BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Talks.cam//talks.cam.ac.uk//
X-WR-CALNAME:Talks.cam
BEGIN:VEVENT
SUMMARY:Origin and Transformation of T Cell Progenitors - Professor Hans-R
 eimer Rodewald\, German Cancer Research Center\, Heidelberg
DTSTART:20111130T123000Z
DTEND:20111130T133000Z
UID:TALK32557@talks.cam.ac.uk
CONTACT:Sue Griffin
DESCRIPTION:We mapped the origin of the majority of T cell progenitors in 
 the thymus to an interleukin 7 receptor (Il7r)-expressing progenitor\, con
 sistent with a lymphoid-primed route from bone marrow to thymus. Most of t
 hese T cell progenitors lacked myeloid potential in vivo\, which argues ag
 ainst the recent notion that T cells and myeloid cells in the thymus share
  a common progenitor. \n\nBy contrast\, using a T cell-biased Cre-deleter\
 , we found that Notch1-deficient T cell progenitors were blocked in their 
 T cell development\, and gave rise to B cells as well as conventional and 
 plasmacytoid dendritic cells in the thymus. A hallmark of T cell progenito
 rs is their lack of self-renewal. \n\nHence\, thymus function is thought t
 o absolutely depend on continuous supply of new progenitors from the bone 
 marrow. We uncovered the ability of the thymus for autonomous\, i.e. bone 
 marrow-independent T cell development. Normally\, fit progenitors from the
  bone marrow prevail over exhausted progenitors in the thymus.\nProgenitor
  deprivation resulted in persistence of thymocytes\, which frequently resu
 lts in T cell acute lymphoblastic leukemia (T-ALL) arising in the thymus. 
 These T-ALL share cellular and molecular hallmarks of human T-ALL. \n\nThe
 se findings suggest that perturbed progenitor turnover can cause genomic i
 nstability and cancer. \n
LOCATION:Lecture Theatre\, Department of Pathology\, Tennis Court Road
END:VEVENT
END:VCALENDAR
