myeloid leukemia-like myeloproliferative disease in mice molecule-1 accelerate the development of BCR/ABL-induced chronic Lack of the adhesion molecules P-selectin and intercellular adhesion

نویسندگان

  • Shawn D. Pelletier
  • Daniel S. Hong
  • Yiguo Hu
  • Yuhua Liu
  • Shaoguang Li
چکیده

http://bloodjournal.hematologylibrary.org/content/104/7/2163.full.html Updated information and services can be found at: (795 articles) Oncogenes and Tumor Suppressors • (4217 articles) Neoplasia • (790 articles) Cell Adhesion and Motility • Articles on similar topics can be found in the following Blood collections http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub_requests Information about reproducing this article in parts or in its entirety may be found online at: http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#reprints Information about ordering reprints may be found online at: http://bloodjournal.hematologylibrary.org/site/subscriptions/index.xhtml Information about subscriptions and ASH membership may be found online at:

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Lack of the adhesion molecules P-selectin and intercellular adhesion molecule-1 accelerate the development of BCR/ABL-induced chronic myeloid leukemia-like myeloproliferative disease in mice.

In vitro studies show that BCR/ABL-expressing hematopoietic cells exhibit altered adhesion properties. No in vivo studies show whether the altered adhesion properties affect BCR/ABL leukemogenesis. Using mice with homozygous inactivation of genes encoding the 2 adhesion molecules P-selectin and intercellular adhesion molecule-1 (ICAM1), we show that the mutant mice develop BCR/ABL-induced chron...

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Selectins and their ligands are required for homing and engraftment of BCR-ABL1+ leukemic stem cells in the bone marrow niche.

We investigated adhesion pathways that contribute to engraftment of breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1)-induced chronic myelogenous leukemia (CML)-like myeloproliferative neoplasia in a mouse retroviral transduction/transplantation model. Compared with normal stem/progenitor cells, BCR-ABL1(+) progenitors had similar expression of very late anti...

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Rac2 GTPase deficiency depletes BCR-ABL+ leukemic stem cells and progenitors in vivo.

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تاریخ انتشار 2004