Objective:To detect Bruton tyrosin kinase (BTK) expression in patients with mantle cell lymphoma (MCL) and analyze its correlation with clinical features and prognosis. Methods:A total of 32 cases of MCL tissues and 10 cases of benign lymph nodes were sampled and stained with immunohistochemical (IHC) staining. Clinical data of these patients were analyzed using SPSS 17.0. Results:BTK was positively expressed in MCL and normal lymphoid tissues and was more strongly expressed in MCL tissue than in normal lym-phoid tissue. Moreover, BTK expression level was correlated with Ki-67 and MIPI scores. Prognosis analysis showed that patients with high BTK expression exhibited shorter progression-free survival (PFS) than patients with low expression levels (P=0.030);however, no significant difference in overall survival (OS) was observed (P=0.073). Single-factor analysis of PFS showed that age≥65 years, ECOG score≥2, bone marrow involvement, strongly positive BTK expression, Ki-67>30%, and MIPI score≥6 are poor prognostic factors for patients with MCL. Only MIPI score≥6 is considered an independent poor prognostic factor in the multivariate analysis. Conclusion:BTK is strongly and positively expressed in patients with MCL, and its expression level is correlated with Ki-67 and MIPI scores. Patients with high-level BTK expression usually exhibit shorter PFS than those with low-level BTK expression;however, owing to short follow-up time and limited sample size, high-level BTK expression cannot be considered an independent poor prognostic factor for PFS.

Myc behaves as a central transcriptional factor, regulating cell proliferation, cell cycle progression, apoptosis, differentiation, metabolism and other functions. In diffuse large B cell lymphomas (DLBCL), Myc abnormality has been identified as an independent prognostic marker. Myc-associated DLBCL tends to have more aggressive phenotypes, lower sensitivity to standard chemotherapeutic regimens, and worse outcomes compared with other types of DLBCL. Myc per se has generally been deemed undruggable, and the pharmacological attempts to directly inhibit Myc have not borne fruits. However, with the understanding of biological functions of Myc, a series of small molecular inhibitors targeting Myc transcription and protein regulation have been developed. The potential antagonistic strategies for Myc mainly include interfering with its stability, decreasing its expression, and acting on the downstream target genes. This review discusses the therapeutic targets for Myc-related DLBCL, with an emphasis on their mechanisms and advances, in the hope to improve the outcomes of these patients.