Showing posts with label tumorigenisis. Show all posts
Showing posts with label tumorigenisis. Show all posts

June 11, 2013

Menin -today's growth promoter, tomorrow's tumor suppressor

Elucidating the Role of Menin During Islet Cell Development in the Human Fetal Pancreas
-Dubrick, Jessica L., (2013).  
University of Western Ontario - Electronic Thesis and Dissertation Repository. Paper 1287.
http://ir.lib.uwo.ca/etd/1287

editor's notes:

Menin functions as a tumor suppressor in adult endocrine cells, but in the fetal pancreas promotes cell survival and proliferation.  At first glance these roles seem very different, almost opposite.  But are they really opposed?

If menin promotes the proliferation of healthy pancreas cells -in particular, cells with at least one functional MEN1 gene- then it would seem that these cells will proliferate faster than those unable to produce menin.  So, cells that are unable to produce menin will represent a decreasing fraction of the cell population. Therefore, even during fetal development, menin's role as a growth promoter offers a tumor suppressive advantage to the developing pancreas, by reducing the percentage of cells that later may pose a tumorigenic risk due to their inability to express menin.

Unless I've got that wrong.

May 29, 2012

DNA - A Graphic Guide to the Molecule that Shook the World

DNA - A Graphic Guide to the Molecule that Shook the World
-Rosenfield I, et al. 2011 Columbia University Press. ISBN 978-0-231-14270-0
  • Don't let the 'comic book' design of this book fool You. This book is a great introduction to DNA and genetics! It's well written -even fun- and it has been extremely helpful in learning the basics of DNA structure, gene transcription, and more. Recommended.

Genome-Wide Analysis of Menin Binding Provides Insights into MEN1 Tumorigenisis

Genome-Wide Analysis of Menin Binding Provides Insights into MEN1 Tumorigenisis -Scacheri, et al. PLoS Genet. 2006 April; 2(4): e51.
  • menin functions as a general regulator of transcription.
  • HLXB9 is overexpressed in islets in the absence of menin.