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Article

Expression of BCR/ABL p210 from a knockin allele enhances bone marrow engraftment without inducing neoplasia.

Cell reports - 17 Oct 2013

Foley Samantha B, Hildenbrand Zacariah L, Soyombo Abigail A, Magee Jeffery A, Wu Yipin, Oravecz-Wilson Katherine I, Ross Theodora S

Abstract excerpt

Chronic myeloid leukemia (CML) and some acute lymphoblastic leukemias are characterized by the t(9;22) chromosome, which encodes the BCR/ABL oncogene. Multiple mouse models of CML express BCR/ABL at high levels from non-Bcr promoters, resulting in the development of leukemias. In contrast, a significant fraction of healthy humans have been found to have BCR/ABL-positive hematopoietic cells. To bridge the gap...

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Share to Bone Marrow Transplantation
Share to Cell Transformation, Neoplastic

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Gene Expression Regulation

Share to Gene Knock-In Techniques

Share to Leukemia, Myeloid

Share to Mice, Transgenic

Source

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Identifiers

PMID: 24095735
DOI: 10.1016/j.celrep.2013.08.037
PMCID: PMC3832111

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

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Expression of BCR/ABL p210 from a knockin allele enhances bone marrow engraftment without inducing neoplasia.PMID 24095735Read ↗

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