**2. The mechanism for malignant transformation of endometriosis**

The exact mechanisms of malignant transformation of endometriosis are not fully established. It is proposed that chronic inflammation and immune dysregulation are the main factors related to the malignant transformation of endometriosis due to most probably iron-triggered oxidative stress leading to genetic alteration [6]. It is reported that endometriotic cysts have more concentration of iron than non-endometrioid counterparts, because of periodic hemorrhage into the cyst with the accumulation of free iron. Moreover, genomic alteration also is a resultant of hyperoestrogenic state associated with endometriosis, leading to inactivation of tumor suppressor genes like p53, PTEN, ARID 1A, and activation of KRAS and p13 oncogenic pathways, thus favoring the development of hormone-dependent malignant diseases like Type-I epithelial ovarian cancer and breast cancers [7]. Some authors have also established an association of endometriosis with ovarian cancer,

*Endometriosis and Cancer DOI: http://dx.doi.org/10.5772/intechopen.102393*

**Figure 2.** *Probable pathway for transformation of endometriosis to cancer.*

breast cancer (BC), cutaneous melanoma, and non-Hodgkin's lymphoma [1, 8]. It is presumed that endometriosis-associated, and endometriosis independent neoplasms may develop from different molecular pathways with distinct genetic alteration with significant clinical and prognostic implications. The estrogen-dependent pathogenesis of ovarian endometrioid carcinomas associated with endometriosis is corroborated also by the increased incidence of synchronous primary endometrial (Type I, estrogen-dependent) and ovarian, endometriosis-associated, endometrioid adenocarcinomas (**Figure 2**).
