Retinoic acid (RA), the principal biologically active retinoid, is essential for normal differentiation of a wide variety of cell types. Vitamin A deficiency predisposes to certain cancers and it has since been discovered that retinoids display antitumorigenic activity in many models. Keratinocytes with a null mutation in the RARgamma and RARalphagamma genes are predisposed to tumorigenesis in vivo. This outcome is reversed by the re-introduction of a functional RAR, suggesting that some retinoid-target gene(s) are implicated in tumour formation in this model. Suppressive subtractive hybridization techniques have been used to isolate RA-responsive genes no longer regulated in RAR-null keratinocytes. This work led to the cloning of gas3, a member of the growth arrest-specific gene family. Our studies have demonstrated that gas3 expression is regulated by RA and is greatly reduced following tumor promotion, indicating that this gene could potentially inhibit epidermal tumorigenesis elicited by retinoids.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.82267 |
| Date | January 2005 |
| Creators | Laforest, Brigitte |
| Publisher | McGill University |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Format | application/pdf |
| Coverage | Master of Science (Division of Experimental Medicine.) |
| Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
| Relation | alephsysno: 002201574, proquestno: AAIMR12478, Theses scanned by UMI/ProQuest. |
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