ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012
Integrative genomic analysis implicates gain of PIK3CA at 3q26 and MYC at 8q24 in chronic lymphocytic leukemia.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 81 citations in OpenAlex.
- Voxtalisib (XL765) in patients with relapsed or refractory non-Hodgkin lymphoma or chronic lymphocytic leukaemia: an open-label, phase 2 trial.The Lancet. Haematology · 2018Trial
- Molecular Pathogenesis and Targeted Treatment of Richter Transformation.Biomedicines · 2026Review
- The Role of mTOR in B Cell Lymphoid Malignancies: Biologic and Therapeutic Aspects.International journal of molecular sciences · 2023Review
- Article
- Case Report: SMARCA4 (BRG1)-deficient undifferentiated carcinoma of gallbladder with genetic analysis.Frontiers in oncology · 2023Article
- Whole-genome sequencing of chronic lymphocytic leukemia identifies subgroups with distinct biological and clinical features.Nature genetics · 2022Article
- Chromothripsis in Chronic Lymphocytic Leukemia: A Driving Force of Genome Instability.Frontiers in oncology · 2021Review
- "Double-Hit" Chronic Lymphocytic Leukemia, Involving theFrontiers in oncology · 2021Review
- Core regulatory circuitries in defining cancer cell identity across the malignant spectrum.Open biology · 2020Review
- The prognostic role of c-MYC amplification in schistosomiasis-associated colorectal cancer.Japanese journal of clinical oncology · 2020Article
- Linear and circular PVT1 in hematological malignancies and immune response: two faces of the same coin.Molecular cancer · 2020Review
- Is There a Role for Dual PI3K/mTOR Inhibitors for Patients Affected with Lymphoma?International journal of molecular sciences · 2020Review
- Phosphoinositide 3-Kinase Signaling in the Tumor Microenvironment: What Do We Need to Consider When Treating Chronic Lymphocytic Leukemia With PI3K Inhibitors?Frontiers in immunology · 2020Review
- Clonal dynamics in chronic lymphocytic leukemia.Hematology. American Society of Hematology. Education Program · 2019Review
- Clonal dynamics in chronic lymphocytic leukemia.Blood advances · 2019Article
- Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Enhancer Architecture and Essential Core Regulatory Circuitry of Chronic Lymphocytic Leukemia.Cancer cell · 2018Article
- Whole-genome sequencing of chronic lymphocytic leukaemia reveals distinct differences in the mutational landscape between IgHVLeukemia · 2018Article
- Copanlisib for treatment of B-cell malignancies: the development of a PI3K inhibitor with considerable differences to idelalisib.Drug design, development and therapy · 2018Review
- Subtype assignment of CLL based on B-cell subset associated gene signatures from normal bone marrow - A proof of concept study.PloS one · 2018Article
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Authors and funding
17 authors at 8 institutions in 3 countries.
Funding
Abstract
purposeThe disease course of chronic lymphocytic leukemia (CLL) varies significantly within cytogenetic groups. We hypothesized that high-resolution genomic analysis of CLL would identify additional recurrent abnormalities associated with short time-to-first therapy (TTFT). EXPERIMENTAL
designWe undertook high-resolution genomic analysis of 161 prospectively enrolled CLLs using Affymetrix 6.0 SNP arrays, and integrated analysis of this data set with gene expression profiles.
resultsCopy number analysis (CNA) of nonprogressive CLL reveals a stable genotype, with a median of only 1 somatic CNA per sample. Progressive CLL with 13q deletion was associated with additional somatic CNAs, and a greater number of CNAs was predictive of TTFT. We identified other recurrent CNAs associated with short TTFT: 8q24 amplification focused on the cancer susceptibility locus near MYC in 3.7%; 3q26 amplifications focused on PIK3CA in 5.6%; and 8p deletions in 5% of patients. Sequencing of MYC further identified somatic mutations in two CLLs. We determined which catalytic subunits of phosphoinositide 3-kinase (PI3K) were in active complex with the p85 regulatory subunit and showed enrichment for the α subunit in three CLLs carrying PIK3CA amplification.
conclusionsOur findings implicate amplifications of 3q26 focused on PIK3CA and 8q24 focused on MYC in CLL.
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