Background: p73 is a member of the p53 family of tumor suppressors. Transactivating isoforms of p73 (TAp73) have p53-like, anti-proliferative and pro-apoptotic activities that are crucial for an efficient chemotherapy response. However, in contrast to p53, which is commonly inactivated in human cancer by point mutations, the TP73 gene is almost never mutated. Instead, the tumor suppressor activity of TAp73 is inhibited through a variety of mechanisms including epigenetic silencing and complex formation with inhibitory proteins. All these mechanisms have in common that they are in principle reversible and therefore amenable to therapeutic intervention. The use of 2 promoters at the N-terminus allows the expression of an isoform containing (TAp73) or not containing (ΔNp73) a complete N terminal transactivation domain, with the latter isoform capable of a dominant negative effect over the former.Aim: Was to investigate the pattern of expression of the 2 isoforms, TAp73 and ÄNp73 in normal lymphoid tissue (normal peripheral blood lymphocytes or reactive lymphoid hyperplasia) and malignant lymphoid neoplasm (acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), B-or T-non Hodgkin lymphomas (NHL)), to detect if there is significant difference in the expression levels between normal and malignant lymphoid tissue.Subjects and Methods: This study involved enrolment of 115 individuals who were classified in to 29 B-NHL patients, 25 T-NHL patients, 16 ALL patients, 18 CLL Patients and 22 Patients with reactive lymphoid hyperplasia. Expression of TAp73 and ΔNp73 was determined by RT-PCR. Results: On comparing the TAp73 expression between the studied disease group we found a significantly higher level of expression in ALL compared to its level in B and T-NHL (p=0.001 and 0.014 respectively) and in CLL compared to its level in B and T-NHL (p=0.000). There was no significant difference between B-NHL and T-NHL cases (p=0.821) and ALL and CLL cases (p=0.113). In comparing the ∆Np73 expression in between studied disease group we found a significantly higher level of expression in ALL compared to t its level in B and T-NHL (p=0.000) and in CLL compared to t its level in B-and T-NHL (p=0.000). There was no significant difference between B-NHL and T-NHL cases (p=0.060) and both ALL and CLL cases (p=0.428). Conclusion: we have demonstrated that TAp73 and ∆Np73 were highly expressed in malignant lymphoid hyperplasia in comparison to normal peripheral blood lymphocytes and nodal reactive lymphoid hyperplasia, especially in ALL and CLL cases while on the other hand the expression of these isoforms were variable in B-NHL and T-NHL patients and this may be due to deletions of 1p36 where p73 gene is localized . High expression levels have been found for ∆Np73, compared toTAp73 in the studied group of malignant lymphoid hyperplasia, indicating an oncogenic role for this isoform. In addition, our finding suggests that increased ∆Np73/TAp73 expression ratio not either isoform alone could play an important role in tumorigenesis. It might occur simultaneously with p53 mutations in lymphomas.