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Knowledge of the genomic alterations of hepatocellular carcinomas (HCC) has significantly contributed to the understanding of the disease pathogenesis and provides the basis for personalized medicine (1). However, it is still a major challenge to translate this information into molecularly plausible and clinically safe therapeutic targets. Specifically, one of the most frequent mutations in HCC affects CTNNB1, encoding β-catenin, and results in an aberrant activation of the Wnt/β-catenin signalling (1). This article is protected by copyright. All rights reserved.
This article was published in the following journal.
Name: Hepatology (Baltimore, Md.)
Hepatocellular carcinomas (HCCs) are known to be highly heterogenous. Within the extensive histopathological and molecular heterogeneity of HCC, tumors with mutations in CTNNB1, encoding β-catenin, (...
CTNNB1, encoding β-catenin, is frequently mutated in hepatocellular carcinoma, the most rapidly growing solid cancer in the US, and activating mutations in this gene are associated with increased exp...
Whilst effects of anti-cancer drugs have been thoroughly explored, little is known about the repercussion of drug cessation. However, this has important clinical relevance since several clinical proto...
The mechanistic target of rapamycin (mTOR) pathway coordinates organismal growth and homeostasis in response to growth factors, nutrients, and cellular energy stage. The pathway regulates several majo...
The objective of our study was to prospectively evaluate the feasibility, safety, and effectiveness of 1-T open MRI-guided percutaneous cryoablation of hepatic dome hepatocellular carcinomas (HCCs).
This study is to determine the maximum tolerated dose and the recommended 188Re-SSS Lipiodol activity for hepatic intra-arterial injection in patients with hepato-cellular carcinoma. The n...
An unmet medical need exists for the successful therapy of patients with advanced hepatocellular and biliary tract malignances, with few and short lived disease responses to chemotherapy f...
Retrospective Study in Patients With Metastatic Renal Cancer Treated With TKI Sequence (Tyrosine Kinase Inhibitors of VEGFR) - mTOR- Axitinib Inhibitors or Anti-VEGF Antibody -Inhibiteurs mTOR - Axitinib
Describe in patients with metastatic kidney cancer treatment modalities with the type sequences: TKI - mTORi - Axitinib or VEGF mAb - mTORi - Axitinib.
After the second protocol amendment two study arms are evaluated in this clinical protocol: PD-0325901 (oral MEK inhibitor) plus PF-05212384 (intravenous PI3K/mTOR inhibitor) and PF-052123...
The purpose of this study is to determine the maximal tolerated dose of idarubicin for chemoembolization of non resectable non metastatic hepatocellular carcinoma.
An adaptor protein, consisting of seven WD REPEATS along its length, that functions as a component of the MECHANISTIC TARGET OF RAPAMYCIN COMPLEX 1 and MTORC2 COMPLEX. It interacts directly with MTOR to enhance its kinase activity and stabilizes the MTOR-RPTOR PROTEIN interaction in nutrient-poor conditions, favoring RPTOR inhibition of MTOR activity.
A carcinoma composed mainly of epithelial elements with little or no stroma. Medullary carcinomas of the breast constitute 5%-7% of all mammary carcinomas; medullary carcinomas of the thyroid comprise 3%-10% of all thyroid malignancies. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1141; Segen, Dictionary of Modern Medicine, 1992)
Drugs that mimic the effects of parasympathetic nervous system activity. Included here are drugs that directly stimulate muscarinic receptors and drugs that potentiate cholinergic activity, usually by slowing the breakdown of acetylcholine (CHOLINESTERASE INHIBITORS). Drugs that stimulate both sympathetic and parasympathetic postganglionic neurons (GANGLIONIC STIMULANTS) are not included here.
Drugs that inhibit the transport of neurotransmitters into axon terminals or into storage vesicles within terminals. For many transmitters, uptake determines the time course of transmitter action so inhibiting uptake prolongs the activity of the transmitter. Blocking uptake may also deplete available transmitter stores. Many clinically important drugs are uptake inhibitors although the indirect reactions of the brain rather than the acute block of uptake itself is often responsible for the therapeutic effects.
Compounds and drugs that inhibit or block the activity of CATECHOL O-METHYLTRANSFERASE enzymes. Drugs in this class are used in management of central nervous system disorders such as PARKINSON DISEASE.