A májsejtrák célzott kezelésének újabb lehetoségei a molekuláris biológiai adatok ismeretében

Translated title of the contribution: New possibilities of targeted therapy in the treatment of hepatocellular carcinoma in view of molecular biology

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Hepatocellular carcinoma (HCC) has a poor prognosis. Approximately 85% of patients are not candidates for curative treatments at the time of diagnosis; hence palliative modalities (transcatheter arterial chemoembolisation, radiofrequency ablation, systemic chemotherapy) are used. Systemic chemotherapies have disappointing results. The increasing knowledge in the molecular biology of HCC will increase the possibilities of targeted therapy. The multi-tyrosine kinase inhibitor sorafenib is the only drug which has approved. The VEGF-inhibitors (bevacizumab, sunitinib), EGFR-blocker agents (erlotinib), as well as the inhibition of mTOR (rapamycin) are promising. Combination of sorafenib or other anti-angiogenic agents with local ablative procedure (transcatheter arterial chemoembolisation, radiofrequency ablation), or with curative hepatectomy also can be favorable. Alteration of Wnt pathway, retinoid compounds, inhibition of the cell cycle as well as the proteosome, and epigenetic therapy can be other potential promising targets in HCC.

Original languageHungarian
Pages (from-to)1763-1768
Number of pages6
JournalOrvosi Hetilap
Volume151
Issue number43
DOIs
Publication statusPublished - Oct 1 2010

Fingerprint

Molecular Biology
Hepatocellular Carcinoma
Drug Therapy
Wnt Signaling Pathway
Retinoids
Hepatectomy
Sirolimus
Epigenomics
Protein-Tyrosine Kinases
Vascular Endothelial Growth Factor A
Cell Cycle
Therapeutics
Pharmaceutical Preparations
sorafenib
sunitinib
Erlotinib Hydrochloride
Bevacizumab

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A májsejtrák célzott kezelésének újabb lehetoségei a molekuláris biológiai adatok ismeretében. / Hagymási, K.; Tulassay, Z.

In: Orvosi Hetilap, Vol. 151, No. 43, 01.10.2010, p. 1763-1768.

Research output: Contribution to journalArticle

@article{b6b4c453dafe4dcba813c69756f13496,
title = "A m{\'a}jsejtr{\'a}k c{\'e}lzott kezel{\'e}s{\'e}nek {\'u}jabb lehetos{\'e}gei a molekul{\'a}ris biol{\'o}giai adatok ismeret{\'e}ben",
abstract = "Hepatocellular carcinoma (HCC) has a poor prognosis. Approximately 85{\%} of patients are not candidates for curative treatments at the time of diagnosis; hence palliative modalities (transcatheter arterial chemoembolisation, radiofrequency ablation, systemic chemotherapy) are used. Systemic chemotherapies have disappointing results. The increasing knowledge in the molecular biology of HCC will increase the possibilities of targeted therapy. The multi-tyrosine kinase inhibitor sorafenib is the only drug which has approved. The VEGF-inhibitors (bevacizumab, sunitinib), EGFR-blocker agents (erlotinib), as well as the inhibition of mTOR (rapamycin) are promising. Combination of sorafenib or other anti-angiogenic agents with local ablative procedure (transcatheter arterial chemoembolisation, radiofrequency ablation), or with curative hepatectomy also can be favorable. Alteration of Wnt pathway, retinoid compounds, inhibition of the cell cycle as well as the proteosome, and epigenetic therapy can be other potential promising targets in HCC.",
keywords = "EGRF-inhibition, hepatocellular carcinoma, molecular biology, mTOR inhibitors, sorafenib, targeted therapy, VEGF-inhibition",
author = "K. Hagym{\'a}si and Z. Tulassay",
year = "2010",
month = "10",
day = "1",
doi = "10.1556/OH.2010.28984",
language = "Hungarian",
volume = "151",
pages = "1763--1768",
journal = "Orvosi Hetilap",
issn = "0030-6002",
publisher = "Akademiai Kiado",
number = "43",

}

TY - JOUR

T1 - A májsejtrák célzott kezelésének újabb lehetoségei a molekuláris biológiai adatok ismeretében

AU - Hagymási, K.

AU - Tulassay, Z.

PY - 2010/10/1

Y1 - 2010/10/1

N2 - Hepatocellular carcinoma (HCC) has a poor prognosis. Approximately 85% of patients are not candidates for curative treatments at the time of diagnosis; hence palliative modalities (transcatheter arterial chemoembolisation, radiofrequency ablation, systemic chemotherapy) are used. Systemic chemotherapies have disappointing results. The increasing knowledge in the molecular biology of HCC will increase the possibilities of targeted therapy. The multi-tyrosine kinase inhibitor sorafenib is the only drug which has approved. The VEGF-inhibitors (bevacizumab, sunitinib), EGFR-blocker agents (erlotinib), as well as the inhibition of mTOR (rapamycin) are promising. Combination of sorafenib or other anti-angiogenic agents with local ablative procedure (transcatheter arterial chemoembolisation, radiofrequency ablation), or with curative hepatectomy also can be favorable. Alteration of Wnt pathway, retinoid compounds, inhibition of the cell cycle as well as the proteosome, and epigenetic therapy can be other potential promising targets in HCC.

AB - Hepatocellular carcinoma (HCC) has a poor prognosis. Approximately 85% of patients are not candidates for curative treatments at the time of diagnosis; hence palliative modalities (transcatheter arterial chemoembolisation, radiofrequency ablation, systemic chemotherapy) are used. Systemic chemotherapies have disappointing results. The increasing knowledge in the molecular biology of HCC will increase the possibilities of targeted therapy. The multi-tyrosine kinase inhibitor sorafenib is the only drug which has approved. The VEGF-inhibitors (bevacizumab, sunitinib), EGFR-blocker agents (erlotinib), as well as the inhibition of mTOR (rapamycin) are promising. Combination of sorafenib or other anti-angiogenic agents with local ablative procedure (transcatheter arterial chemoembolisation, radiofrequency ablation), or with curative hepatectomy also can be favorable. Alteration of Wnt pathway, retinoid compounds, inhibition of the cell cycle as well as the proteosome, and epigenetic therapy can be other potential promising targets in HCC.

KW - EGRF-inhibition

KW - hepatocellular carcinoma

KW - molecular biology

KW - mTOR inhibitors

KW - sorafenib

KW - targeted therapy

KW - VEGF-inhibition

UR - http://www.scopus.com/inward/record.url?scp=77957977057&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957977057&partnerID=8YFLogxK

U2 - 10.1556/OH.2010.28984

DO - 10.1556/OH.2010.28984

M3 - Article

C2 - 20940115

AN - SCOPUS:77957977057

VL - 151

SP - 1763

EP - 1768

JO - Orvosi Hetilap

JF - Orvosi Hetilap

SN - 0030-6002

IS - 43

ER -