ABSTRACT
INTRODUCTION: The inflammatory and immune cells have an important impact on Hodgkin lymphoma (HL). The derived neutrophil-lymphocyte ratio (dNLR) has been confirmed to have a similar prognostic value as the neutrophil-lymphocyte ratio (NLR) in many kinds of tumors, but it has not been explored as a prognostic marker for Hodgkin lymphoma patients. OBJECTIVE: The aim of the study is to evaluate the prognostic value of dNLR and NLR in HL. METHODS: This retrospective study included 213 newly diagnosed HL patients from 2008 to 2019. Then, the prognostic significance of dNLR and NLR in these patients was evaluated. Meanwhile, subgroup analyses based on the Ann Arbor stage and histotype were also carried out. Finally, propensity score matching was used to reduce selection bias. RESULTS: Patients with dNLR ≥ 2.1 showed shorter overall survival (OS) (P = 0.006). Also, patients with NLR ≥ 3.0 showed worse OS (P = 0.005) and progression-free survival (PFS) (P = 0.031). These results were also found in patients with early-stage and mixed cellularity subtype HL. Besides, high dNLR represented an independent prognostic marker for OS and high NLR remained an independent prognostic factor for OS and PFS on multivariable analysis. CONCLUSION: Elevated dNLR and NLR were related to worse survival in HL patients. For the first time, the dNLR has shown the potential to be a new prognostic factor for patients with HL.
ABSTRACT
Glioblastoma multiforme is the most common and aggressive form of primary malignant brain tumor. Previous evidence demonstrates that ß-adrenergic receptors (ß-ARs) are closely associated with the occurrence and development of brain tumors. However, the functional role of ß-ARs in human glioblastoma and the underlying mechanisms are not fully understood. In the present study, by using the MTT assay, western blotting, and the reverse transcription polymerase chain reaction, it was revealed that isoproterenol (ISO), an agonist of ß-ARs, promoted the proliferation of U251 cells but not U87-MG cells, and that this effect was blocked by the ß-ARs antagonist propranolol. It was also demonstrated that ISO transiently induced extracellular signal-related kinase 1/2 (ERK1/2) phosphorylation, and that blocking the mitogen-activated protein kinase pathway by U0126 inhibited ERK1/2 phosphorylation and suppressed U251 cell proliferation. In addition, ß-ARs activation increased the expression of matrix metalloproteinase (MMP) family members MMP-2 and MMP-9 mRNA through ERK1/2 activation. In conclusion, these data suggest that ß-ARs induce ERK1/2 phosphorylation, which may in turn increase MMPs expression to promote U251 cell proliferation. These results provide additional insight into the specific roles of ß-ARs in glioblastoma.
