Coordinatore | ISTITUTO NAZIONALE TUMORI Fondazione Pascale
Organization address
address: Via Mariano Semmola 142 contact info |
Nazionalità Coordinatore | Italy [IT] |
Totale costo | 100˙000 € |
EC contributo | 100˙000 € |
Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | FP7-PEOPLE-2009-RG |
Funding Scheme | MC-IRG |
Anno di inizio | 2011 |
Periodo (anno-mese-giorno) | 2011-01-01 - 2014-12-31 |
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ISTITUTO NAZIONALE TUMORI Fondazione Pascale
Organization address
address: Via Mariano Semmola 142 contact info |
IT (NAPOLI) | coordinator | 100˙000.00 |
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'Many genes that have been shown to cause cancer were originally identified because of their role in embryonic development and in the postnatal control of cell growth and differentiation. The similarities between cancer and development are evident on many levels. Microscopically, cancerous tissues frequently appear as undifferentiated masses, with some tumor types exhibiting embryonic tissue organization. The increased mobility of cancer cells, leading to local invasion or metastasis, is reminiscent of the migratory behavior of cells during development. We aim to have deeper tumor biology knowledge through gene regulatory network (GRN) models. We consider the characterization of GRNs of tissue specific progenitor/stem cells as a paramount to our understanding of cancerogenesis in colon, lung, and pharynx (CLP) tumor cells. This research proposal underlies the hypothesis that some cancer cells are closely related to progenitor cell of respective tissue, therefore the tumor drug selection should resemble proper stem/progenitor cell differentiation signaling pathway perturbation. We believe that such tumor-customized drug treatment will be more successful, it will shed light on the comprehension of drug effect overall. Moreover it will highlight new aspects of developmental and cancer biology mechanisms. We will use spheroid in vitro model and moreover we will adopt mouse model to validate in vitro data. The predicted outcome of this research is the identification of novel gene regulatory interactions that will be investigated for their roles in carcinogenetic tissues.'
A European study is pursuing an interesting approach to investigating cancer progression. They are researching various compounds that induce differentiation in normal cells and wish to apply the same approach in cancer therapy.
Cancer presents several similarities with developmental processes. At the microscopic level, tumour masses often appear as undifferentiated cells with some exhibiting embryonic tissue organization. The migratory and invasive phenotype of cancer cells resembles regular cell movement during development.
This has led scientists of the EU-funded 'Resveratrol-induced molecular markers in cancer and progenitor cells proliferation' (RESVERATROL ROLES) project to investigate the process of organogenesis. Their hypothesis is that understanding the homeostatic balance among progenitor cells and those driven to differentiate, could help address clinical problems such as cancer. Although, cancer cells possess common features with progenitor cells of the tissue of origin, scientists believe they have a perturbed differentiation signalling pathway. To understand carcinogenesis, researchers will characterise gene regulatory networks (GRNs) in tissue-specific stem cells.
From a clinical perspective, the RESVERATROL ROLES study aims to improve cancer treatment by studying natural and chemical substances that increase cellular differentiation. Among others, the effect of the plant-derived phenolic compound resveratrol is being tested for its ability to induce tumour cell differentiation.
The RESVERATROL ROLES project envisages an approach for tumour classification based on similarities to normal tissue progenitor cells. By employing differentiation criteria to select the most suitable drug, researchers are hopeful that drug efficacy will improve while reducing non-specific toxicity.