Two cases (one nodule-in-nodule case and another case with closely attached HCC and HGDN) showed several overlapped driver mutations (CTNNB1 and CEBPA) and CNAs (losses of CDKN2A, RB1, and TP53) between HGDNs and HCCs, suggesting their roles in the early HCC development.
Mutations in ERBB2 and CCND1, and CNAs (gains of CTNNB1, MET, and SMO and losses of PTEN, TP53, and SETD2) were identified as "HCC predominant," suggesting their roles in the progression of HGDN to HCC.
Two cases (one nodule-in-nodule case and another case with closely attached HCC and HGDN) showed several overlapped driver mutations (CTNNB1 and CEBPA) and CNAs (losses of CDKN2A, RB1, and TP53) between HGDNs and HCCs, suggesting their roles in the early HCC development.
Two cases (one nodule-in-nodule case and another case with closely attached HCC and HGDN) showed several overlapped driver mutations (CTNNB1 and CEBPA) and CNAs (losses of CDKN2A, RB1, and TP53) between HGDNs and HCCs, suggesting their roles in the early HCC development.
Mutations in ERBB2 and CCND1, and CNAs (gains of CTNNB1, MET, and SMO and losses of PTEN, TP53, and SETD2) were identified as "HCC predominant," suggesting their roles in the progression of HGDN to HCC.
Mutations in ERBB2 and CCND1, and CNAs (gains of CTNNB1, MET, and SMO and losses of PTEN, TP53, and SETD2) were identified as "HCC predominant," suggesting their roles in the progression of HGDN to HCC.
Mutations in ERBB2 and CCND1, and CNAs (gains of CTNNB1, MET, and SMO and losses of PTEN, TP53, and SETD2) were identified as "HCC predominant," suggesting their roles in the progression of HGDN to HCC.