@article {GONZ{\'A}LEZ-RODILLA4191, author = {IRENE GONZ{\'A}LEZ-RODILLA and VIRGINIA VERNA and ANA-BEL{\'E}N MU{\~N}OZ and JOS{\'E} EST{\'E}VEZ and MERCEDES BOIX and JOS{\'E} SCHNEIDER}, title = {Expression of the Apoptosis-related Genes Bcl-2 and p53 in Clinical Samples from Endometrial Carcinoma Patients}, volume = {31}, number = {12}, pages = {4191--4193}, year = {2011}, publisher = {International Institute of Anticancer Research}, abstract = {Background: Although alterations in the mechanisms of apoptosis are an integral part of the tumor phenotype, their precise role in endometrial carcinoma is still obscure. The aim was to determine whether Bcl-2 plays a similar biological role in endometrial cancer as in breast cancer, endometrial cancer being also a hormone-dependent tumor. Materials and Methods: The expression of the apoptosis-related Bcl-2 and p53 genes, together with Ki67, E-cadherin, c-erb-B2 and estrogen and progesterone receptors were studied in 136 formalin-fixed, paraffin-embedded endometrial carcinoma samples by means of immunohistochemistry. Results: Bcl-2 expression correlated directly and significantly with E-cadherin (r=0.22, p=0.011) estrogen receptor (r=0.18, p=0.04) and progesterone receptor expression (r=0.30, p=0.0006), and inversely with surgical stage (r=-0.20, p=0.024). Mutant p53 expression was directly and significantly associated with increasing patient age (r=0.25, p=0.007), tumor grade (r=0.37, p\<0.001), Ki67 (r=0.47, p\<0.0001), c-erb-B2 expression (r=0.21, p=0.012) and with E-cadherin expression (r=0.19, p=0.026). Conclusion: Bcl-2 and p53 are independently and significantly co-expressed with E-cadherin in endometrial carcinoma. Furthermore, the expression of Bcl-2 is also significantly associated with the expression of both progesterone and estrogen receptors, in that order, suggesting that, analogously to breast cancer, apoptosis is hormonally regulated to some degree also in endometrial cancer.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/31/12/4191}, eprint = {https://ar.iiarjournals.org/content/31/12/4191.full.pdf}, journal = {Anticancer Research} }