Recognizing the connection of apoptotic factors in signaling pathways with diffuse large b cell lymphoma

Background: The cell has developed mechanisms for maintaining hemostasis in defense from unfavorable external and internal influences. Apoptosis with its internal and external signaling pathways is one of those mechanisms. Failure of these mechanisms results in diseases of which the most serious are malignant diseases. Oncogenes which suppress apoptosis are bcl-2 and bclx1and c-myc, as opposed to bax, bad and bid which enhance apoptosis and which are encountered in lymphoma and which are incorporated into external and internal signaling pathway of apoptosis. Aim: disclosure of connections between apoptotic factors in signaling pathways in diffuse large B cell lymphoma DLBCL in relation to achieving first complete remission (CR1). Material and methods: Study was retrospective-prospective. 60 patients were analyzed with de novo DLBCL. Median was 47 months (3-91 months). Patients were divided into the following groups: germinal center B-cell like (GCB), not germinal center B-cell like (non GCB), CR1 and a group of unwanted occurrences (progressive disease, relapse and death). Groups are put in correlation to expressions CD10, CD138 i MUM1, bcl6, bcl2, bclxl, bad, bax, bid and Ki67. Results: Positive correlation was confirmed for bad and bax in the overall sample, GCB group and CR1 group p< 0.0001. Bad that was included into external signaling had positive correlation with bcl6 p=0.006 and CD 10 p=0.03 in overall , GCB and CR 1 group. Negative correlation was confirmed for bclx1 and bid in non GCB group p=0.022. Positive correlation was found for MUM1 and bcl2 p=0.004 and negative correlation CD10 with MUM1 p<0.0001 and bcl2 p=0.048 in non GCB group. Statistics: Spearman's analysis was used, p<0.05 was considered significant Conclusion: We confirmed significant correlation for CD10, bcl6, bad and bax in GCB group. There was significantly negative correlation for bid and bclxl, together with revealing of insufficient inhibition of bid towards bclxl in both external and internal signaling pathway in non GCB group.