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Should Patients with Myelodysplasia and/or Acute Myeloid Leukemia (MDS/AML) Be Screened for Inherited RUNX1 Mutations Prior to Sibling Donor Allografting?.

2007· article· en· W2572471102 on OpenAlexaff
Carolyn Owen, John A. Liu Yin, C. Toze, Donna L. Forrest, Anthony Macheta, Clayton A. Smith, Michael J. Barnett, Tutt N. Andrew, Jude Fitzgibbon

Bibliographic record

VenueBlood · 2007
Typearticle
Languageen
FieldMedicine
TopicAcute Myeloid Leukemia Research
Canadian institutionsVancouver General Hospital
Fundersnot available
KeywordsRUNX1MedicineProbandSiblingPlatelet disorderCEBPAMyeloid leukemiaLeukemiaBone marrowMyeloidInternal medicineOncologyGeneticsImmunologyMutationHaematopoiesisBiologyStem cellGenePlatelet

Abstract

fetched live from OpenAlex

Abstract Background Familial platelet disorder with propensity to myeloid malignancy (FPD/AML) is an autosomal dominant disease characterised by platelet abnormalities and risk of MDS/AML. FPD/AML results from germline mutations in RUNX1. The phenotype is heterogeneous with ∼35% of affected individuals developing MDS/AML. This clinical variability may obscure the diagnosis and prevent appropriate screening. We describe 2 families with novel C-terminal RUNX1 mutations and FPD/AML phenotypes, in which potentially affected siblings were used as haematopoietic stem cell transplant (HSCT) donors prior to identification of the inherited mutation. Methods DNA was collected from members of two families with histories of thrombocytopenia and MDS/AML. Direct PCR sequencing was performed on exons 1 and 3–8 of the RUNX1 gene. Results Pedigree 1 has 4 affected members from 2 generations. The proband (I-1) had a history of chronic thrombocytopenia and developed MDS at age 63 and died of AML at age 64. Her daughter (II-1) presented with MDS at age 37 and underwent 2 HSCTs from II-2, relapsing 8 months after the first and remaining well 6 years after the second HSCT. Individuals II-2 and II-3 were recently noted to have mild thrombocytopenia with normal bone marrow morphologies. DNA from blood and bone marrow of II-2 and II-3 revealed an out-of-frame 7 base pair (bp) deletion in exon 8 (1007_1013del) of RUNX1 at amino acid 336 (Gly336fsTer564). Pedigree 2 has 2 affected individuals from 2 generations. The proband (I-1) had a history of chronic thrombocytopenia since childhood. She developed MDS at age 52 and received an HSCT from her brother (I-2) in 2007 with normal engraftment and no early transplant complications. Her son (II-2) had presented with AML at age 8 and received an HSCT from his sister (II-1) at that time. He remains well 26 years later. DNA from blood and saliva of I-1 revealed a substitution of C for T in exon 7 (877C>T) of [italic[RUNX1, resulting in a stop codon and an early-truncated protein at position 292 (Arg292Ter). Conclusions Two novel, C-terminal RUNX1 mutations are described in families with FPD/AML phenotypes. Both families were investigated after affected individuals received HSCT from siblings (who were also at risk of having inherited the mutation). The sibling donors exhibited normal or near-normal platelet counts prior to HSCT, obscuring a FPD/AML diagnosis. Therefore, all patients with MDS/AML should be screened for a family history of thrombocytopenia and/or MDS/AML and considered for investigation of RUNX1 mutations prior to HSCT. Figure Figure Figure Figure

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)0.001
metaresearch head score (Gemma)0.002
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Theoretical or conceptual · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.003
Threshold uncertainty score0.009

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.002
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0010.000
Science and technology studies0.0010.000
Scholarly communication0.0000.001
Open science0.0000.000
Research integrity0.0020.001
Insufficient payload (model declined to judge)0.0030.001

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 head0.029
GPT teacher head0.312
Teacher spread0.283 · 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 designTheoretical or conceptual
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".

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Citations0
Published2007
Admission routes1
Has abstractyes

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