multifactorial. Currently, epigenetics attempts to explain genetic and environmental interactions and studies changes in gene expression mediated by mechanisms other than the sequence changes of their nucleotides. These epigenetic changes include DNA methylation, histone modification, and interfering RNA. Epigenetic alterations are associated with inflammation and persistence of the lesions. The results of research on the role of these changes in endometriosis are very valuable in the design of future therapeutic strategies.

Currently, epigenetic studies based on FISH technology and comparative genomic hybridization have shown important chromosomal alterations, especially in chromosomes 1, 16, 17, and 22, and it is believed with greater certainty that they are the loci involved in the persistence and progression of chromosomes. Endometriosis cells.

It is in these locations where there has been an instability of DNA information through mechanisms of deletions, translocations, which have led on the one hand to the loss of important genomic information (loss of heterogizity) in endometrial diploid cells, fundamental alterations in the self-regulation, and apoptosis of these aberrant endometrial cells, by mutations as occurs with the P53 gene. These alterations not only occur in the endometriosis cell but are capable of being transmitted to other cells either in an autosomal manner when replicated, or through shared information through a microenvironment mediated by exosomes.

For the researchers, the process of analyzing cultured cells that reproduce the epigenetic changes of an endometriosis cell in vivo has been a feat, but the results of the investigation of the role of these changes in endometriosis have been very valuable and will be useful in the design of future therapeutic strategies (**Figures 1–3**).

**17**

**Conflict of interest**

*Summary of alterations in endometriosis.*

**Appendices and nomenclature**

tating the mobility of heterogeneous groups of cells.

cal properties, behavior, and products of behavior.

this article.

**Figure 3.**

**Figure 2.**

*Clonal aberrations detected by FISH.*

*The Role of the Molecular Genetic Approach in the Pathogenesis of Endometriosis*

I certify that I do not have an actual or potential conflict of interest in relation to

**Exosomes**: are cell-derived vesicles that are present in many and perhaps all eukaryotic fluids, including blood, urine, and cultured medium of cell cultures. **Cadherin**: is a group of cellular adhesive (membrane glycoprotein) that keeps cells tightly bound in time, favoring the organization of tissues and organs, facili-

**Phenotype**: A phenotype is the composite of an organism's observable characteristics or traits, such as its morphology, development, biochemical or physiologi-

*DOI: http://dx.doi.org/10.5772/intechopen.81598*

*The Role of the Molecular Genetic Approach in the Pathogenesis of Endometriosis DOI: http://dx.doi.org/10.5772/intechopen.81598*

**Figure 2.** *Clonal aberrations detected by FISH.*

**Figure 3.**

*Molecular Bases of Endometriosis - The Integration Between Research and Clinical Practice*

Endometriosis, even when in essence it is not a mortal disease, is a major health problem in general due to the disability it causes in young and fertile women, in full

Genetic factors play a predominant role in approximately one-third of chronic disorders in adulthood; so, it is logical to think that endometriosis in turn presents a genetic etiology. Genetic diseases in general can be chromosomal, monogenic, or multifactorial. Currently, epigenetics attempts to explain genetic and environmental interactions and studies changes in gene expression mediated by mechanisms other than the sequence changes of their nucleotides. These epigenetic changes include DNA methylation, histone modification, and interfering RNA. Epigenetic alterations are associated with inflammation and persistence of the lesions. The results of research on the role of these changes in endometriosis are very valuable in

Currently, epigenetic studies based on FISH technology and comparative genomic hybridization have shown important chromosomal alterations, especially in chromosomes 1, 16, 17, and 22, and it is believed with greater certainty that they are the loci involved in the persistence and progression of chromosomes. Endometriosis cells. It is in these locations where there has been an instability of DNA information through mechanisms of deletions, translocations, which have led on the one hand to the loss of important genomic information (loss of heterogizity) in endometrial diploid cells, fundamental alterations in the self-regulation, and apoptosis of these aberrant endometrial cells, by mutations as occurs with the P53 gene. These alterations not only occur in the endometriosis cell but are capable of being transmitted to other cells either in an autosomal manner when replicated, or through shared

For the researchers, the process of analyzing cultured cells that reproduce the epigenetic changes of an endometriosis cell in vivo has been a feat, but the results of the investigation of the role of these changes in endometriosis have been very valuable and will be useful in the design of future therapeutic strategies (**Figures 1–3**).

**3. Conclusions**

reproductive stage.

the design of future therapeutic strategies.

**16**

**Figure 1.**

*Exosomes containing ectonucleotidase could contribute to progression of endometriosis.*

information through a microenvironment mediated by exosomes.

*Summary of alterations in endometriosis.*

## **Conflict of interest**

I certify that I do not have an actual or potential conflict of interest in relation to this article.
