Chemoradiotherapy for untreated Masaoka-Koga stage IVB thymic carcinoma: a single-center retrospective study.

BACKGROUND: Thymic carcinoma (TC) is a rare type of a malignant tumor. The optimal treatment for Masaoka-Koga stage IVB TC patients is controversial due to the rarity of the disease. Chemotherapy is still the preferred option, but the outcomes are unsatisfactory. Whether radiotherapy combined with chemotherapy could improve prognosis remains unclear. METHODS: Untreated stage IVB TC patients who have received first-line chemotherapy were included in the present study. The patients who have undergone surgery were excluded. The primary outcomes were objective response rate (ORR) and progression-free survival (PFS). RESULTS: Sixty-seven patients were included in the study. A total of 31 patients received chemoradiotherapy (ChemoRT cohort), and the remaining 36 patients only received chemotherapy (Chemo cohort). The median follow-up period was 40.3 months. The ORR for the ChemoRT and Chemo cohorts was 61.3 and 27.8%, respectively (P = 0.006). Furthermore, PFS (P = 0.003) and OS (P = 0.046) were significantly superior in the ChemoRT cohort. Radiotherapy maintained a significant favorable effect on PFS in multivariate analysis (P = 0.014), but the effect on OS was insignificant (P = 0.249). There was no advantage in PFS (P = 0.302) in the ChemoRT cohort in patients who received < 4 cycles of chemotherapy. In contrast, radiotherapy significantly improved PFS (P = 0.005) in patients who received ≥ 4 cycles of chemotherapy. CONCLUSIONS: Chemoradiotherapy used as the first-line treatment improved ORR and PFS in Masaoka-Koga stage IVB TC patients. Patients receiving more cycles of chemotherapy may have a better chance to benefit from chemoradiotherapy.

[Value of serum miR-21-3p in predicting acute kidney injury in children with sepsis].

OBJECTIVE: To study the value of serum miR-21-3p combined with serum creatinine (Scr), cystatin C (Cys-C), and kidney injury molecule-1 (KIM-1) in predicting acute kidney injury (AKI) in children with sepsis. METHODS: A total of 142 children who were diagnosed with sepsis from January 2016 to March 2019 were enrolled. According to the presence or absence of AKI, they were divided into AKI group with 49 children and non-AKI group with 93 children. The serum levels of miR-21-3p, Scr, Cys-C, and KIM-1 were measured for the two groups. The receiver operating characteristic (ROC) curve was plotted to analyze the value of serum miR-21-3p, Scr, Cys-C, and KIM-1 in predicting AKI. A Pearson correlation analysis was used to evaluate the correlation of serum miR-21-3p with Scr, Cys-C, and KIM-1. RESULTS: The AKI group had significantly higher serum levels of miR-21-3p, Scr, Cys-C, and KIM-1 than the non-AKI group (P<0.05). The ROC curve analysis showed that the combination of serum miR-21-3p, Scr, Cys-C, and KIM-1 had an area under the ROC curve (AUC) of 0.962 (95%CI: 0.906-0.998), which was significantly larger than the AUC of each index alone (P<0.05), with a sensitivity of 97.0% and a specificity of 91.4%. The correlation analysis showed that the serum level of miR-21-3p was positively correlated with Scr, Cys-C, and KIM-1 in the AKI group (r=0.704, 0.812, and 0.863 respectively, P<0.01). CONCLUSIONS: There is a significant increase in the serum level of miR-21-3p in children with sepsis and AKI, and its combination with Scr, Cys-C, and KIM-1 has a high value in predicting AKI.

Definitive local therapy for extracranial single-organ oligorecurrent non-small-cell lung cancer: A single institutional retrospective study.

Oligometastatic non-small-cell lung cancer (NSCLC) is potentially curable. Oligo-recurrence occurs with oligometastatic disease characterized by well-controlled primary lesion. The purpose of the present study was to explore the value of definitive local therapy (DLT) for extracranial single-organ oligorecurrent NSCLC. A total of 81 patients with NSCLC who had extracranial single-organ oligorecurrence after receiving radical treatment at the Cancer Hospital of the University of Chinese Academy of Sciences from January 2010 to December 2017 were analyzed. The primary endpoint was progression-free survival (PFS), and the secondary endpoint was overall survival (OS). The median follow-up time of the 81 patients was 65.8 months. A total of 39 patients received DLT. A large proportion of patients who did not accept DLTs received specific tyrosine kinase inhibitors (TKIs). The results of multivariate analysis showed that DLT and specific TKI therapy were favorable prognostic factors significantly related to PFS. Further analysis showed that for patients without specific TKI therapy, DLT significantly improved PFS and the 5-year PFS rate. The 5-year OS rate also improved, but the improvement was not significant. For extracranial single-organ oligorecurrent NSCLC, PFS was significantly superior in patients receiving DLT. Among them, for the subgroup of patients who did not receive specific TKI therapy, DLT is expected to improve long-term prognostic outcomes.

CircRNA circ-IQGAP1 Knockdown Alleviates Interleukin-1ß-Induced Osteoarthritis Progression via Targeting miR-671-5p/TCF4.

OBJECTIVE: To explore the function of circular RNA IQ motif-containing GTPase-activating protein 1 (circ-IQGAP1) in interleukin (IL)-1ß-induced osteoarthritis (OA) model and to explore whether circ-IQGAP1 can modulate microRNA-671-5p (miR-671-5p) and transcription factor 4 (TCF4) to regulate chondrocyte apoptosis, inflammatory injury, and extracellular matrix degradation. METHODS: The cartilage tissues were collected from 32 OA patients or normal subjects. Human chondrocyte CHON-001 cells were challenged via different doses of IL-1ß for 24 hours. CHON-001 cells were transfected with circ-IQGAP1 overexpression vector, TCF4 overexpression vector, small interfering RNA (siRNA) for circ-IQGAP1, miR-671-5p mimic, miR-671-5p inhibitor or corresponding negative controls. Circ-IQGAP1, miR-671-5p and TCF4 abundances in cartilage tissues or CHON-001 cells were examined via quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell viability was investigated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT). Cell apoptosis was measured by flow cytometry. The inflammatory injury was analyzed by the secretion levels of inflammatory cytokines (IL-6, IL-8 and tumor necrosis factor-α [TNF-α]) by enzyme-linked immunosorbent assay (ELISA). The extracellular matrix degradation was evaluated by expression of aggrecan and matrix metalloproteinase 13 (MMP13) via western blot. The target relationship of miR-671-5p and circ-IQGAP1 or TCF4 was analyzed via dual-luciferase reporter and RNA immunoprecipitation (RIP) analyses. RESULTS: Circ-IQGAP1 abundance was enhanced in the cartilage tissues from OA patients compared with normal subjects (n = 32), and its expression was increased in CHON-001 cells after treatment of IL-1ß in a dose-dependent pattern. MiR-671-5p expression was decreased in the cartilage tissues from OA patients (n = 32) and IL-1ß-challenged CHON-001 cells. MiR-671-5p expression was negatively associated with circ-IQGAP1 level in OA patients. Circ-IQGAP1 silence mitigated IL-1ß-caused chondrocyte viability reduction, apoptosis promotion, secretion of inflammatory cytokine (IL-6, IL-8 and TNF-α), and extracellular matrix degradation (reduction of aggrecan and increase of MMP13). MiR-671-5p was targeted and inhibited via circ-IQGAP1. MiR-671-5p knockdown attenuated the influence of circ-IQGAP1 interference on IL-1ß-caused chondrocyte apoptosis, inflammatory injury, and extracellular matrix degradation. TCF4 was targeted via miR-671-5p, and TCF4 expression was increased in the cartilage tissues from OA patients (n = 32) and IL-1ß-challenged CHON-001 cells. TCF4 abundance in OA patients was negatively correlated with miR-671-5p expression. MiR-671-5p overexpression alleviated IL-1ß-mediated chondrocyte apoptosis, inflammatory injury, and extracellular matrix degradation via decreasing TCF4 expression. Circ-IQGAP1 silence reduced TCF4 expression via regulating miR-671-5p in IL-1ß-challenged CHON-001 cells. CONCLUSION: Circ-IQGAP1 knockdown attenuated IL-1ß-caused chondrocyte apoptosis, inflammatory injury, and extracellular matrix degradation. Circ-IQGAP1 could regulate miR-671-5p/TCF4 axis to modulate IL-1ß-caused chondrocyte damage. Circ-IQGAP1 might act as a new target for the treatment of OA.