22 research outputs found
The SHAP force plots.
The two representative SHAP force plots of a (A) dead and (B) survival patient. SHAP force plots are effective in interpreting the prediction value of the model in critical instances. The contribution of each feature to the output predicted value is shown with arrows with their force associated with the shapley values. Red arrows indicate features increasing the prediction results (i.e., yield values) to reach the predicted value (output value). Blue arrows show features decreasing the prediction values to reach the same output value. The arrows with positive and negative effects on yield values compensate on a point which is the prediction (output) value.</p
Data_Sheet_3_Calpain2 Upregulation Regulates EMT-Mediated Pancreatic Cancer Metastasis via the Wnt/β-Catenin Signaling Pathway.ZIP
Calpains2 (CAPN2) is a calcium-dependent, non-lysosomal cysteine protease that plays critical roles in normal cellular functions and pathological processes, including tumorigenesis, cancer progression, and metastasis. However, the role and underlying regulatory mechanisms of CAPN2 in pancreatic cancer (PC) are still unknown. We found that CAPN2 is highly expressed in PC tissues and associated with poor PC prognosis by using The Cancer Genome Atlas (TCGA) datasets, Gene Expression Omnibus (GEO) datasets, and PC tissue arrays. CAPN2 downregulation significantly inhibited cell proliferation, migration, and invasion and regulated Wnt/β-catenin signaling pathway-mediated epithelial-mesenchymal transition (EMT) in PC cells. Our findings highlight the significance of CAPN2 in tumor regression and, thus, indicate that CAPN2 could be a promising target for PC treatment.</p
Comparisons of baseline characteristics in all cohorts.
Comparisons of baseline characteristics in all cohorts.</p
Data_Sheet_1_Calpain2 Upregulation Regulates EMT-Mediated Pancreatic Cancer Metastasis via the Wnt/β-Catenin Signaling Pathway.ZIP
Calpains2 (CAPN2) is a calcium-dependent, non-lysosomal cysteine protease that plays critical roles in normal cellular functions and pathological processes, including tumorigenesis, cancer progression, and metastasis. However, the role and underlying regulatory mechanisms of CAPN2 in pancreatic cancer (PC) are still unknown. We found that CAPN2 is highly expressed in PC tissues and associated with poor PC prognosis by using The Cancer Genome Atlas (TCGA) datasets, Gene Expression Omnibus (GEO) datasets, and PC tissue arrays. CAPN2 downregulation significantly inhibited cell proliferation, migration, and invasion and regulated Wnt/β-catenin signaling pathway-mediated epithelial-mesenchymal transition (EMT) in PC cells. Our findings highlight the significance of CAPN2 in tumor regression and, thus, indicate that CAPN2 could be a promising target for PC treatment.</p
Performance of the prediction models using all features.
Performance of the prediction models using all features.</p
The importance of all features derived from random forest in the validation set.
(TIF)</p
SHAP summary plot of the features of the XGBoost model.
The higher the SHAP value of a feature, the higher the probability of in-hospital mortality development. A dot is created for each feature attribution value for the model of each patient, and thus one patient is allocated one dot on the line for each feature. Dots are colored according to the values of features for the respective patient and accumulate vertically to depict density. Red represents higher feature values, and blue represents lower feature values.</p