Daming Gao

Correction: Osteomodulin positively regulates osteogenesis through interaction with BMP2.

CAD manipulates tumor intrinsic DHO/UBE4B/NF-κB pathway and fuels macrophage cross-talk, promoting HCC metastasis

Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Zinc ions activate AKT and promote prostate cancer cell proliferation via disrupting AKT intramolecular interaction.

Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression.

Reversal of lipid metabolism as a therapeutic approach for HCC.

Supplementary Table S1 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Supplementary Table S2 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Figure S6 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Supplementary Table S3 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Figures S3 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Figures S1 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Data from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Supplementary Table S7 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Supplementary Table S5 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Supplementary Table S6 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Figure S4 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Supplementary Figures S1-9 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Figure S5 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Figures S2 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Supplementary Table S2 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Supplementary Table S1 from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Data from Mutant KRAS and CK2 Cooperatively Stimulate SLC16A3 Activity to Drive Intrahepatic Cholangiocarcinoma Progression

Supplementary Table S3 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Supplementary Table S4 from An Inflammatory Checkpoint Generated by <i>IL1RN</i> Splicing Offers Therapeutic Opportunity for <i>KRAS</i>-Mutant Intrahepatic Cholangiocarcinoma

Proteogenomic characterization of small cell lung cancer identifies biological insights and subtype-specific therapeutic strategies

Proteogenomic characterization of small cell lung cancer identifies biological insights and subtype-specific therapeutic strategies.

Pan-cancer proteogenomics expands the landscape of therapeutic targets

Pan-cancer proteogenomics expands the landscape of therapeutic targets.

Overview of recent experimental results on the EAST Tokamak