Evidence map›Paper›PMID 38462571›Full record

ArticleVirchows Archiv : an international journal of pathology2024

Mutational, immune microenvironment, and clinicopathological profiles of diffuse large B-cell lymphoma and follicular lymphoma with BCL6 rearrangement.

Joaquim Carreras, Haruka Ikoma, Yara Yukie Kikuti, Masashi Miyaoka, Shinichiro Hiraiwa, Sakura Tomita, Yusuke Kondo, Atsushi Ito, Shunsuke Nagase, Hisanobu Miura and 5 more

Abstract read
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In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.2field-weighted citation impact, top 6% of its field
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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

15 authors at 4 institutions in 5 countries.

Joaquim CarrerasDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan. joaquim.carreras@tokai.ac.jp.ORCID http://orcid.org/0000-0002-6129-8299
Haruka IkomaDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Yara Yukie KikutiDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Masashi MiyaokaDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Shinichiro HiraiwaDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Sakura TomitaDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Yusuke KondoDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Atsushi ItoDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Shunsuke NagaseDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Hisanobu MiuraDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Hiroshi KawadaDepartment of Hematology, School of Medicine, Tokai University, Tokyo, Japan.
Giovanna RoncadorMonoclonal Antibodies Core Unit, Spanish National Cancer Research Center (CNIO), Madrid, Spain.
Elias CampoDepartment of Pathology, Esther Koplowitz Center (CEK), Centro de Investigacion Biomedica en Red de Cancer (CIBERONC), Hospital Clinic Barcelona, August Pi I Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.ORCID http://orcid.org/0000-0001-9850-9793
Rifat HamoudiResearch Institute for Medical and Health Science, Department of Clinical Sciences, College of Medicine, University of Sharjah, Sharjah, United Arab Emirates.ORCID http://orcid.org/0000-0002-1402-0868
Naoya NakamuraDepartment of Pathology, School of Medicine, Tokai University, Tokyo, Japan.
Tokai University · JPCentro de Investigación Biomédica en Red de Cáncer · ESSpanish National Cancer Research Centre · ESUniversity of Sharjah · AE

Funding

ASPIRE, the technology program management pillar of Abu Dhabi's Advanced Technology Research Council (ATRC), via the ASPIRE Precision Medicine Research Institute Abu Dhabi (AS-PIREPMRIAD) award VRI-20-10Ministry of Education, Culture, Sports, Science and Technology (MEXT) 18K15100Ministry of Education, Culture, Sports, Science and Technology (MEXT) 24590430the Ministry of Education, Culture, Sports, Science and Technology (MEXT) 15K19061the Ministry of Education, Culture, Sports, Science and Technology (MEXT) 23K06454Tokai University School of Medicine research incentive assistant plan 2021-B04
6 · The paper itself

Abstract

BCL6-rearrangement (BCL6-R) is associated with a favorable prognosis of follicular lymphoma (FL), but the mechanism is unknown. We analyzed the clinicopathological, immune microenvironment (immune checkpoint, immuno-oncology markers), and mutational profiles of 10 BCL6-R-positive FL, and 19 BCL6-R-positive diffuse large B-cell lymphoma (DLBCL) cases (both BCL2-R and MYC-R negative). A custom-made panel included 168 genes related to aggressive B-cell lymphomas and FL. FL cases were nodal, histological grade 3A in 70%, low Ki67; and had a favorable overall and progression-free survival. DLBCL cases were extranodal in 60%, IPI high in 63%, non-GCB in 60%, EBER-negative; and had a progression-free survival comparable to that of DLBCL NOS. The microenvironment had variable infiltration of M2-like tumor-associated macrophages (TAMs) that were CD163, CSF1R, LAIR1, PD-L1, and CD85A (LILRB3) positive; but had low IL10 and PTX3 expression. In comparison to FL, DLBCL had higher TAMs, IL10, and PTX3 expression. Both lymphoma subtypes shared a common mutational profile with mutations in relevant pathogenic genes such as KMT2D, OSBPL10, CREBBP, and HLA-B (related to chromatin remodeling, metabolism, epigenetic modification, and antigen presentation). FL cases were characterized by a higher frequency of mutations of ARID1B, ATM, CD36, RHOA, PLOD2, and PRPRD (p < 0.05). DLBCL cases were characterized by mutations of BTG2, and PIM1; and mutations of HIST1H1E and MFHAS1 to disease progression (p < 0.05). Interestingly, mutations of genes usually associated with poor prognosis, such as NOTCH1/2 and CDKN2A, were infrequent in both lymphoma subtypes. Some high-confidence variant calls were likely oncogenic, loss-of-function. MYD88 L265P gain-of-function was found in 32% of DLBCL. In conclusion, both BCL6-R-positive FL and BCL6-R-positive DLBCL had a common mutational profile; but also, differences. DLBCL cases had a higher density of microenvironment markers.

Indexed as

Biomarkers, TumorLymphoma, FollicularLymphoma, Large B-Cell, DiffuseMutationProto-Oncogene Proteins c-bcl-6Tumor MicroenvironmentAdultAgedAged, 80 and overDNA Mutational AnalysisFemaleGene RearrangementHumansMaleMiddle AgedProgression-Free SurvivalBCL6 protein, humanBiomarkers, TumorProto-Oncogene Proteins c-bcl-6BCL6-rearrangementDiffuse large B-cell lymphomaFollicular lymphomaHigh-confidence variant callsMutational profilePrognosis

Identifiers

PMID38462571
OpenAlexW4392759400

What OpenQuestion holds

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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.