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The RNA Editase ADAR1 Promotes Malignant Progenitor Reprogramming in Chronic Myeloid Leukemia.

2012· article· en· W2979877733 on OpenAlexaff
Qingfei Jiang, Leslie Crews-Robertson, Christian Barrett, Hyn-June Chun, Angela Court-Recart, Daniel Goff, Mark D. Minden, Anil Sadarangani, Jessica M. Rusert, Kim‐Hien Dao, Sheldon Morris, Lawrence S.B. Goldstein, Marco A. Marra, Kelly A. Frazer, Catriona Jamieson

Bibliographic record

VenueBlood · 2012
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicRNA regulation and disease
Canadian institutionsBC Cancer AgencyPrincess Margaret Cancer CentreCanada's Michael Smith Genome Sciences Centre
Fundersnot available
KeywordsBiologyReprogrammingProgenitor cellStem cellCancer researchMyeloid leukemiaRNA editingHaematopoiesisMyeloidCell biologyGeneticsCellGene expressionGene

Abstract

fetched live from OpenAlex

Abstract Abstract 2772 While advanced malignancies in Chronic Myeoloid Leukemia (CML) are diverse in phenotype, they often exhibit stem cell properties including enhanced survival, quiescence and self-renewal potential. The molecular etiology of human progenitor reprogramming into self-renewing leukemia stem cells (LSC) has remained elusive. While DNA sequencing has uncovered spliceosome gene mutations that promote alternative splicing and portend leukemic transformation, isoform diversity may also be generated by aberrant RNA editing mediated by adenosine deaminase acting on dsRNA (ADAR) family, which have been shown to promote an embryonic transcriptional program and regulate fetal and adult hematopoietic stem cell (HSC) self-renewal as well as stem cell responses to inflammation. In this study, whole transcriptome sequencing of normal, chronic phase (CP) and functionally validated blast crisis (BC) chronic myeloid leukemia (CML) progenitors revealed increased inflammatory pathway gene expression in concert with BCR-ABL amplification, enhanced expression of interferon-responsive ADAR1 and a propensity for increased A-to-I RNA editing during CML progression. Mechanistic studies demonstrated that lentivirally enforced ADAR1 p150 expression induced expression of the myeloid-skewing transcription factor PU.1 and skewed cell fate towards granulocyte-macrophage progenitors - the initiating LSC population in BC CML. Moreover, lentiviral ADAR1 knockdown reduced BC LSC self-renewal capacity in RAG2−/−gc−/− mice. These data shed new light on the role of ADAR1-directed RNA editing in myeloid progenitor reprogramming and self-renewal potential of malignant progenitors that drive disease progression and therapeutic resistance in CML, and provide a compelling rationale for developing ADAR1-based LSC detection and eradication strategies. Disclosures: No relevant conflicts of interest to declare.

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 distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation 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 score0.107
Threshold uncertainty score0.318

Codex and Gemma teacher scores by category

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 integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

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 head0.009
GPT teacher head0.241
Teacher spread0.232 · 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 teacher head, 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
Published2012
Admission routes1
Has abstractyes

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