Progenitor tumours from E mu-bcl-2-myc transgenic mice have lymphomyeloid differentiation potential and reveal developmental differences in cell survival
Details
Publication Year 1996-08-01,Volume 15,Issue #15,Page 3823-3834
Journal Title
EMBO JOURNAL
Publication Type
Journal Article
Abstract
Mice expressing both a bcl-2 and a myc transgene within the B lymphoid cell compartment invariably develop novel immature haemopoietic tumours. The likely cell of origin of these tumours was identified by a common pattern of cell surface marker expression on a subset of cells comprising similar to 1% of normal mouse bone marrow. The bcl-2-myc tumour cells could be induced to differentiate into either B lymphocytes or macrophages in culture with certain cytokines and feeder cells. Analysis of their progression into the B lymphoid lineage revealed that Igk locus transcription can precede Igh as well as Igk rearrangement. Surprisingly, the undifferentiated tumour cells died rapidly in culture, even in the presence of multiple cytokines, but they proliferated on monolayers of stromal cells derived from haemopoietic tissues. Thus, even with Bcl-2 levels that protect more differentiated cells, these immature bi-potential progenitor cells require a stromal-induced signal for survival. These results provide insight into the process of lineage commitment and suggest new levels of control of cell survival during early steps in haemopoietic development.
Publisher
OXFORD UNIV PRESS UNITED KINGDOM
Keywords
HEMATOPOIETIC STEM-CELLS; PRE-B-CELLS; KAPPA-GENE-TRANSCRIPTION; MURINE FETAL LIVER; LIGHT-CHAIN GENES; MU-HEAVY-CHAIN; BONE-MARROW; C-MYC; GROWTH-FACTOR; IMMUNOGLOBULIN HEAVY
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Creation Date: 1996-08-01 12:00:00
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