Immune checkpoint inhibitors can cause immune-related toxicity in various systems, and myocarditis is the most serious life-threatening toxicity. This report introduces diagnosis and treatment of two cases which developed myocarditis after receiving PD-1 inhibitors therapy. The first case was a 77-yearold male with chordoma, who was treated by third-line sintilimab combined with anlotinib, and presented with symptoms of chest tightness, shortness of breath and upper eyelid ptosis three weeks later. He was diagnosed as immune-checkpoint-inhibitors-related myocarditis and myositis-myasthenia-gravis overlap syndrome based on his clinical symptoms, serum biomarkers, electrocardiogram, echocardiogram, and characteristic findings on cardiac 18F-FDG PET-MRI. Methylprednisolone was given 480 mg/d initially and was gradually reduced to 40 mg/d in 4 weeks, with the myocardial injury biomarkers declined in the same time. The second case was a 69-year-old female with advanced non-small cell lung cancer, who was treated by pemetrexed combined with bevacizumab and camrelizumab, and presented with palpitations 20 days later. She was diagnosed as immune-checkpoint-inhibitors-related myocarditis based on her clinical symptoms, serum biomarkers, electrocardiogram and echocardiogram. Methylprednisolone was given 240 mg/d initially and was gradually reduced to 40 mg/d with good response of myocardial injury biomarkers decline.However, the patient developed fatal myasthenia gravis afterwards, with little response to all treatments. These two cases revealed that, early detection and timely intervention, including discontinuation of immune checkpoint inhibitors and initiation of adequate steroid therapy, can reduce morbidity and mortality and improve prognosis.
Lung cancer is the leading cause of cancer-related mortality worldwide. Despite recent advances in treatment, lung cancer remains an incurable disease. Matrine, an active compound isolated from Sophora flavescens, has been demonstrated to inhibit proliferation and induce apoptosis of tumor cells. However, the protective effects and molecular mechanisms of matrine in lung cancer remain elusive. In the present study, the lung cancer cells H1299 and A549 were used to investigate how matrine affects the proliferation, migration and apoptosis of lung cancer cells in vitro. It was demonstrated that matrine is able to significantly suppress the proliferation and colony formation of lung cancer cells in vitro. Using cell apoptosis analysis, wound-healing and Transwell assays, it was demonstrated that matrine induced cellular apoptosis and inhibited the migration of lung cancer cells. Further experiments revealed that matrine significantly suppressed the phosphorylation of protein kinase B (Akt) and glycogen synthase kinase-3β (GSK-3β). The present results suggested that matrine inhibits lung cancer cell proliferation, and induces cell apoptosis by suppressing the Akt/GSK-3β signaling pathway, which demonstrated that matrine may have therapeutic potential for lung cancer.
Background Acute fibrinous and organizing pneumonia (AFOP) is a very rare form of acute or subacute lung injury, which is characterized by patches of “fibrin balls” distributed within the alveoli. Given the lack of typical clinical manifestations, AFOP is often misdiagnosed as pneumonia, tuberculosis, etc. Definitive diagnosis is obtained from a lung biopsy. Corticosteroids are usually effective. Case presentation We report two cases of patients with histopathological manifestations of AFOP, which were significantly improved after corticosteroid therapy. Previous reports of the clinical and pathological characteristics of AFOP were reviewed to improve clinicians’ understanding of this disease. Conclusions Early identification and diagnosis are very important for AFOP treatment. The prognosis is acceptable after timely and effective treatment.
Background Disappointing clinical efficacy of standard treatment has been proven in refractory metastatic osteosarcoma, and the emerging anti-angiogenic regimens are still in the infantile stage. Thus, there is an urgent need to develop novel therapeutic approach for osteosarcoma lung metastasis. Methods circFIRRE was selected from RNA-sequencing of 4 matched osteosarcoma and adjacent samples. The expression of circFIRRE was verified in clinical osteosarcoma samples and cell lines via quantitative real-time polymerase chain reaction (RT-qPCR). The effect of circFIRRE was investigated in cell lines in vitro models, ex vivo models and in vivo xenograft tumor models, including proliferation, invasion, migration, metastasis and angiogenesis. Signaling regulatory mechanism was evaluated by RT-qPCR, Western blot, RNA pull-down and dual-luciferase reporter assays. Results In this article, a novel circular RNA, circFIRRE (hsa_circ_0001944) was screened out and identified from RNA-sequencing, and was upregulated in both osteosarcoma cell lines and tissues. Clinically, aberrantly upregulated circFIRRE portended higher metastatic risk and worse prognosis in osteosarcoma patients. Functionally, in vitro, ex vivo and in vivo experiments demonstrated that circFIRRE could drive primary osteosarcoma progression and lung metastasis by inducing both tumor cells and blood vessels, we call as “tumorigenic-angiogenic coupling”. Mechanistically, upregulated circFIRRE was induced by transcription factor YY1, and partially boosted the mRNA and protein level of LUZP1 by sponging miR-486-3p and miR-1225-5p. Conclusions We identified circFIRRE as a master regulator in the tumorigenesis and angiogenesis of osteosarcoma, which could be purposed as a novel prognostic biomarker and therapeutic target for refractory osteosarcoma.
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