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Multiple primary lung cancer (MPLC) refers to patients with two or more primary lesions of lung cancer. It can be divided into synchronous MPLC (sMPLC) and metachronous MPLC (mMPLC) based on the timing of occurrence. In recent years, the detection rate of MPLC has gradually increased. However, considerable controversy exists in distinguishing MPLC from intrapulmonary metastasis (IM), especially when the histopathological types are identical. Given the significant differences in treatment strategies and prognosis in clinical practice currently, accurate diagnosis of MPLC is crucial for personalized precision therapy. Molecular genetics and sequencing technologies offer effective strategies for assessing the clonal origin of tumors. There have been reports of coexisting mutations in the epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) fusion genes in non-small cell lung cancer, but case of EGFR mutation following an ALK mutation has not been mentioned. This article accurately diagnoses and retrospectively analyzes the clinical data of a case of ALK mutant adenocarcinoma in a male patient who developed an EGFR mutation with multiple metastases four years after surgery, and reviews the relevant literature. This paper aims to deepen the understanding of mMPLC and provide clinical references for the diagnosis and treatment of such patients. [ABSTRACT FROM AUTHOR]

Lung cancer is the most common malignant disease and the leading cause of cancer death in China. Non-small cell lung cancer (NSCLC) accounts for over 80% of all lung cancers, and the probability of NSCLC gene mutations is high, with a wide variety of types. With the development of next-generation sequencing (NGS) detection technology, more and more patients with rare fusion gene mutations are detected. Neuregulin 1 (NRG1) gene is a rare oncogenic driver that can lead to activation of human epidermal growth factor receptor 3 (Her3/ErbB3) mediated pathway, resulting in tumor formation. In this article, we reported a case of mixed NSCLC with CRISPLD2-NRG1 fusion detected by RNA-based NGS, who responsed to Afatinib well after 1 month of treatment, and magnetic resonance imaging (MRI) showed shrinkage of intracranial lesions. Meanwhile, we also compiled previously reported NSCLC patients with NRG1 rare gene fusion mutation, in order to provide effective references for clinical diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Lung cancer is still the leading cause of cancer death worldwide. Non-small cell lung cancer (NSCLC) is the main pathological type of lung cancer, accounting for about 80%. Approximately 30% of all patients with NSCLC have resectable early and middle stage disease at the time of diagnosis. Recently, the epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have made a major breakthrough in the adjuvant targeted therapy of EGFR-mutated resectable NSCLC, and are recommended by the guidelines for clinical use. In this review, we summarize the clinical research progress of perioperative adjuvant targeted therapy for EGFR-mutated resectable NSCLC, and discuss the key issues in the clinical researches. [ABSTRACT FROM AUTHOR]

Glioma is often recurred after standard treatment due to its complex biological characteristics and the presence of glioma stem cells (GSCs). High-mobility group box 1 (HMGB1) can regulate the malignant progression of glioma through a variety of ways as an oncogene. This article reviews the relationship between HMGB1 gene and the prognosis of glioma patients, tumor pathological grading, GSCs, and the ways including non coding RNA pathway, autophagy pathway, tumor microenvironment, etc., in which HMGB1 gene regulates glioma, so as to provide the reference for the treatment of glioma. [ABSTRACT FROM AUTHOR]

V-Raf murine sarcoma viral oncogene homolog B (BRAF) alteration is one of the most essential driver genes of non-small cell lung cancer (NSCLC). BRAF encodes serine/threonine protein kinases, and its mutations typically lead to protein compositional activation, thereby activating the mitogen-activated protein kinase kinase (MEK) signaling pathway. A promising new approach for the treatment of mutated BRAF and/or downstream MEK may provide customized treatment opportunities for BRAF driven NSCLC patients. However, combination therapy is necessary to overcome the difficulties such as short duration of benefit, poor therapeutic effect of non-V600 BRAF mutations and susceptibility to drug resistance. This article reviewed the progress in structural characteristics, related signaling pathways, mutation types of BRAF gene, and the clinical pathological relationship between BRAF mutations and NSCLC, as well as the therapy, in order to provide more evidences for clinical doctors to make treatment decisions. [ABSTRACT FROM AUTHOR]

Background and objective Transcription factor (TF) can bind specific sequences that either promotes or represses the transcription of target genes, and exerts important effects on tumorigenesis, migration, invasion. Staphylococcal nuclease-containing structural domain 1 (SND1), which is a transcriptional co-activator, is considered as a promising target for tumor therapy. However, its role in lung adenocarcinoma (LUAD) remains unclear. This study aims to explore the role of SND1 in LUAD. Methods Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Clinical Proteomic Tumor Analysis Consortium (CPTAC), and Human Protein Atlas (HPA) database was obtained to explore the association between SND1 and the prognosis, as well as the immune cell infiltration, and subcellular localization in LUAD tissues. Furthermore, the functional role of SND1 in LUAD was verified in vitro. EdU assay, CCK-8 assay, flow cytometry, scratch assay, Transwell assay and Western blot were performed. Results SND1 was found to be upregulated and high expression of SND1 is correlated with poor prognosis of LUAD patients. In addition, SND1 was predominantly present in the cytoplasm of LUAD cells. Enrichment analysis showed that SND1 was closely associated with the cell cycle, as well as DNA replication, and chromosome segregation. Immune infiltration analysis showed that SND1 was closely associated with various immune cell populations, including T cells, B cells, cytotoxic cells and dendritic cells. In vitro studies demonstrated that silencing of SND1 inhibited cell proliferation, invasion and migration of LUAD cells. Besides, cell cycle was blocked at G1 phase by down-regulating SND1. Conclusion SND1 might be an important prognostic biomarker of LUAD and may promote LUAD cells proliferation and migration. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lung cancer is one of the malignant tumors with the highest incidence and mortality rate in China, and its occurrence and development mechanism and treatment methods are the current research focuses. In recent years, the emergence of drugs targeting various tumor driver genes has significantly improved patients' survival and quality of life, setting off a wave of research on new therapeutic targets. Among them, long non-coding RNA (lncRNA) plays a crucial role in the malignant behavior of tumors, which has attracted widespread attention. Shown by a large number of studies, partial members of lncRNA small nucleolar RNA host gene (SNHG) family are aberrantly expressed in many maliglant tumors including non-small cell lung cancer (NSCLC) and participate in cell proliferation, invasion and migration, which may act as a new diagnostic and prognostic biomarker and can be a therapeutic target of NSCLC. In this review, we comprehensively summarize and explore the recent investigation of SNHGs in NSCLC in order to provide new ideas for the diagnosis and treatment of NSCLC [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In advanced non-small cell lung cancer (NSCLC), V-Raf murine sarcoma viral oncogene homolog B1 (BRAF) mutation is highly malignant and has poor prognosis, and currently Dabrafenib in combination with Trametinib is approved for first-line treatment of patients with BRAF V600 mutation. In addition to mutations, BRAF fusion can also occur. With the development of gene detection, the detection of BRAF fusion is gradually increasing, but there is a lack of effective therapeutic strategies for BRAF fusion. In this paper, we review the clinical characteristics, mechanism of action, and clinical treatment of BRAF fusion to provide a basis for the treatment of BRAF fusion in NSCLC patients. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the effects of inhibin subunit beta A antisense RNA 1 (INHBA-AS1) on epithelial-interstitial transformation (EMT) and ornithine metabolic pathway of cervical cancer cells and its mechanism. Methods: Cervical cancer HeLa cells were routinely cultured in vitro and the experiment was divided into 10 groups: control group, negative control (NC) group, sh-INHBA-AS1 group, PluriSIn 1 [stearyl CoA desaturase (SCD) inhibitor] group, NC+PluriSIn 1 group, sh-INHBA-AS1+PluriSIn 1 Group, 10058-F4 (c-Myc inhibitor) group, NC+10058-F4 group, sh-INHBA-AS1+10058-F4 group, sh-INHBA-AS1+OE-c-Myc group. The proliferation ability of cells in each group was detected by plate cloning assay; the apoptosis of cells in each group was detected by flow cytometry; the invasion and migration abilities of cells in each group were detected by Transwell assay; the expressions of INHBA-AS1, c-Myc, SCD and EMT-related genes (N-cadherin, TGF-β and ZEB1) in cells of each group were detected by qPCR; the expressions of c-Myc, SCD, EMT-associated (Ncadherin, TGF-β and ZEB1), S-adenosine-methionine decarboxylase (SAMDC) and spermidine/spermine N1 acetyltransferase (SSAT) proteins in each group were detected by WB method, and the content of ornithine decarboxylase (ODC) in cell supernatant was detected by ELISA. Results: The proliferation, invasion and migration abilities of HeLa cells were significantly decreased after INHBA-AS1 expression was knocked down (all P<0.05). The apoptosis rate was significantly increased (P<0.05). The results of qPCR and WB assay showed that knockdown of INHBA-AS1 could significantly inhibit the expressions of c-Myc, SCD, N-cadherin, TGF-β, ZEB1, and SAMDC in HeLa cells by (all P<0.05), promote the expression of SSAT (P<0.05) and decrease the content of ODC in HeLa cell supernatant (P<0.05). These effects were more significant after further knockdown of INHBA-AS1 compared with c-Myc inhibitor and SCD inhibitor treatments (all P <0.05). Compared with sh-INHBA-AS1 group, further over-expression of c-Myc significantly increased HeLa cell proliferation (P<0.05), SCD and N-cadherin protein expression levels (P<0.05), and the content of ODC in cell supernatant (P<0.05). Conclusion: INHBA-AS1 can regulate the expression of SCD through c-Myc, participate in the ornithine metabolism and EMT process of HeLa cells, and promote the proliferation, invasion, and migration of HeLa cells. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Epidermal growth factor receptor exon 20 insertion (EGFR ex20ins) is one of the earliest driver gene activation mutations in non-small cell lung cancer (NSCLC). However, due to the unique structure of protein variation caused by this mutation, most patients with EGFR ex20ins mutation (except A763_Y764insFQEA) have poor response to the launched first/ second/third generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs). With the successive approval of new specific targeted drugs for EGFR ex20ins in Food and Drug Administration (FDA) and other national regulatory agencies, the development and clinical research of targeted drugs for EGFR ex20ins in China have also developed rapidly and Mobocertinib has been approved recently in China. It is worth noting that EGFR ex20ins is a variant type with strong molecular heterogeneity. How to detect it comprehensively and accurately in clinical practice, so as to enable more patients to benefit from targeted therapy, is a very important and urgent problem to be solved. This review introduces the molecular typing of EGFR ex20ins, then discusses the importance of EGFR ex20ins detection and the differences of various detection methods, and summarizes the research and development of new drugs progress of EGFR ex20ins, in order to optimize the diagnosis and treatment path of EGFR ex20ins patients by selecting accurate, rapid and appropriate detection methods, so as to improve the clinical benefits of the patients. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The correlation between secreted phosphoprotein 1 (SPPf) and immune infiltration and the clinical correlation of SPP1 in head and neck squamous cell carcinoma(HNSC) were analyzed, and the potential value of SPP1 in the prognosis and individualized treatment of HNSC was clarified. The HNSC data from The Cancer Genome Atlas(TCGA) was used to analyze SPP1 expression. The clinical survival data from TCGA was used to evaluate the clinical prognostic value of SPP1. The clusterProfiler package of R language was applied for the enrichment analysis related to SPP1. The CIBERSORT function of R language was used to evaluate the infiltration of 22 kinds of tumor infiltrating immune cells in HNSC. Subsequently, the correlation analysis between tumor infiltrating immune cells and SPP1 expression was performed. Differential expression analysis found that SPP1 was highly expressed in HNSC (PcO.OOl). Clinical correlation analysis found that SPP1 expression was correlated with T stage (P = 0.001) and clinical stage (P = 0.013). The overall survival of patients with high SPP1 expression was significantly shorter than the patients with low SPP\expression (P = 0.020 4). Gene enrichment analysis found that SPP1 was associated with immunological functions and immune-related pathways in HNSC. Analysis of tumor infiltrating immune cells found that in the high SPP1 expression group, the infiltration proportions of M2 macrophages (P = 0.001 1), resting dendritic cells (P = 0.005 5), and activated mast cells (P = 0.048 8) increased, while the infiltration proportions of actived memory CD4+ T lymphocytes (P<0.001), plasma cells (P = 0.026 6), and resting mast cells (P = 0.038 6) decreased. The research results indicate that SPP1 acts as an oncogene in HNSC and is related to the clinical outcome of patients. SPPl may play an important role in the tumor immune microenvironment and may become a valuable prognostic biomarker and immunotherapy target in HNSC. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Lung Cancer is the property of Chinese Journal of Lung Cancer and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Mesenchymal-epithelial transition factor (MET) amplification is an important driver of resistance in epidermal growth factor receptor (EGFR) -mutant non-small cell lung cancer (NSCLC), and the combination of MET proto-oncogene (MET) and EGFR-tyrosine kinase inhibitors (TKIs) has shown promise in overcoming this molecularly defined acquired resistance. Emerging data also demonstrate MET amplification as a resistance driver to TKIs-treated anaplastic lymphoma kinase (ALK)-, RET-, and ROSI-fusion NSCLC. Here, we review the literature on recent research progress of MET amplification as a resistance driver to targeted therapy in oncogene-driven NSCLC and summarize the progress of clinical strategies to overcome the resistance mechanism. [ABSTRACT FROM AUTHOR]

Objective: To explore the clinical value of human papillomavirus (HPV) detection combined with human myeloproliferative oncogene (C-MYC) detection in cervical precancerous lesions-cervical intraepithelial neoplasia (CIN) screening. Methods: A total of 140 cervical intraepithelial neoplasia specimens preserved in the gynecology department of our hospital from June 2018 to December 2020 were selected, the expression of C-MYC was detected by immunohistochemistry, and the expression of HPV16 and HPV18 was detected by PCR and correlated Sexual Analysis. Results: Among the 140 specimens, the positive rates of HPV16 and HPV18 were 62.9% and 61.4%; the positive rates of HPV16 and HPV18 were 26.8% and 24.4% in CIN grade 1 specimens, and 62.7% and 58.8% in grade 2 specimens. Grade specimens were 93.8% and 95.8%, respectively, and there was a difference (P<0.05). The positive rate of C-MYC was 83.6%, and there were differences in the positive rate of C-MYC among the specimens of different CIN grades (P<0.05). Spearsman correlation analysis showed that the positive rate of HPV16, HPV18 and C-MYC was correlated with CIN grade (P<0.05). Two-category Logisitc regression analysis showed that HPV16, HPV18, and C-MYC positive rates were all important risk factors for CIN classification (P<0.05). Conclusion: With the increase of the grade of cervical intraepithelial neoplasia, the positive rate of HPV16 and HPV18 also increases, and the overexpression of C-MYC is associated with the two, which are important risk factors for the aggravation of the patient's disease. [ABSTRACT FROM AUTHOR]

Proteolysis targeting chimeria (PROTAC) degrades target proteins by utilizing the ubiquitin-proteasome pathway, subverting the concept of traditional small molecule inhibitors. Among the common mutation targets of non-small cell lung cancer (NSCLC), PROTAC technology has successfully achieved the effective degradation of kirsten rat sarcoma viral oncogene homolog (KRAS), epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK ) and other proteins in preclinical studies. PROTAC drugs with their unique event-driven advantages, are expected to overcome acquired drug resistance caused by small molecule inhibitors and show good therapeutic potential for undruggable targets, thereby providing a new strategy for the treatment of NSCLC. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background and objective Reticulosome family gene 1 (RTN1) is a reticulosome-encoding gene associated with the endoplasmic reticulum. RTN1 plays a key role in membrane trafficking or neuroendocrine secretion of neuroendocrine cells, while RTN1 serves as a potential diagnostic/therapeutic marker for neurological diseases and cancer. However, the expression of RTN1 and its effect on the immune microenvironment in patients with lung adenocarcinoma have not been reported. In this study, we aimed to investigate the expression of RTN1 in lung adenocarcinoma and its correlation with immune infiltration and survival in lung adenocarcinoma using public databases and bioinformatics network tools. Methods Expression levels of RTN1 mRNA in tumor and normal tissues were analyzed using Tumor Immune Estimation Resource 2.0 (TIMER 2.0) and Gene Expression Profiling Interactive Analysis 2 (GEPIA 2). RTN1 protein expression was examined using the Human Protein Atlas. The clinical prognostic significance of RTN1 was analyzed using the GEPIA2 plotter database. To further confirm the potential function of RTN1, the data were analyzed using gene set enrichment analysis. In addition, We performed dimensionality-reduced clustering analysis at the single-cell sequencing level on two datasets from the Tumor Immune Single-cell Hub (TISCH) database to observe the cellular clustering of RTN1 in different types of immune cells. Using the TIMER online tool to analyze and predict the infiltration abundance of different types of immune cells in the immune microenvironment of lung adenocarcinoma patients in the TCGA cohort; TIMER and CIBERSORT were used to study the relationship between genes co-expressed with RTN1 and its associated tumor-infiltrating immune cells; finally, TIMER was used to analyze the relationship between RTN1 and immune correlations between immune checkpoints. Results We found that RTN1 expression was decreased in patients with lung adenocarcinoma and was closely related to patient prognosis. RTN1 is involved in the process of phagosome formation, hematopoietic cell formation and cell adhesion, and plays an important role in T cell activation. Using cBioPortal and TCGA data to analyze, it is found that RTN1 is significantly associated with BTK, CD4, ECSF1R, MNDA, NCIKAP1L and SNX20. High expression of the above genes may cause significant upregulation of CD4+ T cells, mast cells, monocytes, myeloid dendritic cells and M1 macrophages. The expression of RTN1 is closely related to the common immune checkpoints CD274, CTLA4, HAVCR2, LAG3, PDCD1, PDCD1LG2, TIGIT and SIGLEC15 immune checkpoints. Conclusion RTN1 may act as a tumor suppressor gene and indicate better prognosis. Furthermore, RTN1 is associated with immune infiltration that may be involved in the immunotherapy response in LUAD. However, the related mechanism needs further research. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

With the rapid development and wide application of next generation sequencing (NGS) technology, a series of researches have revealed that concurrent genetic alterations play an important role in the response and resistance of epidermal growth factor receptor (EGFR)-mutant NSCLC to EGFR-tyrosine kinase inhibitor (TKI). Besides, TP53 mutation is the most common co-mutation gene in EGFR-mutant NSCLC, which has been proved to confer a worse prognosis in EGFR- mutated patients treated with first, second and third generation of EGFR-TKIs. Currently, it is still being explored how to select the best treatment strategies for patients with concomitant presence of TP53 mutation in EGFR-mutant NSCLC. Here, we review the literature on recent research progress of TP53 concurrent mutation in EGFR-mutant advanced NSCLC. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Osimertinib-induced interstitial lung disease (ILD) is an uncommon, but fatal pulmonary toxicity in some patients. We report a case of a 64-year-old male with stage IV adeno-non-small cell lung cancer (NSCLC) harboring an exon 19 deletion in the epidermal growth factor receptor (EGFR) treated with osimertinib 80 mg/d for first-line targeted therapy. On day 60 after initiating treatment of osimertinib, the patient developed ILD. Osimertinib was discontinued immediately and oral prednisone 60 mg/d was initiated, ILD improved within 13 d. After balancing the risk and benefit, osimertinib was restarted concurrently with prednisone. The patient showed neither disease progression nor a recurrence of ILD for more than 16 months. Based on our case and literature review, retreatment with osimertinib under steroid coverage could be considered as an effective treatment option after careful risk-benefit assessment for patients with EGFR-mutant NSCLC. [ABSTRACT FROM AUTHOR]

Objective To report the diagnosis and treatment of a patient with meningeal metastases from lung adenocarcinoma, and explore the significance of cerebrospinal fluid (CSF) gene detection for clinical treatment and the efficacy and safety of double - dose icotinib in the treatment of meningeal metastases from lung adenocarcinoma with EGFR gene sensitive mutation. Methods and Results A 56 - year - old female patient with meningeal metastasis from lung adenocarcinoma was examined for CSF and blood double-sample genes. The CSF had an exon 19 deletion mutation in the EGFR gene, and no sensitive mutations were found in blood sample. Oral icotinib hydrochloride 250 mg/time (3 times/d), and chest CT and head MRI enhanced scans were re - examined every 8 weeks, suggesting that the lung tumor was significantly reduced, and the degree of jumbo meningeal enhancement was lessened than before. Right lateral ventricle-peritoneal shunt was performed to effectively reduce intracranila pressure (ICP) and relieve clinical symptoms. Up to September 21, 2019, patient had been taking double doses of icotinib for 589 d, and her condition was stable. The main adverse drug reaction is rash. She is still taking medication and is being followed up. Conclusions For patients with meningeal metastases from lung adenocarcinoma, CSF gene detection of EGFR gene sensitive mutation can guide clinical development of treatment strategies. Double-dose icotinib is effective in treating meningeal metastases from lung adenocarcinoma with EGFR gene sensitive mutation, and is well tolerated and safe. [ABSTRACT FROM AUTHOR]

BACKGROUND: As a non-coding RNA processed by primary transcription, microRNA-21 (miR-21) plays an important role in biological functions such as growth and development, cancer diagnosis and treatment, immune response, osteogenic differentiation and bone regeneration. OBJECTIVE: To review the cellular targets of miR-21 in bone, the molecular mechanisms that regulate bone regeneration, and the role of miR-21 in bone disease. METHODS: With the keywords of “mir-21, bone, osteogenic differentiation of osteoclast differentiation, skeletal muscle, bone regeneration” in English and “miR-21, bone, skeletal muscle, bone regeneration” in Chinese, PubMed, CNKI, and WanFang databases were retrieved by the first author for articles regarding miR-21 published from 2000 to April 2020. Finally 50 articles were retained for review. RESULTS AND CONCLUSION: In recent years, miR-21 has not only been deeply studied as an oncogene, but also received extensive attention in the proliferation, differentiation, metabolism and other aspects of bone cells. Specifically, miR-21 can mediate the growth and development of skeletal muscle by regulating the expression of transforming growth factor β induced gene and other genes. MiR-21 can promote the osteogenesis of bone marrow mesenchymal stem cells by targeting specific signaling pathways and related gene expression. It can also regulate the positive feedback of osteoclast differentiation through c-Fos/tumor suppressor gene programmed death factor 4, and promote the formation of osteoclasts induced by RANKL. It also regulates the differentiation of dendritic cells and indirectly regulates the expression of hypoxia inducible factor 1α and vascular endothelial growth, which mediates the angiogenesis of stem cells. In addition, miR-21 is closely associated with osteoporosis, osteosarcoma, multiple myeloma, knee osteoarthritis and ankylosing spondylitis. [ABSTRACT FROM AUTHOR]

In the past 20 years, with the development of molecular biology, the treatment of non-small cell lung cancer (NSCLC) has been developing. Targeted therapy has improved the survival period of patients with positive mutation of tumor driver gene. More and more targets have been found gradually. Drugs targeting different driving genes have brought the treatment of NSCLC into a promising target era. Among the many driving genes of NSCLC, the fusion of transfection proto oncogene (RET) is the addition of the epidermal growth factor receptor (EGFR), analytic lymphama kinase (ALK) and c-ros oncogene 1-receptor tyrosine kinase (ROS1) are emerging targets. Targeted drugs for RET gene fusion have been constantly updated. Recently, new high selective RET inhibitors blu-667 and loxo-292 have made important breakthroughs. This paper will review the review of the fusion mutation of RET gene in NSCLC, the detection methods, clinicopathological characteristics, targeted treatment and the research progress after drug resistance. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the most common malignant cancers and has high incidence and mortality rates and poor prognosis. Forkhead box ( FOX) transcription factor family can regulate cell growth, differentiation, and tissue development and plays an important role in tumor. This article reviews the association of the molecular expression of the FOX family with the development, progression, and prognosis of HCC and analyzes the mechanism of action of FOX in the progression of HCC. It is pointed out that FOX family is expected to become a new target for HCC treatment. [ABSTRACT FROM AUTHOR]

With the development of precise medicine, targeted therapy has greatly improved the survival and prognosis of patients in advanced non-small cell lung cancer (NSCLC) with oncogenic drivers. However, no matter which kinds of targeted therapy are inevitable to develop therapeutic resistance, treatment options upon exhaustion of targeted therapies are limited. Immune checkpoint inhibitors (ICIs) can bring long-term survival to some patients with advanced NSCLC because of its unique long tailing effect. More and more studies have shown that ICIs can also benefit NSCLC patients with oncogenic drivers. However, the timing of ICIs intervention, the therapeutic regimen and the predictive biomarkers are actually debated, underscoring the need to explore the potential interest of ICIs in these populations. [ABSTRACT FROM AUTHOR]

Over the past several decades, advances in driven targeted therapy has revolutionized the management of oncogene-driven non-small cell lung cancer (NSCLC). However, there are only a few targeted drugs available for patients with rare mutations, such as BRF, HER2, MET, RET, etc. In recent years, immune checkpoint inhibitors (ICIs) have demonstrated promising benefit in NSCLC. Till now, efficacy of ICIs for NSCLC with rare mutation is largely unknown. It is fairly difficult to conduct a large formal prospective controlled trials because of the rarity of these mutation. In this article, currently available real world studies based on convincing clinical evidence will be reviewed, which will ultimately facilitate our rational use of ICIs for NSCLC with rare mutation. [ABSTRACT FROM AUTHOR]

Antibody-drug conjugates (ADCs) are drugs that combine monoclonal antibody drugs targeting specific antigens and small molecule cytotoxic drugs through linker molecules. ADCs combine the advantages of high specificity targeting and potent killing effects, achieving precise and efficient targeting of cancer cells. Nowadays, ADCs are one of the hotspots in cancer drug development. Human epidermal growth factor receptor 2 (HER-2) is a known oncogene that can drive the occurrence and development of various types of tumors. HER-2 is also an important tumor target for ADCs approved for solid tumors. Anti-HER-2 ADCs can not only be used to treat HER-2-positive tumors but also effectively target HER-2-low tumors. The emergence of ADCs has broken the traditional classification of HER-2 in tumors, bringing significant treatment breakthroughs for HER-2-low tumors. Anti-HER-2 ADCs are widely used in the treatment of solid tumors and have substantial evidence for HER-2-low tumors. This article presents the progress of various anti-HER-2 ADCs in HER-2-low tumors including breast cancer, gastrointestinal malignancies, urothelial carcinoma, lung cancer. And this article summarizes the current status of preclinical studies, clinical studies, and safety of anti-HER-2 ADCs in order to provide reference for the clinical use of HER-2-low tumors.

Objectives: This study aimed to explore the effect of pituitary tumor-transforming gene 1 (PTT-G1) on the invasion and proliferation of oral squamous cell carcinoma (OSCC) cell lines under the action of miR-362-3p., Methods: The bioinformatics online database was used to query the expression of PTTG1 in head and neck squamous cell carcinoma (HNSCC). The expression of PTTG1 in the Cal-27, HN-30, and HOK cell lines was detected by Western blot. A wound-healing assay was used to determine the effect of PTTG1 on the migration ability of the OSCC cells. The Transwell assay was used to examine the changes in cell-invasion ability. 5-ethynyl-2'-deoxyuridine (EdU) cell-proliferation assay was used to detect changes in cell-proliferation ability. Bioinformatics approach predicted the upstream miRNA of PTTG1. The targeting relationship between miR-362-3p and PTTG1 was examined by the dual luciferase assay, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of miRNA in OSCC tissues., Results: The ENCORI database showed that PTTG1 expression was up-regulated in OSCC tissues. Western blot confirmed that PTTG1 expression was up-regulated in Cal-27 and HN-30 cells than HOK cells. PTTG1 knockout can inhibit the migration, invasion, and proliferation of Cal-27 and HN-30 cells ( P <0.05). Bioinformatics prediction websites predicted that the upstream miRNA of PTTG1 was miR-362-3p, and PTTG1 can bind to miR-362-3p. Results of qRT-PCR showed that miR-362-3p expression was downregulated in OSCC tissues compared with normal tissue ( P <0.05). Transwell and EdU experiments confirmed that miR-362-3p knockdown can promote the invasion and proliferation of Cal-27 and HN-30 after PTTG1 knockdown., Conclusions: miR-362-3p can inhibit the invasion and proliferation of Cal-27 and HN-30 cells by targeting PTTG1.

Background: Transcription factor (TF) can bind specific sequences that either promotes or represses the transcription of target genes, and exerts important effects on tumorigenesis, migration, invasion. Staphylococcal nuclease-containing structural domain 1 (SND1), which is a transcriptional co-activator, is considered as a promising target for tumor therapy. However, its role in lung adenocarcinoma (LUAD) remains unclear. This study aims to explore the role of SND1 in LUAD., Methods: Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Clinical Proteomic Tumor Analysis Consortium (CPTAC), and Human Protein Atlas (HPA) database was obtained to explore the association between SND1 and the prognosis, as well as the immune cell infiltration, and subcellular localization in LUAD tissues. Furthermore, the functional role of SND1 in LUAD was verified in vitro. EdU assay, CCK-8 assay, flow cytometry, scratch assay, Transwell assay and Western blot were performed., Results: SND1 was found to be upregulated and high expression of SND1 is correlated with poor prognosis of LUAD patients. In addition, SND1 was predominantly present in the cytoplasm of LUAD cells. Enrichment analysis showed that SND1 was closely associated with the cell cycle, as well as DNA replication, and chromosome segregation. Immune infiltration analysis showed that SND1 was closely associated with various immune cell populations, including T cells, B cells, cytotoxic cells and dendritic cells. In vitro studies demonstrated that silencing of SND1 inhibited cell proliferation, invasion and migration of LUAD cells. Besides, cell cycle was blocked at G1 phase by down-regulating SND1., Conclusions: SND1 might be an important prognostic biomarker of LUAD and may promote LUAD cells proliferation and migration.

Extrachromosomal DNA (ecDNA) is a small segment of circular DNA located outside the chromosome, which has the function of self-replication. Recently, amplification of oncogenes on ecDNA has been proved to be a common phenomenon in tumor cells, and has some characteristics worth studying, such as correlation with patients' poor prognosis. Multiple chromosomal events are involved in the formation of ecDNA, and its amplification can directly increase the number of DNA copies of extra-chromosomal oncogenes and accelerate the generation and development of tumors. Moreover, the segregation pattern of unequal transmission of parental ecDNA cells to offspring not only increases tumor heterogeneity, but also enhances tumor adaptation to environment and response to therapy. This article reviews the current status and potential significance of ecDNAin tumor cells. [ABSTRACT FROM AUTHOR]

Lung micropapillary adenocarcinoma is characterized by frequent metastasis, lymph node infiltration, high recurrence rate and low overall survival rate as a high-grade lung adenocarcinoma. Special oncogenic pathway is activated and immune microenvironment is established in this subtype of tumor. This article reviews the Pathological phenomena and molecular features of micropapillary adenocarcinoma studied in recent years, aiming to deepen the understanding of micropapillary lesions and lay the foundation for formulating specific treatment strategies. [ABSTRACT FROM AUTHOR]

Background and objective Leptomeningeal metastasis (LM) are a severe complication of non-small cell lung cancer (NSCLC), and normally accompanied by poor prognosis. For the patients with targetable mutations, epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are the preferred treatment, but the acquired TKI resistance is inextricable. The aim of this study is to analyze the different gene mutation spectrum and mutation frequency of the cerebrospinal fluid (CSF) and plasma in NSCLC patients with LM, and screen out the drug-resistant mutations so as to guide the choice of treatment accurately. Methods The paired CSF and plasma samples were collected from the NSCLC-LM patients with acquired TKI resistance. Next generation sequencing (NGS) was used to detect the gene variations of circulating tumor DNA (ctDNA). Results A total of 18 NSCLC patients with LM were collected. Of the basic mutations, 11 cases (61.11%) were EGFR, 6 cases (33.33%) were anaplastic lymphoma kinase (ALK), and 1 case (5.56%) was ROS proto-oncogene 1, receptor tyrosine kinase (ROS1). Tumor protein p53 gene (TP53) and mesenchymal-epithelial transition factor (MET) were the two most frequently accompanying mutated genes in CSF ctDNA. The detected mutation rate of CSF samples was higher than that of plasma samples (100.00% vs 66.67%, P=0.006), and the maximum allelic fractions were all higher in CSF than in plasma (P<0.001). Abundant single-nucleotide variations (SNV) and copy number variants (CNV) were detected in CSF, the amount of both of which were more than in blood. In addition, the CSF and plasma samples of patients treated with several TKIs had more SNV mutations than patients who received only a single TKI treatment. Conclusion For the patients of NSCLC, ctDNA in CSF could reveal genomic alterations of LM more exactly and overally than it in plasma, thus could be an optimal source of liquid biopsy for guiding therapy, monitoring therapeutic effect, and predicting prognosis. [ABSTRACT FROM AUTHOR]

Signal transduction and activator of transcription 3 (STAT3) is an oncogene with transcription activity. STAT3 is widely involved in multiple cellular physiological or pathological processes including cancer oncogenesis, metastasis and immunology modulation. The abnormal activation of STAT3 is associated with the oncogenesis or poor prognosis of multiple epithelium original malignant tumors (head and neck squamous cell carcinoma, colorectal cancers, glioma, hepatocellular carcinoma and lung cancer). Additionally, RNA interference or small molecular inhibitor treatment can inhibit the expression or activation of STAT3 in tumor cells and immune escape. Based on the domestic and foreign literature reports and the progress of our own research, this review article provides a brief summary of the latest progress on STAT3 signaling pathway in head and neck cancer research. [ABSTRACT FROM AUTHOR]

Young adult lung cancer is defined as a group of patients refers to whose onset age is less than 40 years old and ≥18 years old. Compare with elder lung cancer, the clinical symptoms of them are not typical, the stage is usually late at the time of discovery, and most of them have regional lymphatic metastasis or distant metastasis. Current study found that young adult lung cancer has a relatively unique genetic background, the abundance of tumor-driving genes is high, and it is closely related to its clinical manifestation and prognosis. Young adult lung cancer is the focus of attention in the field of cancer in recent years. This article reviewed the literature on the clinical features, gene phenotypic characteristics and prognosis of young adult lung cancer in order to provide provide some references and clues for the study on young adult lung cancer. [ABSTRACT FROM AUTHOR]

Patients with sensitive epidermal growth factor receptor (EGFR) mutations often respond to tyrosine kinase inhibitors (TKIs), but acquired resistance will eventually develop. The most common mechanisms of acquired resistance include secondary EGFR mutation, MET amplification, and histologic transformation. Besides, gene fusions could also mediate the process of acquired resistance. Various gene fusions including rearranged during transfection (RET), v-raf murine sarcoma viral oncogene homolog B1 (BRAF) and anaplastic lymphoma kinase (ALK) could take place after TKIs resistance, the incidence of which is around 1%. The clinical cases and experiments both in vitro and in vivo have proved the role of gene fusions in EGFR-TKI resistance. The combination of EGFR inhibitors and gene fusion inhibitors might be an effective therapeutic method. The understanding of gene fusions at EGFR-TKI resistance may contribute to the subsequent diagnosis and treatment strategy. [ABSTRACT FROM AUTHOR]

Background and objective Occurrence at a younger age has been demonstrated to be associated with a distinct biology in non-small cell lung cancer. However, genomics and clinical characteristics among younger patients with lung adenocarcinoma remain to be determined. Here we studied the potentially targetable genetic alterations by next-generation sequencing (NGS) assay in young Chinese patients with lung adenocarcinoma. Methods Eighty-nine surgically resected lung adenocarcinoma tissue samples from patients aged less than 45 years were collected with informed consent from all patients. Targeted NGS assays were used to identify actionable genetic alterations in the cancer tissues. Additionally, the genomic and clinical pathologic characteristics of 95 patients with lung adenocarcinoma who received NGS testing over the same period were analyzed retrospectively. Results The frequencies of targetable genetic alterations in 184 patients with lung adenocarcinoma were analyzed by defined age categories, which unveiled a distinctive molecular profile in the younger group, aged less than 45 years. Notably, higher frequency of anaplastic lymphoma kinase (ALK) and human epidermal growth factor receptor 2 (HER2) genetic alterations were associated with young age. However, a reverse trend was observed for kirsten rat sarcoma viral oncogene (K^AS), serine/threonine kinase 11 (STK11) and epidermal growth factor receptor (EGFR) exon 20 mutations, which were more frequently identified in the older group, aged more than 45 years. Furthermore, concurrent EGFR/tumor protein p53 (TP53) mutations were much more prevalent in the younger patients (81.6% vs 44.9%), which might have a poor response to treatment with EGFR-tyrosine kinase inhibitor (EGFR-TKI). Conclusion NGS assay revealed a distinctive genetic profile in younger patients with adenocarcinoma. High frequency of concurrent EGFR/TP53 mutations was found in the younger patients, which especially warranted personalized treatment in this population. [ABSTRACT FROM AUTHOR]

Background and objective Pulmonary epithelial-myoepithelial carcinoma is a very rare type of salivary gland lung tumor. No standard treatment plan yet. This article intends to analyze the clinical characteristics of pulmonary epithelial-myoepithelial carcinoma and discuss the diagnosis and treatment of pulmonary epithelial-myoepithelial carcinoma. Methods The clinical data of a patient with pulmonary epithelial-myoepithelial carcinoma were analyzed and other relevant clinical literatures were reviewed. Results Epithelial cells immunohistochemically expressed cytokeratin and myoepithelial cells immunohistochemically expressed SMA and S-100. The next-generation sequencing was mainly HRAS gene mutation and the express of PD-L1 protein was negative. Conclusion Most of the patients with Pulmonary epithelial-myoepithelial carcinoma have a good prognosis. Diagnosis mainly depends on microscopic examination and immunohistochemistry. The treatment of pulmonary epithelial-myoepithelial carcinoma is mainly surgical resection. The effect of radiotherapy and chemotherapy is not clear. [ABSTRACT FROM AUTHOR]

BRAF gene mutation is found in about 2%-4% of the patients with non-small cell lung cancer (NSCLC). This type of NSCLC is characterized by high malignancy, low efficacy of chemotherapy and poor prognosis. Although the combination treatment of BRAF inhibitor and MEK inhibitor has achieved remarkable results in advanced NSCLC patients with BRAF V600E mutation, which has been written into the National Comprehensive Cancer Network (NCCN) guidelines, severe side effects of the combination therapy are frequently observed. There isn't effective treatment strategy after drug resistance, and targeted therapy for non-V600E mutation patients is still lacking. In this paper, we summarized the researches on expression of immune markers in NSCLC patients with mutant BRAF and analyzed the studies on efficacy of immune checkpoint inhibitor (ICI), so as to provide more options for prolonging survival of the patients. [ABSTRACT FROM AUTHOR]