ArticleCancer research2017
Mutational Landscape and Gene Expression Patterns in Adult Acute Myeloid Leukemias with Monosomy 7 as a Sole Abnormality.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 31 citations in OpenAlex.
- The nomograms for predicting overall and cancer-specific survival in elderly patients with early-stage lung cancer: A population-based study using SEER database.Frontiers in public health · 2022Trial
- [Clinical characteristics and prognostic analysis of pediatric acute myeloid leukemia with -7/7q- abnormalities].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- Mutation dynamics from diagnosis to relapse in acute myeloid leukemia with chromosomal 7 deletions.Leukemia & lymphoma · 2025Article
- Emergence and Cytogenetic Clonal Evolution of Chromosome 7 Abnormalities in Myeloid Malignancies: Investigating the Role of Telomere Dysfunction.International journal of molecular sciences · 2025Article
- CD37 in acute myeloid leukemia: a novel surface target for drug delivery.Blood advances · 2025Article
- Genomic characterization of AML with aberrations of chromosome 7: a multinational cohort of 519 patients.Journal of hematology & oncology · 2024Article
- Insights into the Clinical, Biological and Therapeutic Impact of Copy Number Alteration in Cancer.International journal of molecular sciences · 2024Review
- BCL7A is silenced by hypermethylation to promote acute myeloid leukemia.Biomarker research · 2023Article
- Inhibitor of DNA binding proteins revealed as orchestrators of steady state, stress and malignant hematopoiesis.Frontiers in immunology · 2022Review
- Large-Scale Identification of Clonal Hematopoiesis and Mutations Recurrent in Blood Cancers.Blood cancer discovery · 2021Article
- BRM: the core ATPase subunit of SWI/SNF chromatin-remodelling complex-a tumour suppressor or tumour-promoting factor?Epigenetics & chromatin · 2019Review
- Article
- Selective targeting of NAMPT by KPT-9274 in acute myeloid leukemia.Blood advances · 2019Article
- Not Only Mutations Matter: Molecular Picture of Acute Myeloid Leukemia Emerging from Transcriptome Studies.Journal of oncology · 2019Review
- Formaldehyde, Hematotoxicity, and Chromosomal Changes-Response.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Article
- Response to letter to the editor of Carcinogenesis by Pira et al., 2017.Carcinogenesis · 2017Article
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14 authors at 1 institution in 1 country.
Funding
Abstract
Monosomy of chromosome 7 is the most frequent autosomal monosomy in acute myeloid leukemia (AML), where it associates with poor clinical outcomes. However, molecular features associated with this sole monosomy subtype (-7 AML), which may give insights into the basis for its poor prognosis, have not been characterized. In this study, we analyzed 36 cases of -7 AML for mutations in 81 leukemia/cancer-associated genes using a customized targeted next-generation sequencing panel (Miseq). Global gene and miRNA expression profiles were also determined using paired RNA and small RNA sequencing data. Notably, gene mutations were detected in all the major AML-associated functional groups, which include activated signaling, chromatin remodeling, cohesin complex, methylation, NPM1, spliceosome, transcription factors, and tumor suppressors. Gene mutations in the chromatin remodeling groups were relatively more frequent in patients <60 years of age, who also had less mutations in the methylation and spliceosome groups compared with patients ≥60 years of age. Novel recurrent mutational events in AML were identified in the SMARCA2 gene. In patients ≥60 years of age, the presence of spliceosome mutations associated with a lower complete remission rate (P = 0.03). RNA sequencing revealed distinct gene and miRNA expression patterns between the sole -7 and non -7 AML cases, with reduced expression, as expected, of many genes and miRNAs mapped to chromosome 7, and overexpression of ID1, MECOM, and PTPRM, among others. Overall, our findings illuminate a number of molecular features of the underlying aggressive pathobiology in -7 AML patients. Cancer Res; 77(1); 207-18. ©2016 AACR.
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