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Identification of Meis1 Target Genes Involved in the Induction of AML in Collaboration with NUP98-HOXD13.

2006· article· en· W2559698750 on OpenAlexaff
Lars Palmqvist, Bob Argiropoulos, R. Keith Humphries

Bibliographic record

VenueBlood · 2006
Typearticle
Languageen
FieldMedicine
TopicAcute Myeloid Leukemia Research
Canadian institutionsBC Cancer Agency
Fundersnot available
KeywordsHox geneBiologyHomeoboxCancer researchDownregulation and upregulationTranscription factorLeukemiaMolecular biologyCell biologyGeneticsGene

Abstract

fetched live from OpenAlex

Abstract Meis1, a homeodomain-containing HOX cofactor, cooperates with multiple native and NUP98-HOX fusion proteins to accelerate the onset of AML. We have recently shown that enforced overexpression of Meis1 in NUP98-HOX transduced bone marrow (bm) cells leads to a marked elevation in the tyrosine receptor molecule, Flt3 transcription and subsequent activation of Flt3 signaling pathways (Blood. Aug 1, 2006). Furthermore, overexpression of wildtype Flt3 is sufficient to collaborate with NUP98-HOX fusions to induce AML in mice, albeit with a longer disease latency than NUP98-HOX+Meis1-mediated AML. To further study the molecular mechanisms underlying Meis1’s strong pro-leukemic effect together with HOX proteins, we conducted a structure-function analysis of Meis1 in the context of NUP98-HOXD13 (ND13) leukemogenesis. We show that the homeodomain (ΔHD, amino acids 272–335) is required for Meis1 collaboration with ND13 while the N-terminal domain (ΔN, amino acids 1–67) is dispensable for leukemogenesis but decelerates the disease onset. Interestingly, primary bm cells transduced with ND13-Meis1ΔHD or ND13-Meis1ΔN revealed no significant upregulation of Flt3 mRNA levels in either case. These results suggest that Meis1 triggers additional Flt3-independent pathways to accelerate leukemia development. Thus, the retained leukemogenic properties of ND13-Meis1ΔN and the longer latency observed for NUP98-HOX fusions and Flt3 overexpression to induce leukemia point to additional roles for Meis1 in induction of leukemia independent of its ability to upregulate Flt3. To search for these additional Meis1-induced leukemic pathway(s), we used the Affymetrix GeneChip MOE430 to compare the gene expression profiles of bm cells transduced with ND13, ND13+Meis1, ND13+Meis1ΔHD and Meis1ΔN. Interestingly, the gene array results indicate that only a relatively small number of genes (72 increased and 64 decreased) differed significantly between the non-leukemic Meis1ΔHD and the leukemic Meis1 bm cells and these genes are all strong candidates as to be direct Meis1 target genes. A significant number of these genes are involved in cytokine receptor pathways as revealed by gene ontology analysis and, furthermore, promoter analysis revealed the presence of putative Hox, Meis1 and Pbx binding sites in several of these. The gene array results also indicate that only a small fraction of genes differed significantly between the non-leukemic Meis1ΔHD and the leukemic Meis1ΔN bm cells suggesting that these genes could be involved in Flt3-independent Meis1 leukemogenic activity.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.005

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0020.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.014
GPT teacher head0.270
Teacher spread0.257 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2006
Admission routes1
Has abstractyes

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