ReviewOncogene2001
Modeling Philadelphia chromosome positive leukemias.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 74 citations in OpenAlex.
- Differentiation therapy in acute myeloid leukaemia: molecular basis, clinical progress, and future perspectives.Frontiers in medicine · 2026Review
- Creation of Philadelphia chromosome by CRISPR/Cas9-mediated double cleavages on BCR and ABL1 genes as a model for initial event in leukemogenesis.Cancer gene therapy · 2023Article
- Stabilization of fatty acid synthesis enzyme acetyl-CoA carboxylase 1 suppresses acute myeloid leukemia development.The Journal of clinical investigation · 2021Article
- Increased sensitivity of BCR-ABL-induced B-ALL to imatinib by releasing leukemia B cell differentiation blockage.International journal of clinical and experimental pathology · 2020Article
- Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics.Leukemia · 2017Article
- Novel working hypothesis for pathogenesis of hematological malignancies: combination of mutations-induced cellular phenotypes determines the disease (cMIP-DD).Journal of biochemistry · 2016Review
- Article
- Mechanisms determining the fate of hematopoietic stem cells.Stem cell investigation · 2015Review
- The molecular basis of myeloid malignancies.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2014Review
- Expression of BCR/ABL p210 from a knockin allele enhances bone marrow engraftment without inducing neoplasia.Cell reports · 2013Article
- CCN3 suppresses mitogenic signalling and reinstates growth control mechanisms in Chronic Myeloid Leukaemia.Journal of cell communication and signaling · 2012Article
- Mouse models as tools to understand and study BCR-ABL1 diseases.American journal of blood research · 2011Article
- Targeted therapy of chronic myeloid leukemia.Biochemical pharmacology · 2010Review
- Array-based genomic resequencing of human leukemia.Oncogene · 2010Article
- CCN3: a key growth regulator in Chronic Myeloid Leukaemia.Journal of cell communication and signaling · 2009Article
- Sustained suppression of Bcr-Abl-driven lymphoid leukemia by microRNA mimics.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Age-related defects in B lymphopoiesis underlie the myeloid dominance of adult leukemia.Blood · 2007Article
- Article
- Role of Dok-1 and Dok-2 in leukemia suppression.The Journal of experimental medicine · 2004Article
- Role of Dok-1 and Dok-2 in myeloid homeostasis and suppression of leukemia.The Journal of experimental medicine · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ph chromosome has been genetically linked to CML and ALL. Its chimeric fusion gene product, BCR-ABL, can generate leukemia in mice. This review will discuss selected model systems developed to study BCR-ABL induced leukemia and focuses on what we have learned about the human disease from these models. Five main experimental approaches will be discussed including: (i) Reconstitution of mice with bone marrow cells retrovirally transduced with BCR-ABL; (ii) Transgenic mice expressing BCR-ABL; (iii) Knock-in mice with BCR-ABL expression driven from the endogenous bcr locus; (iv) Development of CML-like disease in mice with loss of function mutations in heterologous genes; and (v) ES in vitro hematopoietic differentiation coupled with regulated BCR-ABL expression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.