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[New molecular targets in pancreatic cancer].
Bull Cancer 2008; 95(5):503-12BC

Abstract

The understanding of the biology of pancreatic carcinoma has greatly benefited from studies of genetic alterations and molecular expression in experimental models as well as in pre-cancerous and cancerous tissues by mean of molecular amplification and large scale transcriptome analysis. P16, TP53, DPC4/Smad4 tumor suppressor pathways are genetically inactivated in the majority of pancreatic carcinomas, whereas oncogenic k-ras is activated. The activating mutation of the K-ras oncogene on codon 12 seems to occur early in pancreatic carcinogenesis and detecting its mutation in tumor samples could have a clinical relevance in term of positive (improvement of current histological diagnosis) and differential diagnosis (versus chronic pancreatitis) of pancreatic cancer. At a late stage of tumor development, an increase of telomerase activity, an over expression of growth factors and/or their receptors (EGF, nerve growth factor, gastrin, bombesin), of proangiogenic factors (VEGF, FGF, PDGF), of invasiveness factors (metalloproteinases, E-cadherin, beta integrin, urokinase and tissue plasminogen activator) occur. All these molecular events contribute to the progression and to the metastatic potential of this carcinoma. New markers and targets are currently studied among microRNA and epigenetics events such as methylation and acetylation. Among all these molecular markers, some are now tested for their potential clinical interest in term of diagnosis or therapeutic target.

Authors+Show Affiliations

Inserm U858, Institut de médecine moléculaire et Service de gastro-entérologie et nutrition, CHU Rangueil, TSA 50032, 31059 Toulouse Cedex 9.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

fre

PubMed ID

18541514

Citation

Torrisani, Jérôme, et al. "[New Molecular Targets in Pancreatic Cancer]." Bulletin Du Cancer, vol. 95, no. 5, 2008, pp. 503-12.
Torrisani J, Bournet B, Cordelier P, et al. [New molecular targets in pancreatic cancer]. Bull Cancer. 2008;95(5):503-12.
Torrisani, J., Bournet, B., Cordelier, P., & Buscail, L. (2008). [New molecular targets in pancreatic cancer]. Bulletin Du Cancer, 95(5), pp. 503-12. doi:10.1684/bdc.2008.0632.
Torrisani J, et al. [New Molecular Targets in Pancreatic Cancer]. Bull Cancer. 2008;95(5):503-12. PubMed PMID: 18541514.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [New molecular targets in pancreatic cancer]. AU - Torrisani,Jérôme, AU - Bournet,Barbara, AU - Cordelier,Pierre, AU - Buscail,Louis, PY - 2007/10/29/received PY - 2008/02/11/accepted PY - 2008/6/11/pubmed PY - 2008/7/17/medline PY - 2008/6/11/entrez SP - 503 EP - 12 JF - Bulletin du cancer JO - Bull Cancer VL - 95 IS - 5 N2 - The understanding of the biology of pancreatic carcinoma has greatly benefited from studies of genetic alterations and molecular expression in experimental models as well as in pre-cancerous and cancerous tissues by mean of molecular amplification and large scale transcriptome analysis. P16, TP53, DPC4/Smad4 tumor suppressor pathways are genetically inactivated in the majority of pancreatic carcinomas, whereas oncogenic k-ras is activated. The activating mutation of the K-ras oncogene on codon 12 seems to occur early in pancreatic carcinogenesis and detecting its mutation in tumor samples could have a clinical relevance in term of positive (improvement of current histological diagnosis) and differential diagnosis (versus chronic pancreatitis) of pancreatic cancer. At a late stage of tumor development, an increase of telomerase activity, an over expression of growth factors and/or their receptors (EGF, nerve growth factor, gastrin, bombesin), of proangiogenic factors (VEGF, FGF, PDGF), of invasiveness factors (metalloproteinases, E-cadherin, beta integrin, urokinase and tissue plasminogen activator) occur. All these molecular events contribute to the progression and to the metastatic potential of this carcinoma. New markers and targets are currently studied among microRNA and epigenetics events such as methylation and acetylation. Among all these molecular markers, some are now tested for their potential clinical interest in term of diagnosis or therapeutic target. SN - 1769-6917 UR - https://www.unboundmedicine.com/medline/citation/18541514/[New_molecular_targets_in_pancreatic_cancer]_ L2 - http://www.jle.com/medline.md?issn=0007-4551&vol=95&iss=5&page=503 DB - PRIME DP - Unbound Medicine ER -