Hepatic metastases have variable appearances depending on the primary tumor and are characterized Raf inhibitor as hypervascular or hypovascular, enhancing more or less than surrounding parenchyma (Fig. 7). Hypervascular metastases are seen with neuroendocrine tumors, renal cell carcinoma, thyroid carcinoma, melanoma, and sarcoma. Metastases from other primaries tend to be hypovascular. Internal hemorrhage may occur with metastases from renal cell carcinoma, melanoma, and lung cancer, often demonstrating

T1 hyperintensity (Fig. 8). Hepatobiliary imaging with Eovist and DWI can be useful for detection of small hepatic metastases, demonstrating improved sensitivity over traditional MRI and CT.17-22, 85, 86 MRI is a highly specific and accurate modality for FLL characterization. An experienced MR radiologist is essential to maintain high-quality Y27632 liver MR protocols, determine appropriate indications for hepatocyte versus extracellular contrast agents, and guide management. Although many hepatic lesions have characteristic imaging features, consideration of the clinical context, in particular the presence or absence of underlying liver disease when considering

HCC or ICC, is essential to confidently diagnose and direct management in these patients. “
“During liver development and regeneration, hepatocytes undergo rapid cell division and face an increased risk of DNA damage associated with active DNA replication. The mechanism that protects proliferating hepatocytes from replication-induced DNA damage remains unclear. Nucleostemin (NS) is known to be up-regulated during liver regeneration, and loss of NS is associated with increased DNA damage in cancer cells. To determine whether NS is involved in protecting the genome integrity of proliferating hepatocytes, we created an albumin promoter-driven NS conditional-null (albNScko) mouse model. Livers of albNScko mice begin to show loss of NS in developing Inositol monophosphatase 1 hepatocytes from the first postnatal week and increased DNA damage and hepatocellular injury at 1-2 weeks of age. At 3-4 weeks, albNScko

livers develop bile duct hyperplasia and show increased apoptotic cells, necrosis, regenerative nodules, and evidence suggestive of hepatic stem/progenitor cell activation. CCl4 treatment enhances degeneration and DNA damage in NS-deleted hepatocytes and increases biliary hyperplasia and A6+ cells in albNScko livers. After 70% partial hepatectomy, albNScko livers show increased DNA damage in parallel with a blunted and prolonged regenerative response. The DNA damage in NS-depleted hepatocytes is explained by the impaired recruitment of a core DNA repair enzyme, RAD51, to replication-induced DNA damage foci. Conclusion: This work reveals a novel genome-protective role of NS in developing and regenerating hepatocytes.