Evidence map›Paper›PMID 39191762›Full record

ArticleBlood cancer journal2024

Multi-omics profiling of longitudinal samples reveals early genomic changes in follicular lymphoma.

Baoyan Bai, Jillian F Wise, Daniel Vodák, Sigve Nakken, Ankush Sharma, Yngvild Nuvin Blaker, Marianne Brodtkorb, Vera Hilden, Gunhild Trøen, Weicheng Ren and 13 more

Abstract read
In one paragraph

Article in Blood cancer journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  5. Review
  6. Article
  7. Design, processing, and modeling for longitudinal multiomics microbiome data.Frontiers in cellular and infection microbiology · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

Baoyan Bai *Department of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0001-7017-4442
Jillian F Wise *Department of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Daniel VodákNorwegian Cancer Genomics Consortium, CancerGenomics.no, Oslo, Norway.
Sigve NakkenNorwegian Cancer Genomics Consortium, CancerGenomics.no, Oslo, Norway.ORCID 0000-0001-8468-2050
Ankush SharmaDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0002-1399-7503
Yngvild Nuvin BlakerDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Marianne BrodtkorbKG Jebsen Centre for B-cell malignancies, Institute for Clinical Medicine, University of Oslo, Oslo, Norway.
Vera HildenDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Gunhild TrøenDepartment of Pathology, Oslo University Hospital, Oslo, Norway.
Weicheng RenDivision of Immunology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Susanne LorenzNorwegian Cancer Genomics Consortium, CancerGenomics.no, Oslo, Norway.
Michael S LawrenceMassachusetts General Hospital Cancer Center and Department of Pathology, Harvard Medical School, Charlestown, MA, USA.
Ola MyklebostNorwegian Cancer Genomics Consortium, CancerGenomics.no, Oslo, Norway.ORCID 0000-0002-2866-3223
Eva KimbyUnit for Hematology and Department of Medicine at Karolinska Institutet, Huddinge, Stockholm, Sweden.ORCID 0000-0003-3078-6131
Qiang Pan-HammarströmDivision of Immunology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-1990-8804
Chloé B SteenDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Leonardo A Meza-ZepedaNorwegian Cancer Genomics Consortium, CancerGenomics.no, Oslo, Norway.
Klaus BeiskeDepartment of Pathology, Oslo University Hospital, Oslo, Norway.
Erlend B SmelandDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Eivind HovigNorwegian Cancer Genomics Consortium, CancerGenomics.no, Oslo, Norway.ORCID 0000-0002-9103-1077
Ole Christian LingjærdeKG Jebsen Centre for B-cell malignancies, Institute for Clinical Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0003-3565-4912
Harald Holte *KG Jebsen Centre for B-cell malignancies, Institute for Clinical Medicine, University of Oslo, Oslo, Norway. hhe@ous-hf.no.ORCID 0000-0001-9799-9428
June Helen Myklebust *Department of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. j.h.myklebust@medisin.uio.no.ORCID 0000-0003-0394-9986

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follicular lymphoma (FL) is the most common indolent type of B-cell non-Hodgkin lymphoma. Advances in treatment have improved overall survival, but early relapse or transformation to aggressive disease is associated with inferior outcome. To identify early genetic events and track tumor clonal evolution, we performed multi-omics analysis of 94 longitudinal biopsies from 44 FL patients; 22 with transformation (tFL) and 22 with relapse without transformation (nFL). Deep whole-exome sequencing confirmed recurrent mutations in genes encoding epigenetic regulators (CREBBP, KMT2D, EZH2, EP300), with similar mutational landscape in nFL and tFL patients. Calculation of genomic distances between longitudinal samples revealed complex evolutionary patterns in both subgroups. CREBBP and KMT2D mutations were identified as genetic events that occur early in the disease course, and cases with CREBBP KAT domain mutations had low risk of transformation. Gains in chromosomes 12 and 18 (TCF4), and loss in 6q were identified as early and stable copy number alterations. Identification of such early and stable genetic events may provide opportunities for early disease detection and disease monitoring. Integrative analysis revealed that tumors with EZH2 mutations exhibited reduced gene expression of numerous histone genes, including histone linker genes. This might contribute to the epigenetic dysregulation in FL.

Indexed as

GenomicsLymphoma, FollicularMutationAdultAgedAged, 80 and overCREB-Binding ProteinDNA Copy Number VariationsExome SequencingFemaleHumansLongitudinal StudiesMaleMiddle AgedMultiomicsCREB-Binding ProteinCREBBP protein, human

Identifiers

PMID39191762
PMCPMC11350178

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Registered trials

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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.