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The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and <t>RT‐qPCR</t> (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.
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The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and <t>RT‐qPCR</t> (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.
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The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and <t>RT‐qPCR</t> (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.
Primescript Rt Master Mix, supplied by Beijing CWBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and <t>RT‐qPCR</t> (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.
Primescript Rt Reagent Kit, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and <t>RT‐qPCR</t> (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.
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The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and <t>RT‐qPCR</t> (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.
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The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and <t>RT‐qPCR</t> (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.
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Image Search Results


The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and RT‐qPCR (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.

Journal: Cancer Medicine

Article Title: Machine Learning–Driven Integration of Cancer Cell Phenotypes Predicts Cisplatin Sensitivity

doi: 10.1002/cam4.71373

Figure Lengend Snippet: The CSP26G model was applicable for predicting the response to cisplatin in external samples. (A) Schematic representative of A549CR cell establishment and photo images of parental A549 and established A549CR cells are shown. (B) The viabilities of A549 and A549CR cells at 72 h after cisplatin treatment were compared by the MTT assay. Scale bars: 100 μm. Mean ± SD. Significance levels denoted * p < 0.05, ** p < 0.01, and *** p < 0.001. (C) RNA‐seq (resistant/sensitive in the training data for CSP26G) and RT‐qPCR (A549CR/A549) showed positive correlation. The x‐ and y‐axes were shown in log 2 scale, with r denoting the Pearson correlation coefficient and its associated p ‐value. RT‐qPCR data were normalized to GAPDH before fold change calculation. (D) Survival analysis was performed using the Kaplan–Meier method on NSCLC patients with pathological stage II and IIIA ( N = 407) from TCGA, based on CSP26G output results. The solid green and solid orange lines are the survival curves for the sensitive and resistant groups, respectively. The light green and orange shading on the plot represents the 95% CI for each group. Censored patients are shown as markers on the curve. Statistical analysis was conducted using the log‐rank test. (E) ROC curves at 2, 4, 6, and 8 years of treatment in TCGA data were used to estimate predictive accuracies of CSP26G. (F) Forest plot of multivariate Cox proportional hazards regression for overall survival. Hazard ratios and 95% CI are shown for CSP26G prediction score, age, TNM classifications (T, primary tumor and local invasion; N, regional lymph node involvement; M, distant metastasis). Due to the single level of the M stage, its hazard ratio, 95% CI and p ‐value could not be calculated.

Article Snippet: Total RNA was extracted using the RNeasy mini kit (Qiagen, Hilden, Germany). cDNA was prepared using the ReverTra Ace qPCR RT Master Mix with gDNA Remover (Toyobo, Osaka, Japan).

Techniques: MTT Assay, RNA Sequencing, Quantitative RT-PCR