ArticleLeukemia2006
Identification of a molecular signature for leukemic promyelocytes and their normal counterparts: Focus on DNA repair genes.
Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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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.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Dysregulation of HOXA genes in acute myeloid leukemia and targeted therapy.NPJ precision oncology · 2025Review
- Micro-RNA-140-3p Acts as a Tumor Suppressor Gene in Acute Promyelocytic Leukemia by Targeting Hepatocyte Growth Factor.Cell biochemistry and biophysics · 2025Article
- Therapeutic targeting of PARP with immunotherapy in acute myeloid leukemia.Frontiers in pharmacology · 2024Review
- Discovery of druggable cancer-specific pathways with application in acute myeloid leukemia.GigaScience · 2022Article
- Targeting PARP proteins in acute leukemia: DNA damage response inhibition and therapeutic strategies.Journal of hematology & oncology · 2022Review
- Review
- Review
- PARP goes the weasel! Emerging role of PARP inhibitors in acute leukemias.Blood reviews · 2021Review
- IGFBP7 activates retinoid acid-induced responses in acute myeloid leukemia stem and progenitor cells.Blood advances · 2020Article
- Deficiency of nucleotide excision repair is associated with mutational signature observed in cancer.Genome research · 2019Article
- High-Resolution Single-Cell DNA Methylation Measurements Reveal Epigenetically Distinct Hematopoietic Stem Cell Subpopulations.Stem cell reports · 2018Article
- ZYH005, a novel DNA intercalator, overcomes all-trans retinoic acid resistance in acute promyelocytic leukemia.Nucleic acids research · 2018Article
- Gene and protein analysis reveals that p53 pathway is functionally inactivated in cytogenetically normal Acute Myeloid Leukemia and Acute Promyelocytic Leukemia.BMC medical genomics · 2017Article
- Meta-Analysis of Gene Expression Profiles in Acute Promyelocytic Leukemia Reveals Involved Pathways.International journal of hematology-oncology and stem cell research · 2017Article
- DNA damage accumulation and repair defects in acute myeloid leukemia: implications for pathogenesis, disease progression, and chemotherapy resistance.Chromosoma · 2014Review
- Notch signaling in acute promyelocytic leukemia.Leukemia · 2013Article
- DNA damage and repair in human cancer: molecular mechanisms and contribution to therapy-related leukemias.International journal of environmental research and public health · 2012Review
- Data recovery and integration from public databases uncovers transformation-specific transcriptional downregulation of cAMP-PKA pathway-encoding genes.BMC bioinformatics · 2009Article
- High throughput digital quantification of mRNA abundance in primary human acute myeloid leukemia samples.The Journal of clinical investigation · 2009Article
- HOX proteins and leukemia.International journal of clinical and experimental pathology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute promyelocytic leukemia (APL) is a clonal expansion of hematopoietic precursors blocked at the promyelocytic stage. Gene expression profiles of APL cells obtained from 16 patients were compared to eight samples of CD34+-derived normal promyelocytes. Malignant promyelocytes showed widespread changes in transcription in comparison to their normal counterpart and 1020 differentially expressed genes were identified. Discriminating genes include transcriptional regulators (FOS, JUN and HOX genes) and genes involved in cell cycle and DNA repair. The strong upregulation in APL of some transcripts (FLT3, CD33, CD44 and HGF) was also confirmed at protein level. Interestingly, a trend toward a transcriptional repression of genes involved in different DNA repair pathways was found in APL and confirmed by real-time polymerase chain reactor (PCR) in a new set of nine APLs. Our results suggest that both inefficient base excision repair and recombinational repair might play a role in APLs development. To investigate the expression pathways underlying the development of APL occurring as a second malignancy (sAPL), we included in our study eight cases of sAPL. Although both secondary and de novo APL were characterized by a strong homogeneity in expression profiling, we identified a small set of differentially expressed genes that discriminate sAPL from de novo cases.
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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.