Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-1-22
pubmed:abstractText
Multiple members of the A, B, and C clusters of Hox genes are expressed in hematopoietic cells. Several of these Hox genes have been found to display distinctive expression patterns, with genes located at the 3' side of the clusters being expressed at their highest levels in the most primitive subpopulation of human CD34+ bone marrow cells and genes located at the 5' end having a broader range of expression, with downregulation at later stages of hematopoietic differentiation. To explore if these patterns reflect different functional activities, we have retrovirally engineered the overexpression of a 5'-located gene, HOXA10, in murine bone marrow cells and demonstrate effects strikingly different from those induced by overexpression of a 3'-located gene, HOXB4. In contrast to HOXB4, which causes selective expansion of primitive hematopoietic cells without altering their differentiation, overexpression of HOXA10 profoundly perturbed myeloid and B-lymphoid differentiation. The bone marrow of mice reconstituted with HOXA10-transduced bone marrow cells contained in high frequency a unique progenitor cell with megakaryocytic colony-forming ability and was virtually devoid of unilineage macrophage and pre-B-lymphoid progenitor cells derived from the transduced cells. Moreover, and again in contrast to HOXB4, a significant proportion of HOXA10 mice developed a transplantable acute myeloid leukemia with a latency of 19 to 50 weeks. These results thus add to recognition of Hox genes as important regulators of hematopoiesis and provide important new evidence of Hox gene-specific functions that may correlate with their normal expression pattern.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-1348930, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-1354076, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-1375263, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-1402659, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-1676505, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-1712489, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-1987478, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-2576652, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-2822260, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-2902929, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-6943564, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7506075, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7518789, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7527557, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7622039, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7678830, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7741726, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7758949, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7774011, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7823932, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7830794, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7890597, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7905617, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7913880, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-7949119, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8078582, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8097318, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8104786, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8563752, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8563753, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8563754, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8643691, http://linkedlifedata.com/resource/pubmed/commentcorrection/8972230-8724694
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0270-7306
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
495-505
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:8972230-Acute Disease, pubmed-meshheading:8972230-Animals, pubmed-meshheading:8972230-B-Lymphocytes, pubmed-meshheading:8972230-Bone Marrow Cells, pubmed-meshheading:8972230-Bone Marrow Transplantation, pubmed-meshheading:8972230-Cell Differentiation, pubmed-meshheading:8972230-DNA-Binding Proteins, pubmed-meshheading:8972230-Female, pubmed-meshheading:8972230-Gene Transfer Techniques, pubmed-meshheading:8972230-Genes, Homeobox, pubmed-meshheading:8972230-Hematopoiesis, pubmed-meshheading:8972230-Hematopoietic Stem Cells, pubmed-meshheading:8972230-Homeodomain Proteins, pubmed-meshheading:8972230-Humans, pubmed-meshheading:8972230-Leukemia, Myeloid, pubmed-meshheading:8972230-Lymphoid Tissue, pubmed-meshheading:8972230-Male, pubmed-meshheading:8972230-Mice, pubmed-meshheading:8972230-Mice, Inbred C3H, pubmed-meshheading:8972230-Mice, Inbred C57BL, pubmed-meshheading:8972230-RNA, Messenger, pubmed-meshheading:8972230-Retroviridae
pubmed:year
1997
pubmed:articleTitle
Overexpression of HOXA10 in murine hematopoietic cells perturbs both myeloid and lymphoid differentiation and leads to acute myeloid leukemia.
pubmed:affiliation
Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, Canada.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.
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