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BACKGROUND: Pulmonary sarcomatoid carcinoma (PSC), a rare subtype of non-small cell lung cancer (NSCLC), is poorly differentiated and highly aggressive. Treatment is limited, and the prognosis is poor. Pembrolizumab is an anti-programmed death (PD)-1 antibody with good efficacy in NSCLC. Recent studies have demonstrated that PD-ligand 1 (PD-L1) overexpression is common in PSCs, which suggests that anti-PD-L1 treatment is an ideal option. However, the response to pembrolizumab in PSC has not been studied. CASE SUMMARY: We present a PSC case with PD-L1 overexpression that significantly benefited from pembrolizumab. A 73-year-old Chinese male was detected with a right lung lesion. Pathological analysis of the right upper lobectomy confirmed PSC. The PD-L1 test revealed overexpression (TPS: 90%). Multiple metastases occurred 1 mo after surgery, representing stage IV PSC. Neither first-line chemotherapy nor second-line antiangiogenic agents showed any benefit. Radiotherapy (1200 cGy) was administered to relieve chest wall pain. The patient received the PD-1 inhibitor pembrolizumab (100 mg) as third-line therapy; however, because of fever and severe infection, he refused to receive immunotherapy any longer. Thus, only one dose of pembrolizumab was administered. Deep sustained remission of most of the metastases was achieved except for lesions in the right adrenal gland, which first shrank and then progressed. The patient died because of disease progression in the right adrenal gland. He achieved a progression-free survival time of 8 mo and an overall survival time of 9 mo with third-line pembrolizumab. CONCLUSION: Our findings highlight and offer direct evidence of the efficacy of pembrolizumab in PD-L1-overexpressing PSCs. Combined radiotherapy and immunotherapy may enhance treatment efficacy.

This article has been retracted, and the online PDF has been watermarked “RETRACTION”. The retraction notice is available at http://doi.org/10.3233/MGC-220954.

Background For treatment of advanced lung cancer, immune checkpoint inhibitors (ICIs) + chemotherapy or the combination of dual ICIs has become the standard first-line treatment in recent years. Considering the differences among patients’ immune systems, the response to ICIs may vary. Therefore, we aimed to evaluate the predictive implications of patient age and Eastern Cooperative Oncology Group (ECOG) performance status (PS) for the efficacy of ICIs for the treatment of lung cancer. Methods We searched the PubMed, Cochrane Library, Web of Science, and EMBASE databases for articles published between January 2010 and September 2020 that compared overall (OS) and progression-free survival (PFS) rates between patients with lung carcinoma who were administered ICIs and control treatments. Results Twenty-four trials including 15,584 patients were selected. ICIs significantly improved the OS rates in patients aged

Scutellarin plays an anti-tumor role in A549 lung cancer cells, but the underlying mechanism is unclear. In this study, scutellarin was used to treat A549 cells for 12, 24, and 48 h, followed by the addition of Tempo, a selective scavenger of mitochondrial reactive oxygen species (ROS) and SB431542, a transforming growth factor (TGF)-β1 receptor inhibitor. A dihydroethidium fluorescence probe was used to measure the intracellular ROS level, Cell Counting Kit-8 (CCK-8) was used to detect cell viability, and flow cytometry was performed to examine apoptosis. Western blots were used to detect the total protein level of TGF-β1, p-smad2, and cleaved caspase-3 in A549 cells. The results showed that scutellarin significantly inhibited cell viability and increased apoptosis. Scutellarin also promoted intracellular ROS production, TGF-β1/smad2 signaling pathway activation, and cleaved caspase-3 expression, which was partly reversed by Tempo. Moreover, scutellarin-induced intracellular ROS production and cleaved caspase-3 expression were inhibited by blocking the TGF-β1/smad2 pathway with SB431542. In conclusion, scutellarin promoted apoptosis and intracellular ROS accumulation, which could be abrogated by Tempo and SB431542 treatment in A549 cells. Our study indicated that scutellarin induced A549 cell apoptosis via the TGF-β1/smad2/ROS/caspase-3 pathway.

Renal cell cancer is a common malignant tumor of the urinary system. Ursolic acid (UA) serves an important antitumor role in certain types of cancer, such as lung cancer, breast cancer and hepatocellular carcinoma; however, to the best of our knowledge, the effect of UA on renal cancer has not yet been investigated. In the present study, A498 cells were treated with different concentrations of UA for 12, 24 and 48 h, and then MCC950, an inhibitor of the NLR family pyrin domain-containing 3 (NLRP3) receptor, was added to block NLRP3 signaling. The proliferation of A498 cells was analyzed using an MTS assay and invasiveness was analyzed using a Transwell assay. The expression levels of NLRP3, cleaved caspase-1, IL-1β and MMP-2 were detected using western blotting. The present results demonstrated that the invasiveness of A498 cells was significantly decreased following UA treatment (P

C21H16BrNO5, monoclinic, P21/c (no. 14), a = 10.146(5) Å, b = 8.188(4) Å, c = 22.204(4) Å, β = 90.720(9)°, V = 1844.4(12) Å3, Z = 4, R gt(F) = 0.051, wR ref(F 2) = 0.142, T = 296(2) K.

C26H27NO4, monoclinic, P21/c (no. 14), a = 12.034(4) Å, b = 15.247(5) Å, c = 12.991(4) Å, β = 115.379(6)°, V = 2153.6(12) Å3, Z = 4, R gt(F) = 0.0531, wR ref(F 2) = 0.1447, T = 296 K.

In this study, we attempted to solve two important challenges in systems biology. First, although the Michaelis–Menten (MM) model provides local kinetic information, it is hard to generalize MM models to model a large system because increasingly large amounts of experimental data are necessary for the parameter identification. In addition, it is not possible to develop an MM model that provides information about the strength of the interactions in the system. Second, although the dynamic simulation of various signal transduction pathways is important in cancer research, it is impossible to theoretically derive a mathematical model to describe the cancer molecular mechanism. Predictive computational approaches can be used to analyze the dynamics of a system and to determine the dysfunction of a regulatory process. In this report, we first propose a pseudo-dynamic pathway to describe protein interactions in an MM system. We then discuss the dynamic behavior of two large-scale systems (antigrowth-signal-induced cell cycle and apoptotic-signal-transduction mechanism). These two systems were constructed through the in-series and organic integration, respectively, of MM modules with Petri net modules; moreover, more than 30% additional reactions were added during this integration step. We then described an extremely large multi-stream system (growth signal transduction); however, the analysis of this system to obtain dynamic predictions is critical but appears impossible. Thus, we introduced a fuzzy concept that can be used to develop a physically realizable model prototype. In the future, through step-by-step in vivo modifications, researchers will be able to develop a complete model of cancer metabolism to achieve accurate predictions.

A new spectrophotometric method for the determination of zinc is proposed. The chromogenic agent Hydrazidazol forms a 1:1 chelate with zinc in the presence of Triton X-100 in a medium containing 20-40% ethanol. The molar absorptivity and conditional formation constant have been found to be 2.7 x 1O(4) l.mole(-1).cm(-1) (at 640 nm) and 10(5.32) respectively. Beer's law is obeyed for zinc over the range of 0.2-0.8 mug/ml with a standard deviation of 0.024 mug/ml. The method can be applied to the determination of zinc in cadmium metal and its oxide after preconcentration by selective extraction of zinc thiocyanate into ethyl acetate in the presence of EDTA and thiosulphate as masking agents.