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lung-cancer

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Journal Articles
Journal Articles
Cancer Res (2022) 82 (22): 4219–4233.
Published: 15 November 2022
... signaling and the impact of their perturbation remain unknown for numerous recalcitrant cancers. Here, we characterize WNT pathway activity in small cell lung cancer (SCLC) and determine the functional role of WNT signaling using genetically engineered mouse models. β-Catenin, a master mediator of canonical...
Includes: Supplementary data
Journal Articles
Cancer Res (2022) 82 (21): 4016–4030.
Published: 02 November 2022
... evasion in non–small cell lung cancer (NSCLC) in a CD8+ T-cell-dependent manner. Mechanistically, CYP4F2 induced expression of immune checkpoint PD-L1 and production of proangiogenic factors IL6 and TGFβ in cancer-associated fibroblasts (CAF) via the 20-HETE-GPR75-STAT3-c-Jun axis. Tumors...
Includes: Supplementary data
Journal Articles
Cancer Res (2022) 82 (21): 4079–4092.
Published: 02 November 2022
... Uppaluri; Cloud P. Paweletz; Juan J. Miret; Patrick H. Lizotte; Prafulla C. Gokhale; Pasi A. Jänne; David A. Barbie Immunotherapy has shown limited efficacy in patients with EGFR-mutated lung cancer. Efforts to enhance the immunogenicity of EGFR-mutated lung cancer have been unsuccessful...
Includes: Supplementary data
Journal Articles
Cancer Res (2022) 82 (20): 3734–3750.
Published: 17 October 2022
.... Exploring the function of CD248 has the potential to provide biological insights into tumor-supportive stroma and potential therapeutic targets. Here, we investigated the role of stromal CD248 in lung cancer. In orthotopic lung cancer transplantation models, tumor volume, density of vessels and pericytes...
Includes: Supplementary data
Journal Articles
Cancer Res CAN-22-1289.
Published: 10 October 2022
... between lncRNAs and c-Myc/E2F1-related signaling pathways could provide important insights into cancer biology. In this study, we used integrated bioinformatic analyses and found that the lncRNA MNX1-AS1 is upregulated in non-small cell lung cancer (NSCLC) via copy number gain and c-Myc-mediated...
Includes: Multimedia, Supplementary data
Journal Articles
Cancer Res (2022) 82 (19): 3435–3448.
Published: 04 October 2022
.... Vogel; Alejandro Suárez-Bonnet; Simon L. Priestnall; Philip East; Sarah J. Ross; George Kassiotis; Miriam Molina-Arcas; Charles Swanton; Reuben Harris; Julian Downward Mutations in oncogenes such as KRAS and EGFR cause a high proportion of lung cancers. Drugs targeting these proteins...
Includes: Supplementary data
Journal Articles
Cancer Res CAN-22-1039.
Published: 26 September 2022
... supports lung tumorigenesis and is a potential therapeutic target in lung cancer. A better understanding of the importance of tumor cell-autonomous versus systemic autophagy in lung cancer could facilitate clinical translation of autophagy inhibition. Here, we exploited inducible expression of Atg5 shRNA...
Includes: Supplementary data
Journal Articles
Cancer Res (2022) 82 (17): 3058–3073.
Published: 02 September 2022
...Demetra P. Kelenis; Kathia E. Rodarte; Rahul K. Kollipara; Karine Pozo; Shreoshi Pal Choudhuri; Kyle B. Spainhower; Sarah J. Wait; Victor Stastny; Trudy G. Oliver; Jane E. Johnson Genomic studies support the classification of small cell lung cancer (SCLC) into subtypes based on the expression...
Includes: Supplementary data
Images
Gene expression in <span class="search-highlight">lung</span> <span class="search-highlight">cancer</span> PDX models.  A,  Hierarchical clustering of ...
Published: 15 November 2022
Figure 4. Gene expression in lung cancer PDX models. A, Hierarchical clustering of gene expression percentile rank z-score for all lung cancer PDX samples and platforms. The heatmap is based on correlation values of expression percentile rank z-score expression for LUSC and LUAD PDX samples from sequencing and array platforms. The top horizontal color bars indicate the library preparation methods and platforms, subtype designation, and passage number. Sample labels are indicated by model ID, sample ID, and library preparation/platform. B, Expression (quantile-normalized raw RSEM counts) correlation of nearest template prediction genes between TCGA (LUAD, n = 230; LUSC, n = 178) and PDX (LUAD, n = 36; LUSC, n = 24) samples for LUAD and LUSC. The color bars indicate the subtype labels for TCGA and subtype predictions for PDX. C, Proportion of PDX models with mutations reported to be enriched in LUAD and LUSC subtypes as indicated on the left. LUAD subtypes: proximal-inflammatory (PIF), proximal-proliferative (PPR), terminal respiratory unit (TRU). LUSC subtypes: basal (BAS), classical (CLA), primitive (PRI), and secretory (SEC). Figure 4. Gene expression in lung cancer PDX models. A, Hierarchical clustering of gene expression percentile rank z-score for all lung cancer PDX samples and platforms. The heatmap is based on correlation values of expression percentile rank z-score expression for LUSC and LUAD PDX samples from sequencing and array platforms. The top horizontal color bars indicate the library preparation methods and platforms, subtype designation and passage number. Sample labels are indicated by model ID, sample ID, and library preparation/platform. B, Expression (quantile-normalized raw RSEM counts) correlation of nearest template prediction genes between TCGA (LUAD: n = 230; LUSC: n = 178) and PDX (LUAD: n = 36; LUSC: n = 24) samples for LUAD and LUSC. The color bars indicate the subtype labels for TCGA and subtype predictions for PDX. C, Proportion of PDX models with mutations reported to be enriched in LUAD and LUSC subtypes as indicated on the left. LUAD subtypes: proximal-inflammatory (PIF), proximal-proliferative (PPR), terminal respiratory unit (TRU). LUSC subtypes: basal (BAS), classical (CLA), primitive (PRI), and secretory (SEC). More
Images
MLL inhibition enhancing chemotherapy sensitivity of <span class="search-highlight">lung</span> <span class="search-highlight">cancer</span> cells.  A–...
Published: 15 November 2022
Figure 4. MLL inhibition enhancing chemotherapy sensitivity of lung cancer cells. A–D, A549 cells were treated with siNC or siMLL-2, and the generated cells were treated with cisplatin or ET. The cell proliferation was measured by the CCK8 assay at day 3 ( A and B ), and the colony-forming activity was determined at day 7 ( C and D ). Right, quantification of colony numbers. n = 3. E, The A549, H1299, H157, H1975, and H1944 cells were cotreated with MI-3 and DDP for 72 hours and cell proliferation was measured by CCK8 assays. n = 3. F, The H157 cells were stably transfected with the empty vector or KrasG12V-overexpressing plasmid via the lentiviral. The transfected cells were cotreated with MI-3 and DDP for 72 hours and cell proliferation was measured by CCK8 assays. n = 3. Data are represented as mean ± SD in A – F . The P values were determined by two-tailed unpaired t tests. Figure 4. MLL inhibition enhancing chemotherapy sensitivity of lung cancer cells. A–D, A549 cells were treated with siNC or siMLL-2, and the generated cells were treated with cisplatin or ET. The cell proliferation was measured by the CCK8 assay at the day 3 (A and B), and the colony-forming activity were determined at the day 7 (C and D), the quantification of colony numbers showed in the right. n = 3. E, The A549, H1299, H157, H1975, and H1944 cells were cotreated treated with MI-3 and DDP for 72 hours and cell proliferation was measured by CCK8 assays. n = 3. F, The H157 cells were stably transfected with the empty vector or KrasG12V-overexpressing plasmid via the lentiviral. The transfected cells were cotreated with MI-3 and DDP for 72 hours and the cell proliferation was measured by CCK8 assays. n = 3. Data are represented as mean ± SD in A–F. The P values were determined by two-tailed unpaired t tests. More
Journal Articles
Cancer Res OF1.
Published: 26 August 2022
... , Kim DH , Im K , Lee H , . The reversible fourth-generation EGFR tyrosine kinase inhibitor OBX02-011 overcomes C797S-mediated resistance in lung cancer . Cancer Res 2022 [Online only]. doi: 10.1158/0008-5472.CAN-22-0394 . 2. Choi YJ , Kim D-S , Sung...
Journal Articles
Journal Articles
Cancer Res OF1–OF10.
Published: 25 August 2022
... is an irreversible third-generation EGFR tyrosine kinase inhibitor (TKI) that was initially developed to overcome the EGFR T790M mutation and is used as a standard therapy in patients with advanced non–small cell lung cancer (NSCLC) with EGFR-activating mutations. Despite the remarkable initial efficacy, osimertinib...
Includes: Supplementary data
Images
CD73 is regulated by oncogenic <em>MET</em> in <span class="search-highlight">lung</span> <span class="search-highlight">cancer</span> cells.  ...
Published: 02 November 2022
Figure 4. CD73 is regulated by oncogenic MET in lung cancer cells. A, H69/H69M HGF-derived isogenic model and immunoblot of CD73 at basal expression. B, Flow cytometry of CD73 in H69M at basal condition. Red, isotype control. C, Immunoblot of different lung cancer cell lines used in the study. Protein basal status is indicated. D, Immunoblot showing the levels of MET and CD73 in the EBC1 cells after MET KO targeting MET (#1KO). Scr, scramble control. ACTIN, total protein-loading control (up). Flow cytometry assay of CD73 levels in the MET scr and KO EBC1 cells (down). E, Immunoblot of the indicated proteins in the cell lines after treatment with 0.1 μmol/L crizotinib (CRZ) and 30 nmol/L trametinib (TRAM). F , Immunoblot of the indicated proteins in the cell lines after treatment with 0.05 μmol/L HGF and 0.1 μmol/L crizotinib. Figure 4. CD73 is regulated by oncogenic MET in lung cancer cells. A, H69/H69M HGF derived isogenic model and IB of CD73 at basal expression. B, Flow cytometry of CD73 in H69M at basal condition. Isotype control in red. C, IB of different lung cancer cell lines used in the study. Protein basal status are indicated. D, IB showing the levels of MET and CD73 in the EBC1 cells after MET KO targeting MET (#1KO). Scr, scramble control. ACTIN, total protein-loading control (up). Flow citometry assay of CD73 levels in the MET scr and KO EBC1 cells (down). E, IB of the indicated proteins in the cell lines after treatment with 0.1 μmol/L crizotinib (CRZ) and 30 nmol/L trametinib (TRAM). F, IB of the indicated proteins in the cell lines after treatment with 0.05 μmol/L HGF and 0.1 μmol/L crizotinib (CRZ). More
Journal Articles
Cancer Res (2022) 82 (16): 2826–2828.
Published: 16 August 2022
...Christian Rolfo; Umberto Malapelle; Alessandro Russo In recent years, there has been tremendous therapeutic progress for advanced lung cancer, leading to the identification of a multitude of therapeutic targets and significantly expanding the list of potential target genes to be tested. However...
Journal Articles
Cancer Res (2022) 82 (16): 2838–2847.
Published: 16 August 2022
...; Joseph B. Shrager; Ash A. Alizadeh; Maximilian Diehn Genomic profiling of bronchoalveolar lavage (BAL) samples may be useful for tumor profiling and diagnosis in the clinic. Here, we compared tumor-derived mutations detected in BAL samples from subjects with non–small cell lung cancer (NSCLC) to those...
Includes: Supplementary data
Journal Articles
Cancer Res (2022) 82 (15): 2692–2703.
Published: 03 August 2022
...Jennifer A. Karlow; Siddhartha Devarakonda; Xiaoyun Xing; Hyo Sik Jang; Ramaswamy Govindan; Mark Watson; Ting Wang Non–small cell lung cancer (NSCLC) is one of the most commonly diagnosed and deadliest cancers worldwide, with roughly half of all patients initially presenting with both primary...
Includes: Supplementary data
Images
Coexpression of CD248, OPN, and SERPINE1 in human <span class="search-highlight">lung</span> <span class="search-highlight">cancer</span>–associated pe...
Published: 17 October 2022
Figure 8. Coexpression of CD248, OPN, and SERPINE1 in human lung cancer–associated pericytes. A, IF microscopy compared the coexpression of the pericyte marker αSMA with CD248 (left), OPN (middle), or SERPINE1 (right) in large (diameter > 5 cm, n = 10) and small (diameter < 3 cm, n = 10) human NSCLC tissues. There was a significant increase in the areas double positive for αSMA/CD248, αSMA/OPN, and αSMA/SERPINE1 in large lung tumors compared with small ones. Data were from five HPF per section and two sections per tumor (n = 10) and are presented as mean percentage plus SEM. B, A positive correlation existed between any two of the αSMA+CD248+, αSMA+OPN+, and αSMA+SERPINE1+ area percentages in human lung cancer tissues. The Pearson correlation coefficient (r) was calculated to assess the strength of correlation (n = 20, tissues in A ). C, Colocalization of CD248 with pericyte marker αSMA, OPN, and SERPINE1 in human lung cancer tissues in IF confocal microscopy. The intensity profiles (bottom) along selected lines (X1–X2) indicated overlapping fluorescence signals. Scale bar, 20 μm. D, Schematic illustration of how CD248 enhanced Wnt/β-catenin signaling to increase Opn and Serpine1 expressions in mouse pericytes. Without CD248 (left), the majority of LGALS3 was tethered to LGALS3BP and so was LRP6 to IGFBP4. Combined, the absence of CD248 in mice resulted in reduced Wnt/β-catenin signaling and the expression of its downstream genes, including Serpine1, Opn, Ccnd1, and Myc. In contrast, in the presence of CD248 (right), a significant proportion of LRP6 and LGALS3 was displaced from the association with IGFBP4 and LGALS3BP, respectively. The increased amounts of released LRP6 and LGALS3 antagonized the inhibition of GSK3β on β-catenin and enhanced the transcription of Serpine1, Opn, and other Wnt target genes. Finally, the augmented production of OPN and SERPINE1 proteins by pericytes stimulated the angiogenesis of neighboring endothelial cells, which promoted lung tumor growth. **, P < 0.01. Figure 8. Coexpression of CD248, OPN, and SERPINE1 in human lung cancer–associated pericytes. A, IF microscopy compared the coexpression of the pericyte marker αSMA with CD248 (left), OPN (middle), or SERPINE1 (right) in large (diameter > 5 cm, n = 10) and small (diameter < 3 cm, n = 10) human NSCLC tissues. There was a significant increase in the areas double positive for αSMA/CD248, αSMA/OPN, and αSMA/SERPINE1 in large lung tumors compared with small ones. Data were from five HPF per section, and two sections per tumor (n = 10) and presented as mean percentage plus SEM. B, A positive correlation existed between any two of the αSMA+CD248+, αSMA+OPN+, and αSMA+SERPINE1+ area percentages in human lung cancer tissues. The Pearson correlation coefficient (r) was calculated to assess the strength of correlation (n = 20, tissues in A). C, Colocalization of CD248 with pericyte marker αSMA, OPN, and SERPINE1 in human lung cancer tissues in IF confocal microscopy. The intensity profiles (bottom) along selected lines (X1–X2) indicated overlapping fluorescence signals. Scale bar, 20 μm. D, Schematic illustration of how CD248 enhanced Wnt/β-catenin signaling to increase Opn and Serpine1 expressions in mouse pericytes. Without CD248 (left), the majority of LGALS3 was tethered to LGALS3BP and so was LRP6 to IGFBP4. Combined, the absence of CD248 in mice resulted in reduced Wnt/β-catenin signaling and the expression of its downstream genes, including Serpine1, Opn, Ccnd1, and Myc. In contrast, in the presence of CD248 (right), a significant proportion of LRP6 and LGALS3 was displaced from the association with IGFBP4 and LGALS3BP, respectively. The increased amounts of released LRP6 and LGALS3 antagonized the inhibition of GSK3β on β-catenin and enhanced the transcription of Serpine1, Opn, and other Wnt target genes. Finally, the augmented production of OPN and SERPINE1 proteins by pericytes stimulated the angiogenesis of neighboring endothelial cells, which promoted lung tumor growth. More
Journal Articles
Cancer Res (2022) 82 (12_Supplement): 1168.
Published: 15 June 2022
...Lin Song; Thaidy Y. Rodriguez; Adam Olshen; Eric Collisson 11% of non-small cell lung cancer (NSCLC) patients harbor NF1 mutations. The enrichment of NF1 mutations in lung adenocarcinoma (LUAD) cases that otherwise lack activated oncogene mutations indicates that NF1 loss may play a necessary role...