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ALDH Genes and Reactive Aldehydes Play Important Roles in HSCs and Leukemia and May Be Exploited to Treat AML

2013· article· en· W2980861407 on OpenAlexaff
Maura Gasparetto, Craig T. Jordan, Mohammad Minhajuddin, Daniel A. Pollyea, Vasilis Vasilou, Philip Reigan, R. Keith Humphries, Clayton A. Smith

Bibliographic record

VenueBlood · 2013
Typearticle
Languageen
FieldMedicine
TopicAcute Myeloid Leukemia Research
Canadian institutionsBC Cancer Agency
Fundersnot available
KeywordsLeukemiaAcute leukemiaBiologyCancer researchHaematopoiesisReactive oxygen speciesCell biologyDNA damageSignal transductionChemistryStem cellBiochemistryImmunologyDNA

Abstract

fetched live from OpenAlex

Abstract ALDH1A1 is expressed at high levels in normal HSCs and we previously reported that its function might involve metabolism of compounds termed reactive aldehydes. We also reported that loss of ALDH1A1 led to a compensatory increase in a related isoform, ALDH3A1, which also metabolizes reactive aldehydes. Double knockouts for both ALDH1A1/3A1 accumulate reactive aldehydes, which appear to impact a number of cellular processes including signal transduction and gene expression. As reactive aldehydes also cause DNA damage, we hypothesized that excess accumulation of reactive aldehydes may predispose to leukemic transformation of HSCs. In support of this, we found that ALDH1A1/3A1 double knockout HSCs readily form acute leukemia following transduction with a NUP98-HOXA10 fusion gene, which rarely causes leukemic transformation in wild type HSCs. Furthermore, in human AML, frequent absence of ALDH1A1 and the universal absence of ALDH3A1 was observed. A human AML cell line, Kasumi-1, was found to be ALDH1A1/3A1 deficient and to have high levels of intracellular reactive aldehydes. In addition, Kasumi-1 was highly sensitive to DNA damage and cell death following exposure to exogenous 4-HNE, a prototypic reactive aldehyde. In contrast, normal CD34+ HSCs were relatively resistant to 4-HNE. Based on these observations, we further hypothesized that treatment of ALDH1A1/3A1 deficient AMLs with clinically relevant compounds that further increase intracellular 4-HNE levels would selectively eliminate AML while sparing normal CD34+ HSCs. To test this, Kasumi-1 were exposed to a series of compounds including the pro-oxidant Arsenic tri-oxide (ATO), the sesquiterpene lactone parthenolide (PTL) and 4-HC, the active metabolite of cyclophosphamide (Cy) and a substrate of ALDH1A1. All increased intracellular 4-HNE levels and DNA damage. Exposure to combinations of 4-HC, ATO and PTL induced high levels of cell death in Kasumi-1. In contrast, Kasumi-1 cells engineered to express ALDH1A1 through lentiviral gene transfer and normal CD34+ HSCs were relatively resistant to several of these treatments. Primary ALDH1A1/3A1- AMLs were also relatively sensitive to treatment with these same compounds. In conclusion, ALDHs and reactive aldehydes may play important roles in HSCs and leukemia and exploitation of their biology may lead to novel therapies for AML and possibly other cancers. As an initial application of this treatment strategy, we are developing a clinical trial to treat patients with relapsed/refractory ALDH1A1/3A1 deficient AML with Cy/ATO. 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 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 score0.001
Threshold uncertainty score0.003

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 integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

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 head0.018
GPT teacher head0.274
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
Published2013
Admission routes1
Has abstractyes

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