ArticleLeukemia2011
Identification of recurring tumor-specific somatic mutations in acute myeloid leukemia by transcriptome sequencing.
Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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
36 citing papers in PubMed, 60 citations in OpenAlex.
- Significance of expression of ITGA5 and its splice variants in acute myeloid leukemia: a report from the Children's Oncology Group.American journal of hematology · 2013Trial
- The Polo-Like Kinase 1 (PLK1) inhibitor NMS-P937 is effective in a new model of disseminated primary CD56+ acute monoblastic leukaemia.PloS one · 2013Trial
- Cullin-3 adaptor SHKBP1 inhibits SQSTM1/p62 oligomerization and Keap1 sequestration.The Journal of cell biology · 2026Article
- Calpain activity is negatively regulated by a KCTD7-Cullin-3 complex via non-degradative ubiquitination.Cell discovery · 2023Article
- Molecular and clinical characteristics of IDH mutations in Chinese NSCLC patients and potential treatment strategies.Cancer medicine · 2022Article
- The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021Review
- Candidate gene expression and coding sequence variants in Warmblood horses with myofibrillar myopathy.Equine veterinary journal · 2021Article
- Erythrocytosis with JAK2 GGCC_46/1 haplotype and without JAK2 V617F mutation is associated with CALR rs1049481_G allele.Leukemia · 2021Article
- Genome-wide Identification and Analysis of Splicing QTLs in Multiple Sclerosis by RNA-Seq Data.Frontiers in genetics · 2021Article
- KCells · 2020Article
- KCTD15 is overexpressed in human childhood B-cell acute lymphoid leukemia.Scientific reports · 2019Article
- KCTD: A new gene family involved in neurodevelopmental and neuropsychiatric disorders.CNS neuroscience & therapeutics · 2019Review
- Structural complexity in the KCTD family of Cullin3-dependent E3 ubiquitin ligases.The Biochemical journal · 2017Article
- The impact of RNA sequence library construction protocols on transcriptomic profiling of leukemia.BMC genomics · 2017Article
- Understanding of leukemic stem cells and their clinical implications.Molecular cancer · 2017Review
- Article
- Inconsistency and features of single nucleotide variants detected in whole exome sequencing versus transcriptome sequencing: A case study in lung cancer.Methods (San Diego, Calif.) · 2015Article
- Class III Receptor Tyrosine Kinases in Acute Leukemia - Biological Functions and Modern Laboratory Analysis.Biomarker insights · 2015Review
- Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic lesions are crucial for cancer initiation. Recently, whole genome sequencing, using next generation technology, was used as a systematic approach to identify mutations in genomes of various types of tumors including melanoma, lung and breast cancer, as well as acute myeloid leukemia (AML). Here, we identify tumor-specific somatic mutations by sequencing transcriptionally active genes. Mutations were detected by comparing the transcriptome sequence of an AML sample with the corresponding remission sample. Using this approach, we found five non-synonymous mutations specific to the tumor sample. They include a nonsense mutation affecting the RUNX1 gene, which is a known mutational target in AML, and a missense mutation in the putative tumor suppressor gene TLE4, which encodes a RUNX1 interacting protein. Another missense mutation was identified in SHKBP1, which acts downstream of FLT3, a receptor tyrosine kinase mutated in about 30% of AML cases. The frequency of mutations in TLE4 and SHKBP1 in 95 cytogenetically normal AML patients was 2%. Our study demonstrates that whole transcriptome sequencing leads to the rapid detection of recurring point mutations in the coding regions of genes relevant to malignant transformation.
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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.