Expression analysis of BCL-2 in endometrial hyperplasia and carcinoma : The powers and limitations

I read the arthicle by Krishna Kumar et al. which examined BCL-2 expression in normal endometrium, endometrial hyperplasia and endometrial adenocarcinoma(1). They found that BCL-2 expression in the endometrium of patients with endometrial hyperplasia was significantly higher than the normal endometrial tissue. A notable decrease in BCL-2 levels was also observed in endometrioid adenocarcinoma when compared to endometrial hyperplasia. Based on these results, authors suggested that alternative mechanisms other than failure of apoptosis, may be implicated in endometrial carcinogenesis. These findings are important because BCL-2 expression plays an important role in maintaining a favorable antiapoptotic microenvironment which influences tumor progression. Moreover, it is vastly upregulated in most of the cancers, allowing cancer cells don't stop growing and dividing. For these reasons, BCL-2 has been a hot topic in cancer research including endometrioid adenocarcinoma and several studies about this issue have been published recently. Unfortunately, various papers have reported conflicting results. For instance, some investigators have observed increased expression of BCL-2 in the endometrial carcinoma, particularly in low-grade endometrioid types, while others have found its reduced expression in people with this carcinomas(2). Addressing the root causes of these conflicts are complex because myriad different molecules involved in apoptosis regulation and BCL-2 make up only a small fraction among them. In fact, BCL-2 is a member of a large family of proteins which consists of various anti-apoptotic members (such as BCL-2 or BCL-xL) and pro-apoptotic members( like BAX and BAK). They exhibit specific pattern of activation, localisation and response to signalling molecules. All of these can influence multiple cell fate choices with the outcomes of cell death or survival.