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      Chemotherapeutic Agents for the Treatment of Hepatocellular Carcinoma: Efficacy and Mode of Action

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          Abstract

          Hepatocellular carcinoma (HCC) is a dreaded malignancy that every year causes half a million deaths worldwide. Being an aggressive cancer, its incidence exceeds 700,000 new cases per year worldwide with a median survival of 6-8 months. Despite advances in prognosis and early detection, effective HCC chemoprevention or treatment strategies are still lacking, therefore its dismal survival rate remains largely unchanged. This review will characterize currently available chemotherapeutic drugs used in the treatment of HCC. The respective mode(s) of action, side effects and recommendations will be also described for each drug.

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          Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins.

          Shona Kerr, I Kerr, G Stark … (1994)
          Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.
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            Structure, Recognition, and Processing of Cisplatin-DNA Adducts.

            Elizabeth Jamieson, Stephen Lippard (1999)
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              The role of signaling pathways in the development and treatment of hepatocellular carcinoma.

              S. Whittaker, R Marais, A X Zhu (2010)
              Hepatocellular carcinoma (HCC) is a highly prevalent, treatment-resistant malignancy with a multifaceted molecular pathogenesis. Current evidence indicates that during hepatocarcinogenesis, two main pathogenic mechanisms prevail: (1) cirrhosis associated with hepatic regeneration after tissue damage caused by hepatitis infection, toxins (for example, alcohol or aflatoxin) or metabolic influences, and (2) mutations occurring in single or multiple oncogenes or tumor suppressor genes. Both mechanisms have been linked with alterations in several important cellular signaling pathways. These pathways are of interest from a therapeutic perspective, because targeting them may help to reverse, delay or prevent tumorigenesis. In this review, we explore some of the major pathways implicated in HCC. These include the RAF/MEK/ERK pathway, phosphatidylinositol-3 kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway, WNT/beta-catenin pathway, insulin-like growth factor pathway, hepatocyte growth factor/c-MET pathway and growth factor-regulated angiogenic signaling. We focus on the role of these pathways in hepatocarcinogenesis, how they are altered, and the consequences of these abnormalities. In addition, we also review the latest preclinical and clinical data on the rationally designed targeted agents that are now being directed against these pathways, with early evidence of success.
              Article 0 comments Cited 279 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Rev
                Journal ID (iso-abbrev): Oncol Rev
                Journal ID (publisher-id): OR
                Title: Oncology Reviews
                Publisher: PAGEPress Publications, Pavia, Italy
                ISSN (Print): 1970-5565
                ISSN (Electronic): 1970-5557
                Publication date (Electronic): 28 May 2014
                Publication date Collection: 17 March 2014
                Volume: 8
                Issue: 1
                Electronic Location Identifier: 246
                Affiliations
                [1 ]Department of Chemistry, Mansoura University , Egypt
                [2 ]Department of Biochemistry, Mansoura University , Egypt
                [3 ]Department of Zoology, Mansoura University , Egypt
                [4 ]Department of Botany, Mansoura University , Egypt
                Author notes
                Department of Biochemistry, Faculty of Science, Mansoura University, El-Gomhorya Street, 35516 Mansoura, Egypt. 0020.1018933660 - 0020.502.397900. amrbiochem@ 123456googlemail.com ; amrnigm@ 123456mans.edu.eg

                Contributions: the authors contributed equally to this work.

                Conflict of interests: the authors declare no potential no conflict of interests.

                Article
                DOI: 10.4081/oncol.2014.246
                PMC ID: 4419609
                PubMed ID: 25992234
                SO-VID: ba3a4448-a20a-4ff0-814a-cf82e4f5d412
                Copyright © ©Copyright S. Shaaban et al.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 04 February 2014
                Date accepted : 06 March 2014
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 151, Pages: 11
                Categories
                Subject: Review

                Keywords: liver cancer,hepatocellular carcinoma,molecular therapies,chemoresistance
                Data availability:
                Keywords: liver cancer, hepatocellular carcinoma, molecular therapies, chemoresistance

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