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EGFR-TKI resistance poses a significant challenge in the treatment landscape of non-small cell lung cancer (NSCLC), prompting extensive research into mechanisms and therapeutic strategies. In this study, we conduct a bibliometric analysis to elucidate evolving research hotspots and trends in EGFR-TKI resistance, offering insights for clinical interventions and scientific inquiries. Publications spanning from 1996 to 2024, focusing on EGFR-TKI resistance in NSCLC, were sourced from the Web of Science Core Collection. Utilizing VOSviewer 1.6.19, CiteSpace 6.2. R2, and Scimago Graphica 1.0.35, we analyzed these articles to identify countries/regions and institutions, Journals, publications, key contributors, collaborations, and emerging topics. An analysis of 8051 articles by 38,215 researchers from 86 countries shows growing interest in EGFR-TKI resistance mechanisms. Since 1996, publications have steadily increased, surpassing 500 per year after 2016, with a sharp rise in citations. Research articles make up 84% of publications, emphasizing scholarly focus. Global collaboration, especially among researchers in China, the US, and Japan, is strong. Leading institutions like Dana-Farber and Harvard, along with journals such as \"Lung Cancer\", are key in sharing findings. Professors Yi-Long Wu and William Pao are prominent contributors. Keyword analysis reveals core themes, including first-generation EGFR-TKIs, emerging agents like osimertinib, and research on the T790M mutation. EGFR-TKI resistance remains a critical issue in NSCLC treatment, driving ongoing research efforts worldwide. Focusing future research on clear identification of resistance mechanisms will guide post-resistance treatment strategies, necessitating further exploration, alongside the validation of emerging drugs through clinical trials. Moreover, \"chemo+\" treatments following EGFR-TKI resistance require more clinical data and real-world evidence for assessing safety and patient outcomes. As research advances, a multidisciplinary approach will be key to overcoming these challenges. Continued innovation in treatment could greatly enhance patient survival and quality of life.

Background Neutrophil‐to‐lymphocyte ratio (NLR) and platelet‐to‐lymphocyte ratio (PLR) are closely related to the prognosis of patients with non‐small cell lung cancer, but their effect on extensive‐stage small cell lung cancer (ES‐SCLC) remains uncertain. Methods This retrospective study was conducted in ES‐SCLC patients treated with first‐line atezolizumab or durvalumab and platinum‐etoposide. Clinical data from three hospitals were analyzed. Significant risk factors for survival were identified using descriptive statistics and Cox regression. Homogeneity was assessed using t‐tests or nonparametric tests. Kaplan‐Meier analysis revealed an association between high NLR level and median PFS and OS. Results A total of 300 ES‐SCLC patients were included in the study. Cox regression analysis revealed that an elevated NLR level after the second treatment cycle (defined as NLRT2) was an independent prognostic factor for survival. Stratifying patients based on median NLRT2 showed significant differences in both PFS (HR: 1.863, 95% CI: 1.62–2.12, p < 0.001) and OS (HR: 2.581, 95% CI: 2.19–3.04, p < 0.001) between NLR ≥ 1.75 and NLR < 1.75 groups. mPFS and mOS were 8.2 versus 6.1 months and 13.7 versus 9.5 months, respectively. NLR was also associated with treatment efficacy and occurrence of irAEs. Further stratification based on NLR and irAEs showed that in the NLR < 1.75 group, patients with irAEs had prolonged mPFS and mOS. In the NLR ≥ 1.75 group, only mPFS showed a significant difference between patients with and without irAEs. Conclusion NLRT2 and irAEs can predict the prognosis of ES‐SCLC patients with first‐line ES‐SCLC receiving PD‐L1 inhibitors combined with chemotherapy. NLRT2 (NLR level after the second treatment cycle) and (immune‐related adverse events) irAEs can predict the prognosis of ES‐SCLC patients with first‐line ES‐SCLC receiving PD‐L1 inhibitors combined with chemotherapy.

Recurrent fusions of receptor tyrosine kinases (RTKs) are often driving events in tumorigenesis that carry important diagnostic value and are potentially targetable by the increasing number of tyrosine kinase inhibitors (TKIs). Here, we characterized the spectrum of 1324 RTK fusions with intact kinase domains in solid tumors by DNA-based high-throughput sequencing. Overall, the prevalence of RTK fusions were 4.7%, with variable frequencies and diverse genomic structures and fusion partners across cancer types. Cancer types, such as thyroid cancers, urological cancers and neuroendocrine tumors are selective in the RTK fusions they carry, while others exhibit highly complex spectra of fusion events. Notably, most RTKs were promiscuous in terms of the partner genes they recombine with. A large proportion of RTK fusions had one of the breakpoints localized to intergenic regions. Comprehensive genomic profiling revealed differences in co-mutational patterns pre- and post-TKI treatments across various RTK fusions. At baseline, multiple cases were detected with co-occurring RTK fusions or concomitant oncogenic mutations in driver genes, such as KRAS and EGFR . Following TKI resistance, we observed differences in potential on- and off-target resistance mutations among fusion variants. For example, the EML4 - ALK v3 variant displayed more complex on-target resistance mechanisms, which might explain the reduced survival outcome compared with the v1 variant. Finally, we identified two lung cancer patients with MET + and NTRK1 + tumors, respectively, who responded well to crizotinib treatment. Taken together, our findings demonstrate the diagnostic and prognostic values of screening for RTK fusions using DNA-based sequencing in solid tumors.

Treatment of advanced non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutation with EGFR-tyrosine kinase inhibitors (EGFR-TKIs) can achieve good disease control, but it will inevitably produce drug resistance. About 3%-10% of the resistance mechanism is small cell transformation. Two cases of stage IV lung adenocarcinoma with EGFR mutation were reported and the disease was controlled after EGFR-TKIs treatment. In case 1, progression-free survival (PFS) before small cell carcinoma transformation was 16 months, and in case 2, PFS before small cell carcinoma transformation was 24 months. Subsequent biopsy after disease progression indicated a shift to small cell lung cancer. Case 1 PFS after small cell carcinoma transformation was 6 months, and case 2 PFS after small cell carcinoma transformation was 8 months, and overall survival (OS) was 36 months, which significantly prolonged the patient's survival. At the same time, the literature of such drug resistance mutations wa

COVID-19 is an infectious pneumonia caused by 2019-nCoV. The number of newly confirmed cases and confirmed deaths continues to remain at a high level. RT–PCR is the gold standard for the COVID-19 diagnosis, but the computed tomography (CT) imaging technique is an important auxiliary diagnostic tool. In this paper, a deep learning network mutex attention network (MA-Net) is proposed for COVID-19 auxiliary diagnosis on CT images. Using positive and negative samples as mutex inputs, the proposed network combines mutex attention block (MAB) and fusion attention block (FAB) for the diagnosis of COVID-19. MAB uses the distance between mutex inputs as a weight to make features more distinguishable for preferable diagnostic results. FAB acts to fuse features to obtain more representative features. Particularly, an adaptive weight multiloss function is proposed for better effect. The accuracy, specificity and sensitivity were reported to be as high as 98.17%, 97.25% and 98.79% on the COVID-19 dataset-A provided by the Affiliated Medical College of Qingdao University, respectively. State-of-the-art results have also been achieved on three other public COVID-19 datasets. The results show that compared with other methods, the proposed network can provide effective auxiliary information for the diagnosis of COVID-19 on CT images.

Objective. To study the effects of camrelizumab accompanied by first-line chemotherapy on serum SCC, VEGF levels, and adverse reactions in people undergoing advanced lung squamous cell carcinoma. Methods. Data sources of the study subjects were 60 people suffering from advanced squamous cell carcinoma of the lung hospitalized from January 2018 to October 2019. They were assigned to two groups, including the control group and the observation group in a random manner, and each consisted of 30 patients. Those in the observation group received camrelizumab (SHR-1210), and gemcitabine plus cisplatin (GP) chemotherapy were treated in the control group. Finally, according to the results, we compare the data of patients in both groups so as to find out the similarities and differences. Results. Among them, the effective efficiency of clinical treatment in the control group reached 36.67%, and that in the observation group reached 56.67%. Intuitively, it can be concluded that the control group showed lower results than the observed group. The observed group turned out to have higher periodic survival and progression free survival (PFS) of patients than the other group. During and after the cycle treatment, the data of SCC and VEGF were reduced to some extent, but the control group appeared to have a more evident reduction rate than the other group. Conclusion. SHR-1210 combined with chemotherapy has a considerable effect in practical application and has excellent clinical performance.

The functionally graded composite structures with viscoelastic polymers inherits the excellent performance of functionally graded composites and also possesses large damping performance, which has broad application prospects in the aerospace and mechanical engineering fields. However, due to the complexity of the structure itself, there is limited literature available on its theoretical modeling for efficient solutions. To predict its dynamic performance, a simplified dynamic model of the functionally graded composite structures with viscoelastic polymers is established. This model takes into account the displacement transfer relationship between the functional graded composite layer and the viscoelastic polymer layer. The governing differential equations are obtained by applying the Navier method and complex modulus theory. These equations are then solved using the Rayleigh–Ritz method. The validity of the theoretical model is confirmed by comparing it with existing literature and the results obtained from ANSYS software. Additionally, the model that has been developed is used to analyze how the graded index and elastic modulus of the structure, as well as its geometric parameters, affect its vibration and damping characteristics.

BNIP3 is reported to be involved in hypoxia-induced mitochondrial defect and cell death in cardiomyocytes. However, little is known about the specific function and molecular mechanism of BNIP3-mediated mitophagy in myocardial ischemia–reperfusion injury (MIRI). Herein, this study explored the mechanism regulating BNIP3-modulated mitophagy in MIRI. Rat cardiomyocytes (H9c2 cells) underwent transfection and hypoxia/reoxygenation (H/R) treatment, followed by cell viability and apoptosis detection. Gain-of-function assays were conducted in rats before MIRI modeling, followed by the monitoring of cardiac changes and the evaluation of cardiac function, myocardial infarction area, and apoptosis in myocardial tissues. The levels of creatine kinase MB (CK-MB), cardiac troponin I (cTnI), lactic dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), p62, and LC3 II/LC3 I were tested in rat serum or H9c2 cells. The co-localization of LC3 and TOMM20 was analyzed. The interaction of BNIP3 with YTHDF2 was assessed. H/R treatment decreased cell viability and p62 and SOD levels while elevating cell apoptosis, the levels of CK-MB, cTnI, LDH, MDA, ROS, and LC3 II/LC3 I, the number of autophagosomes, and the co-localization of LC3 and TOMM20 in cardiomyocytes, which were neutralized by downregulating BNIP3 or upregulating YTHDF2. Moreover, upregulation of YTHDF2 repressed myocardial injury and mitophagy in MIRI rats. Mechanistically, YTHDF2 mediated BNIP3 expression by recognizing methylated BNIP3. Upregulation of BNIP3 counteracted the suppressive effect of YTHDF2 overexpression on H/R-induced injury and mitophagy in cardiomyocytes. The RNA methylation reading protein YTHDF2 ameliorated MIRI by downregulating BNIP3 via m 6 A modification.

Light is one of the important environmental factors affecting the growth and development of facility vegetables. In this experiment, we investigated the effects of different light intensities on the growth, nutritional quality and flavonoid accumulation of celery under hydroponic and full LED light conditions. Four light intensities of 40, 100, 200, or 300 µmol·m -2 ·s -1 were set up in the experiment, and three harvest periods were set up on the basis of different light intensities, which were 15, 30, and 45 d after treatment (labeled as S1, S2, and S3, respectively). The results showed that the plant height and aboveground biomass of celery increased with the increase of light intensity, and the light intensity of 200 μmol·m -2 ·s -1 was beneficial to increase the contents of chlorophyll, carotenoids, total phenols, vitamin C, cellulose, total flavones and apigenin in celery. During the S1-S3 period, the activities of PAL, CHS, CHI and ANS increased gradually under 200 and 300 μmol·m -2 ·s -1 light intensity treatments, and the activities of FNS and CHS enzymes were the highest under 200 μmol·m -2 ·s -1 light intensity treatment. The expression and ANS activity of Ag3GT , a key gene for anthocyanin synthesis, reached the maximum value at 300 μmol·m -2 ·s -1 , and the expression level and FNS activity of AgFNS , a key gene for apigenin synthesis, reached a maximum value at 200 μmol·m -2 ·s -1 . In general, the anthocyanin content was the highest at 300 μmol·m -2 ·s -1 , and the apigenin content was the highest at 200 μmol·m -2 ·s -1 . In conclusion, light intensity of 200 µmol·m -2 ·s -1 treatment was more favorable for celery growth and nutrient synthesis.