Evidence map›Paper›PMID 40316697›Full record

ArticleLeukemia2025

TP53 and CDKN2A alterations define a poor prognostic subgroup in patients with nodal T follicular helper cell lymphoma.

Yuta Ito, Joji Shimono, Keisuke Kawamoto, Kanako C Hatanaka, Yasunori Kogure, Mariko Tabata, Yuki Saito, Kota Mizuno, Sara Horie, Yosuke Mizukami and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
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

22 authors.

Yuta Ito *Division of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0001-7259-4870
Joji Shimono *Department of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan.
Keisuke Kawamoto *Department of Pathology, Kurume University School of Medicine, Kurume, Japan.
Kanako C HatanakaCenter for Development of Advanced Diagnostics, Hokkaido University Hospital, Sapporo, Japan.
Yasunori KogureDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0003-1158-5131
Mariko TabataDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0002-8013-7327
Yuki SaitoDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0003-2686-9604
Kota MizunoDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Sara HorieDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0001-8668-4623
Yosuke MizukamiDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Junji KoyaDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Koichi MurakamiDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan.
Takanori TeshimaDepartment of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan.ORCID 0000-0002-0941-271X
Yutaka HatanakaResearch Division of Genome Companion Diagnostics, Hokkaido University Hospital, Sapporo, Japan.ORCID 0000-0003-3128-1477
Kenichi ChibaDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.
Ai OkadaDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.
Yuichi ShiraishiDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.
Hiroaki MiyoshiDepartment of Pathology, Kurume University School of Medicine, Kurume, Japan.ORCID 0000-0002-2356-3725
Yoshihiro MatsunoDepartment of Surgical Pathology, Hokkaido University Hospital, Sapporo, Japan.
Koichi OhshimaDepartment of Pathology, Kurume University School of Medicine, Kurume, Japan. ohshima_kouichi@med.kurume-u.ac.jp.
Keisuke KataokaDivision of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan. kkataoka-tky@umin.ac.jp.ORCID 0000-0002-8263-9902
Masao NakagawaDepartment of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan. nakagawam@med.hokudai.ac.jp.ORCID 0000-0002-8602-6054

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nodal T follicular helper cell lymphoma (nTFHL) exhibits unique immunophenotypes and somatic alterations, while the prognostic value of these alterations remains unclear. By analyzing 173 nTFHL cases, we identified 36 driver genes, including 4 novel ones (TET3, HLA-C, NRAS, and KLF2). Then, we classified nTFHL cases into four molecular subgroups by major driver alterations. TR-I (+) and TR-I (-) were characterized by TET2 and/or RHOA mutations with and without IDH2 mutations; AC53 by TP53 and/or CDKN2A alterations and aneuploidy; and NSD with no subgroup-defining alterations (namely without any of the above alterations). AC53 exhibited the worst survival, while NSD, particularly those lacking driver alterations, showed the best prognosis. nTFHL had a better prognosis than peripheral T-cell lymphoma, not otherwise specified, when TP53 and/or CDKN2A alterations were absent. Multivariable analyses showed that AC53, the presence of driver alterations, and international prognostic index high-risk were independently associated with worse survival. Finally, we developed a simple prognostic index (mTFHL-PI), which classified patients into three risk categories with a median OS of 181, 67, and 20 months, respectively. Our study identifies novel prognostic factors, namely TP53 and/or CDKN2A alterations and the presence of driver alterations, demonstrating the clinical relevance of molecular classification in nTFHL.

Indexed as

Biomarkers, TumorCyclin-Dependent Kinase Inhibitor p16Lymphoma, FollicularMutationTumor Suppressor Protein p53AdultAgedAged, 80 and overFemaleHumansMaleMiddle AgedPrognosisSurvival RateBiomarkers, TumorCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16TP53 protein, humanTumor Suppressor Protein p53

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.