Aagaardwillard3283
urgical resection.
Using an RF algorithm, clinical characteristics can be combined with intraoperative FS analysis to significantly improve intraoperative judgment accuracy for low- and high-risk tumors, and may serve as a reliable complementary method when FS evaluation is equivocal, improving the accuracy of the extent of surgical resection.
Although the prognosis of non-small cell lung cancer (NSCLC) can be assessed based on pathological type, disease stage and inflammatory indicators, the prognostic scoring model of NSCLC still needs to improve.
is associated with poor prognosis of partial tumors, but its prognostic relationship with NSCLC is poorly understood. In this study, the role of
in NSCLC was studied to evaluate relationship with disease prognosis and potential therapeutic target.
The clinicopathological and paracancerous tissues of patients with NSCLC primarily diagnosed in Tangdu Hospital from 2009 to 2013 were collected. Follow-up of patients were made every three months and the last follow-up period was December 2018. The expression of
was assessed by immunohistochemistry (IHC). Then, weighted gene co-expression network analysis (WGCNA) was used to analyze the relationship between
expression and the prognosis of lung adenocarcinoma (LUAD) patients. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG)analysis showed that
-related genes
and
were significantly associated with LUAD prognosis.
The high expression of
is related to the poor prognosis of LUAD, and it is expected to become a therapeutic target and prognostic evaluation therapy for LUAD in the future. However, the relevant results need to be further studied and verified.
The high expression of HDAC11 is related to the poor prognosis of LUAD, and it is expected to become a therapeutic target and prognostic evaluation therapy for LUAD in the future. However, the relevant results need to be further studied and verified.
Squamous cell carcinoma (SCC) is the major histological type in lung cancer (LC). The tumor microenvironment (TME) drives tumor progression and metastasis. In the TME, cancer-associated fibroblasts (CAFs) play key roles in carcinogenesis. However, the roles of CAFs in lung SCC remain unknown. In this study, we evaluated whether the CAF phenotype was determined by various CAF-related proteins and whether CAF-related protein expression contributed to clinical outcomes in patients with lung SCC.
We examined the associations of CAF- and epithelial-mesenchymal transition (EMT)-related markers expressed in CAFs, including α-smooth muscle actin (α-SMA), CD10, podoplanin, fibroblast-specific protein 1 (FSP1), platelet-derived growth factor receptor (PDGFR) α, PDGFRβ, adipocyte enhancer-binding protein 1 (AEBP1), fibroblast activation protein (FAP), tenascin-C, Zinc finger E-box binding homeobox 1 (ZEB1), and twist homolog 1 gene (TWIST1), in 108 lung SCC tissues using immunohistochemistry. In addition, cluster anBP1 overexpression played key roles in prediction of a poor prognosis in patients with lung SCC.
Small cell lung cancer (SCLC) and Ewing's sarcoma (ES) at the disseminated stage are not amenable to therapy and have a dismal prognosis with low survival rates. Despite representing different tumor entities, treatment for both malignancies relies on cytotoxic chemotherapy that has not considerably changed for the past decades. The genomic background has been extensively studied and found to comprise inactivation of p53 and RB1 in case of SCLC and EWSR1/FLI1 rearrangement in case of ES resulting in aggressive tumors in adults with heavy tobacco consumption and as bone tumor in juveniles, respectively. Idasanutlin New therapeutic modalities are urgently needed to improve the outcomes of both tumor entities, especially in patients with metastatic disease or recurrences. This review summarizes the common cell biologic and clinical characteristics of difficult-to-treat SCLC and ES and discusses their refractoriness and options to improve the therapeutic efficacy.
PubMed and Euro PMC were searched from January 1
, 2012 tective drug concentration at the tumor cell level to a significant degree leaving therapeutic interventions of any kind ineffective.
The global chemoresistance of SCLC and ES may be explained by physiological resistance at the tumor level and formation of larger spheroids that contain quiescent and hypoxic tumor cells in regions that occlude therapeutics. This type of chemoresistance is difficult to overcome and prevent the accumulation of effective drug concentration at the tumor cell level to a significant degree leaving therapeutic interventions of any kind ineffective.
Glycosylation is crucial for the stability and biological functions of proteins. The aberrant glycosylation of critical proteins plays an important role in multiple cancers, including lung adenocarcinoma (LUAD). STT3 oligosaccharyltransferase complex catalytic subunit A (STT3A) is a major isoform of N-linked glycosyltransferase that catalyzes the glycosylation of various proteins. However, the functions of STT3A in LUAD are still unclear.
The expression profiles of STT3A were initially analyzed in public data sets and then validated by quantitative real-time polymerase chain reaction, Western blot and immunohistochemistry assays in clinical LUAD samples. The overall survival (OS) between patients with high and low STT3A expression was compared using a Kaplan-Meier curve with a log-rank analysis. STT3A was knocked-out using CRISPR/Cas9 and inhibited by NGI-1. Cell Counting Kit-8, colony formation assay, wound-healing, transwell assay, and flow cytometry were performed to assess the cellular functions of STnaling pathways and could serve as a novel prognostic biomarker and potential therapeutic target for LUAD patients.
STT3A promotes LUAD progression via the MAPK and PI3K/AKT signaling pathways and could serve as a novel prognostic biomarker and potential therapeutic target for LUAD patients.
The rechallenge of immune checkpoint inhibitors (ICI) is now an optional strategy for patients who discontinued ICI due to immune-related adverse events (irAEs) or disease progression. However, little data is available for the prognosis and prognostic factors of patients receiving ICI rechallenge treatment in advanced lung cancer patients. Our study aimed to explore the efficacy, prognosis and safety of patients who received anti-programmed cell death-1/programmed cell death ligand 1 (anti-PD-1/PD-L1) inhibitor rechallenge.
In our retrospective cohort study, data of advanced lung cancer patients who received anti-PD-1/PD-L1 inhibitor and discontinued due to irAEs or disease progression were collected from December 2016 to August 2021. Enrolled patients were categorized into two groups rechallenge group (R group) and non-rechallenge group (NR group). Progression-free survival (PFS), overall survival (OS), disease control rate (DCR) and safety data were analyzed. Cox model and subgroup analysis were analyze95; P=0.144), and the DCR of the rechallenge subgroup was 40% after ICI rechallenge.
ICI rechallenge might be an attractive option for patients who discontinue treatment due to irAEs. For patients with disease progression, further research should be conducted. The recurrence of irAEs and their early onset during the second round of ICI should be considered.
ICI rechallenge might be an attractive option for patients who discontinue treatment due to irAEs. For patients with disease progression, further research should be conducted. The recurrence of irAEs and their early onset during the second round of ICI should be considered.
To explore the feasibility of the depth ratio method partitioning the lung parenchyma and the depth distribution of lung nodules in pulmonary segmentectomy.
Based on the measurement units, patients were allocated to the chest group, the lobar group, and the symmetrical 3 sectors group. In each unit, the center of the respective bronchial cross-section was set as the starting point (O). Connecting the O point with the center of the lesion (A) and extending to the endpoint (B) on the pleural, the radial line (OB) was trisected to divide the outer, middle, and inner regions. The depth ratio and relevant regional distribution were simultaneously verified using 2-dimensional (2D) coronal, sagittal, and axial computed tomography images and 3-dimensional (3D) reconstruction images.
Two hundred and nine patients were included in this study. The median age was 53 (IQR, 44.5-62) years and 64 were males. The intra-group consistency of the depth ratio region partition was 100%. The consistency of the inter-group region partition differed among the three groups (Kappa values 0.511, 0.517, and 0.923). The chest group, lobar group, and symmetrical 3 sectors group had 69.4%, 26.3%, and 4.8% mediastinum disturbance, respectively (P<0.001).
The depth ratio method in the symmetrical 3 sectors of the lung maximally eliminated the disturbance of the mediastinal structures and more accurately trisected the lung parenchymal in 3D space. Sublobar resection based on subsegments strategy is feasible for outer 2/3 pulmonary nodules when depth ratio is used as the measurement method.
The depth ratio method in the symmetrical 3 sectors of the lung maximally eliminated the disturbance of the mediastinal structures and more accurately trisected the lung parenchymal in 3D space. Sublobar resection based on subsegments strategy is feasible for outer 2/3 pulmonary nodules when depth ratio is used as the measurement method.
The genetic nature of cancer provides the rationale to support the need for molecular diagnosis and patient selection for individualised antineoplastic treatments that are the best in both tolerability and efficacy for each cancer patient, including non-small cell lung cancer (NSCLC) patients. Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations represent the prevalent oncogenic driver in NSCLC, being detected in roughly one-third of cases and KRAS G12C is the most frequent mutation found in approximately 13% of patients.
This paper gives an overview of the numerous scientific efforts in recent decades aimed at KRAS inhibition.
Sotorasib is the first approved KRAS G12C inhibitor that has been shown to provide a durable clinical benefit in patients with pre-treated NSCLC with KRAS G12C mutation. Together with the development of new targeted drugs, the development of strategies to control resistance mechanisms is one of the major drivers of research that is exploring the use of KRAS inhibitors not only alone, but also in combination with other targeted therapies, chemotherapy and immunotherapy.
This review will describe the major therapeutic developments in KRAS mutation-dependent NSCLC and will analyse future perspectives to maximise benefits for this group of patients.
This review will describe the major therapeutic developments in KRAS mutation-dependent NSCLC and will analyse future perspectives to maximise benefits for this group of patients.
Osimertinib is standard of care for
-mutated non-small cell lung cancer (NSCLC) patients. The efficacy of the drug in patients with mutations other than the common deletion in exon 19 and L858R in exon 21 is largely unknown.
We identified patients with uncommon
-mutations from two prospective clinical phase II, single-arm studies for previously treated patients and untreated patients, respectively, and pooled data for this analysis. All patients received treatment with osimertinib 80 mg daily until radiological progression or death. The primary endpoint of both trials was objective response rate (ORR), with progression-free survival (PFS), overall survival (OS) and intracranial efficacy as key secondary endpoints. Circulating tumour DNA (ctDNA) was analysed before and two weeks after treatment initiation in the first line cohort.
Of 299 enrolled patients in the two trials, 21 patients with uncommon mutations were identified; 12 patients had a single mutation (G719X or L861Q), one patient had L861Q and an exon 20 insertion, and 8 patients had compound mutations with G719X and either L861Q or S768I.
