Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As a broad generalization, there appears to be little intrinsic difference in the biological behaviour of the common malignant liver tumours in respect of presentation, clinical course, clinical features and prognosis. Whatever the tumour's origin, patients present with some combination of abdominal pain, hepatomegaly, weight-loss and general malaise and death occurs within 3 years of the onset of symptoms. It is the state of the non-tumorous liver (cirrhotic/non-cirrhotic) and the anatomical site of the tumour (as with hilar cholangiocarcinomas) that are responsible for any significant differences. Metastatic carcinoid tumours, epithelioid haemangioendotheliomas, stage IV-S neuroblastomas and the fibrolamellar variant of HCC are exceptions to this rule with a genuinely better prognosis.
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PMID:The clinical features and natural history of malignant liver tumours. 303 58

In the present study, repeated hepatic dearterialization combined with intra-arterial infusion chemotherapy was performed in patients with unresectable tumors of the liver. Of 36 patients, 16 had primary liver tumors (13 hepatocellular carcinomas and 3 cholangiocellular carcinomas), while 20 had metastatic tumors (7 gastric carcinomas, 10 colon carcinomas, 2 pancreatic carcinomas, and 1 gastric carcinoid). A significantly better survival outcome was found in those with intra-arterial infusion chemotherapy and those without cirrhosis. In the HCC cases, those with the therapy tended to show a better survival as compared with the natural history. Remarkable tumor regression was found in four (67%) of six patients with metastases of gastric cancer.
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PMID:[Efficacy of repeated hepatic dearterialization combined with intra-arterial infusion chemotherapy for unresectable tumors of the liver]. 757 66

The use of helical CT, infusing pump and non-ionic contrast media has enabled the evaluation of different hepatic circulatory phases during contrast injection. Starting the acquisition of scans 20 to 30 seconds after the injection at a rate of 3 to 4 ml/sec the arterial enhancing of the liver is depicted. THROMBOSIS OR COMPRESSION OF THE PORTAL VEIN: Hypervascular triangle-shaped was with peripheral base can be seen, secondary to the increased arterial flow to compensate for the diminished portal flow. ARTERIOPORTAL SHUNTS: This condition can be caused by tumors such hepatocellular adenocarcinomas and hemangiomas, trauma, interventional procedures, cirrhosis, AVMs and surgery. INFLAMMATORY LESIONS: Hypervascular areas can be seen during the arterial phase in abscesses or cholecystitis, returning to their normal condition in the arterial phase. ANATOMIC VARIANTS: Third veins coming from the periphery (capsular veins, accessory cystic vein and an aberrant gastric vein) supply enhanced blood earlier than the portal circulation. OTHER CAUSES: In liver cirrhosis diffuse hyperattenuated areas can be seen during the arterial circulation. In right-sided heart failure, pericardial disease and Budd-Chiari Syndrome, "mosaic areas" can also be noted. In other patients these perfusion disorders were considered unknown. TUMORS: The well-differentiated hepatocellular carcinoma is a lesion with a predominant arterial blood supply, thus appearing in general hyperdense in this phase. Hemangiomas may appear as highly hyperdense lesions in the arterial phase and can be misinterpreted as HCC if smaller than 2 cm. (30% of cases). Focal nodular hyperplasia is a benign lesion (vascular malformation associated with focal nodules of hepatocellular hyperplasia) with increased arterial blood supply. Hepatic adenomas show an important hypervascularity during the arterial phase and, if large, they may present a small central scar and or capsule. Low or high-grade dysplastic nodules can sometimes be seen as hypervascular areas during the arterial phase. Although most metastasis are depicted as hypodense lesions sometimes they can show arterial hypervascularity such as carcinoid and pancreatic islet cell metastasis.
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PMID:[Liver hyperdensity during arterial phase on CT exams]. 1147 23

Atiprimod is a novel anticancer and antiangiogenic drug candidate which is currently being evaluated in patients with liver carcinoid and multiple myeloma. In this study, we report that atiprimod selectively inhibited proliferation and induced apoptosis in HCC cells that expressed either hepatitis B virus (HBV) or hepatitis C virus, through deactivation of protein kinase B (Akt) and signal transducers and activators of transcription 3 (STAT3) signaling. In HepG2 AD38 cells, which express HBV genome under the control of a tetracycline-off promoter, both Akt and STAT3 were constitutively activated in response to HBV expression. However, this constitutive activation was not sensitive to lamivudine, a drug that inhibits HBV replication without affecting its gene expression, suggesting that HBV replication per se might not be responsible for the activation. Interestingly, the electrophoretic mobility of p-STAT3 protein bands on immunoblot was slower when AD38 cells were cultured in the absence of tetracycline, suggesting a differential phosphorylation in response to HBV expression. In HCC cells, interleukin 6 stimulates the phosphorylation of STAT3 both at serine 727 and at tyrosine 705 positions. The interleukin 6-stimulated activation of STAT3 and Akt was inhibited not only by atiprimod but also by LY294002, a phosphoinositide-3-kinase-specific inhibitor, and by NS398, a cyclooxygenase-2-selective inhibitor. The combination of these compounds did not produce any additive effect, implying that the mechanisms by which HBV activates Akt and STAT3 might also involve phosphoinositide-3-kinase and cyclooxygenase-2. Collectively, these results suggest that atiprimod could be useful as a multifunctional drug candidate for the treatment of HCC in humans.
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PMID:Deactivation of Akt and STAT3 signaling promotes apoptosis, inhibits proliferation, and enhances the sensitivity of hepatocellular carcinoma cells to an anticancer agent, Atiprimod. 1723 71

A 60-year-old woman was admitted to our hospital because of upper abdominal discomfort and body weight loss. Abdominal CT showed multiple liver tumors with early enhancement and delayed washout. There were no abnormal findings in other organs. IVR-CT showed hypervascular masses, but it is not a typical tumor staining of HCC. To obtain the diagnosis, we performed laparoscopic partial liver resection in the left lateral segment. Histological examination suggested a primary hepatic carcinoid a tumor. But primary hepatic carcinoid tumor is comparatively rare, so we underwent further examinations. Two months later after the liver resection, the tumor of pancreatic tail was detected by CT and MRI. We could obtain the diagnosis of pancreatic endocrine tumor by EUS-FNA. We conducted a distal pancreatectomy with splenectomy and partial colonic resection. She had no symptom related to neuroendocrinology. The final diagnosis was non-functional endocrine carcinoma of pancreas. After that, we added extended right hepatic lobectomy with radiofrequency ablation in left lobe. The woman remains alive without a recurrence after the surgery.
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PMID:[Non-functional pancreatic endocrine carcinoma with multiple liver metastases--a case report]. 2122 76