The biology and treatment of Epstein-Barr virus-positive diffuse large B cell lymphoma, NOS.

EBV positive Diffuse Large B-cell lymphoma, not otherwise specified (EBV+DLBCL-NOS) referred to DLBCL with expression of EBV encoded RNA in tumor nucleus. EBV+DLBCL-NOS patients present with more advanced clinical stages and frequent extranodal involvement. Although rituximab-containing immunochemotherapy regimens can significantly improve outcomes in patients with EBV+DLBCL, the best first-line treatment needs to be further explored. Due to the relatively low incidence and regional variation of EBV+DLBCL-NOS, knowledge about this particular subtype of lymphoma remains limited. Some signaling pathways was abnormally activated in EBV+DLBCL-NOS, including NF-κB and JAK/STAT pathways) and other signal transduction pathways. In addition, immune processes such as interferon response, antigen-presenting system and immune checkpoint molecule abnormalities were also observed. Currently, chimeric antigen receptor T-cell (CAR-T) therapy, chemotherapy combined with immunotherapy and novel targeted therapeutic drugs are expected to improve the prognosis of EBV+DLBCL-NOS patients, but more studies are needed to confirm this.

Radiotherapy with continued EGFR-TKIs for oligoprogressive disease in EGFR-mutated non-small cell lung cancer: A real-world study.

BACKGROUND: Epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) develops resistance to tyrosine kinase inhibitors (TKIs). Here, we evaluated the efficacy of radiotherapy and continuation of TKIs in patients with advanced NSCLC with oligoprogression after EGFR-TKIs. METHODS: From January 2011 to January 2019, 33 patients with EGFR-mutated NSCLC on TKIs were treated by radiotherapy and continuation of TKIs for oligoprogressive disease. The primary endpoints were median progression-free survival 1 (mPFS1), mPFS2, and median overall survival (mOS). PFS1 was measured from the start of EGFR-TKIs therapy to the oligoprogression of the disease. PFS2 was measured from the date of oligoprogression to the further progression of the disease, while OS was calculated from oligoprogression to death from any cause or was censored at the last follow-up date. RESULT: The mPFS1, mPFS2, and mOS were 11.0 (95% CI, 4.4-17.6), 6.5 (95% CI, 1.4-11.6) and 21.8 (95% CI, 14.8-28.8) months, respectively. Univariate analysis showed that EGFR mutation type (p = 0.024), radiotherapy method (p = 0.001), and performance status (p = 0.017) were significantly correlated with PFS2. Univariate analysis showed that sex (p = 0.038), smoking history (p = 0.031), EGFR mutation type (p = 0.012), and radiotherapy method (p = 0.009) were significantly correlated with OS. Multivariate analysis suggested that radiotherapy method (p = 0.001) and performance status (p = 0.048) were prognostic factors for PFS2, and radiotherapy method (p = 0.040) was a prognostic factor for OS. CONCLUSION: Radiotherapy with continued TKIs is effective for EGFR-mutated NSCLC with oligoprogression, and it should be conducted as soon as possible. T790M+ patients have higher sensitivity to radiotherapy, and patients with good performance status and stereotactic body radiation therapy have better PFS2 and OS.

[Research Progress of Immunotherapy for Non-small Cell Lung Cancer 
with Drive Gene Mutation].

Lung cancer is the most lethal malignancy around the world and non-small cell lung cancer (NSCLC) accounts for 80% of all cases. Most of the NSCLC patients has "driver gene mutations" and targeted therapy achieved a relatively good efficacy, but some patients progressed or relapsed after treatment. Previous studies demonstrated that immune checkpoint inhibitor could improve the prognosis of advanced-stage NSCLC and prolong the survival time. However, the efficacy of immune therapy varies in NSCLC patients with different immune and molecular features. The efficacy of immune therapy was controversial in NSCLC patients with driver gene mutation. The present review will summarize the immune characteristics of NSCLC patients with driver mutation and the directions of immunotherapy for patients with driver mutation.
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