CKB (Creatine Kinase B)

Our study establishes a robust and scalable method that integrates single-cell spheroids with proteomics to model and quantify ITH in CRC. By capturing clinically relevant diversity across morphology, viability, proteomic profiles and drug response, this approach provides a foundation for translating spheroid- and proteomics-based assays into personalized therapeutic testing.

These include multiple endocrine neoplasia type 2A (MEN2A), medullary thyroid carcinoma (MTC), Hirschsprung disease, and pheochromocytoma. The existence and use of a database classifying variants in the RET gene plays a fundamental role in molecular diagnostics and personalized medicine.

These results indicate that disabling the CK-pCr energy-buffering system reprograms cellular energetics toward apoptosis and less aggressive phenotypes. Our findings support targeting the CK pathway as a tractable metabolic vulnerability and a rational partner for cytotoxic regimens, with pathway-specific signaling alterations representing downstream consequences of central energetic collapse.

ENO1 and CKB serve as clinically meaningful markers-ENO1 indicating metastatic potential and CKB predicting overall prognosis-while also representing promising therapeutic targets. These findings bridge molecular metabolism-immune crosstalk with clinical outcomes, offering novel perspectives for integrating metabolic intervention and immunotherapy in PCa management.

c-Myb - CKB - N-cadherin axis was identified as pathway regulating OSA cell migration and metastasis.

Our findings suggested that expanded mCAs were significantly associated with all-cause and cause-specific deaths and could serve as a complement to the FI in providing a more comprehensive perspective on mortality risk, especially for cancer mortality.

Our findings suggest that platelet-related CKB may be linked to metastatic potential in lung cancer and represent a previously underrecognized component in cancer-associated biochemical alterations. This study provides novel insights into the non-canonical roles of platelets in cancer biology and highlights CK isoenzyme profiling as a clinically relevant tool for tumor characterization.

In this large-scale prospective cohort study of Chinese adults, we demonstrated that adherence to a healthy lifestyle was significantly associated with a reduced risk of frailty-related cancer. Our findings highlight the importance of integrating healthy lifestyle factors into cancer prevention strategies for frail populations.

Efficacy evidence from case reports spans over 500 genes, 2800 molecular profiles, and 300 tumor types, including several rare cancers and pediatric tumor types. CKB is a powerful resource for leveraging case reports to identify treatment options for patients with rare cancers and oncogenic variants, patients for whom multiple therapies exist, and patients experiencing resistance to first-line therapy.

We also introduced ArGO-LDHA-1, a covalent inhibitor targeting LDHA's hyperreactive arginine residues, showing potential to enhance chemotherapy efficacy. This work highlights the biological significance of arginine residues and provides a platform for large-scale profiling of arginine reactivity.

Lean patients with MASLD have worse liver outcomes and greater risk of all-cause mortality, but similar risk of HCC and extrahepatic cancer, and lower CVD risk.

Here, we demonstrate that CKB is essential for CK enzymatic activity in several cancer cell lines, including NSCLC (H1299), osteosarcoma (143B), and ovarian adenocarcinoma (OVCAR8). Moreover, we demonstrate that CKB promotes metastasis of H1299 cells to the lung and liver in vivo, a process associated with enhanced anoikis resistance.