Survivin is one of the inhibitors of apoptosis proteins (IAP) that might play an important role in the pathogenesis of diffuse large B cell lymphoma (DLBCL). The present study was designed to investigate the clinical and prognostic significance of survivin expression in nodal DLBCL. We analyzed lymph node biopsy specimens obtained from 56 patients with newly diagnosed nodal DLBCL, treated with immunochemotherapy (R-CHOP). The expression of survivin was analyzed using the standard immunohistochemical method on formalin-fixed and routinely processed paraffin-embedded lymph node specimens and evaluated semiquantitatively as a percentage of tumor cells. Survivin immunoexpression (>45 % positive tumor cells) was found in 22 (39.28 %) and observed as cytoplasmic staining in 15 patients, or mixed (cytoplasmic and nuclear) staining in 7 patients. A significant difference in survivin immunoexpression was noticed between the GCB and the non-GCB subtypes of DLBCL (p = 0.031). However, survivin immunoexpression had no significant association with IPI, “bulky” disease, extranodal localization, hemoglobin, Ki-67 immunoexpression or other clinicopathological parameters. A univariate analysis showed that survivin positivity was an unfavorable factor for therapy response and a predictor of shorter survival in patients with DLBCL (p = 0.048 and p = 0.034, respectively). Patients with survivin overexpression experienced a relapse more often than patients without expression of this apoptotic protein (27.3 vs. 11.8 %), but this difference did not reach statistical significance (p = 0.131). The results of this study showed that disregulation of survivin expression had an important role in the determination of the course of the disease in patients with nodal DLBCL treated with R-CHOP. Therefore, survivin represents a potential target for therapeutic intervention in DLBCL.
An unusual case of acute myeloblastic leukemia (AML) with indolent clinical course and spontaneous remission in the terminal phase is described. A 63-year-old male has been diagnosed to suffer from AML, subtype M2. Chromosomal analysis showed 46,XY,del(6)(q21). Clinical course was slowly progressive ("smoldering" AML). The patient did not require cytoreductive drugs, and occasional supportive therapy was his only treatment. Five years from diagnosis patient exhibited spontaneous remission of the disease, accompanied with disappearance of del(6q) clone. Six months after, relapse occured and patient died from CNS bleeding. Additional curiosity in this case is the fact that patient's older brother died of acute lymphoblastic leukemia at the age of 71 years. Possible mechanisms of spontaneous remission of AML and genetic predisposition for human leukemia are discussed with a review of the literature.
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