Abstract Objectives Clinical documentation consumes substantial clinician time, potentially detracting from patient care. Generative artificial intelligence (AI) may support drafting discharge summaries and patient referral documents, but feasibility in non-Western-language oncology settings using real-world electronic health record (EHR) data remains insufficiently evaluated. This study assessed feasibility in a Japanese cancer hospital using an enterprise AI system. Methods Medical records from 61 consenting adult patients at Chiba Cancer Center were analyzed. Although the plan aimed at comprehensive EHR data, actual input was limited to extractable text (physician notes, nursing records); structured laboratory data and imaging, endoscopy, and pathology reports were not directly used, and existing summaries and external referrals were excluded to avoid information leakage. Data were converted to JavaScript Object Notation; GaiXer generated 31 discharge summaries and 30 referral documents. Four evaluators scored them; ≥80/100 was an exploratory threshold for draft-level practical utility. Feedback drove one refinement cycle. Results Generated documents scored approximately 60 to 70. A score ≥80 was reached by 9 of 31 discharge summaries in each evaluation; for referrals, none reached the threshold initially, whereas 5 of 30 did after refinement. Discharge summary scores did not substantially improve; referral scores did. Raw percent agreement among three nonphysician evaluators was high, although chance-corrected agreement varied. Wilcoxon signed-rank tests showed no significant change for discharge summaries ( p = 0.866) but significant improvement for referrals ( p = 0.006). Conclusion This feasibility study suggests AI may support drafting these documents in a secure environment using real-world Japanese EHR data, although the generated documents did not consistently reach the predefined threshold for draft-level utility. Findings should not be interpreted as demonstrating workload reduction or maximum performance under ideal data conditions. Future studies should evaluate larger datasets, multiple institutions and models, blinded evaluations, actual editing time, clinician acceptance, and workflow impact.
N. Michihata, Hiroshi Ishii, H. Tsujimura et al.· Applied Clinical Informatics· 0 citations
MYCN is a key oncogenic driver in hepatocellular carcinoma (HCC) and a therapeutic challenge due to the historical undruggability of MYC transcription factors (TFs). Using a high-throughput MYCN promoter-luciferase reporter, we identified PhiKan 083 (PK83), a small molecule previously recognized as a mutant p53 activator, that dose-dependently suppresses MYCN expression in HCC cells. PK83 impaired the proliferation and survival of MYCN-high HCC cells, inducing DNA damage, apoptosis, and loss of clonogenic and spheroid growth potential, while sparing MYCN-low HCC cells and normal hepatocytes. Structure-activity analysis revealed that polar, hydrogen-bond-capable substituents on PK83's tricyclic scaffold are critical for its activity. Although PK83 broadly activates p53 signaling, its cytotoxicity in MYCN-high cells is not strictly dependent on intact p53, as confirmed in p53-knockout systems. Transcriptome profiling and pathway analysis demonstrated robust suppression of MYC/MYCN targets along with modulation of pathways linked to stress, differentiation, and metabolism. In primary HCC tumors, PK83-downregulated TFs, including oncogenic TFs ZMIZ1 and TARBP1, positively correlated with MYCN, whereas upregulated stress-responsive TFs ATF3 and FOSL2 showed a negative correlation. These findings suggest that PK83 suppresses MYCN expression and preferentially affects MYCN-high HCC cells in a p53-independent manner, warranting further preclinical investigation of PK83 and related compounds in MYCN-associated cancers.