Evidence map›Paper›PMID 42262647›Full record

Trial reportInternational journal of hematology2026

TFH phenotype and response to tucidinostat in relapsed/refractory PTCL: analysis of patients from a phase IIb trial.

Koji Izutsu, Ayumi Fujimoto, Shinya Rai, Dai Maruyama, Ken Ohmachi, Akihiko Yokohama, Kunihiro Tsukasaki, Toshiki Uchida, Junya Kuroda, Ilseung Choi and 10 more

Abstract readClinical Trial, Phase II
PubMed Publisher
In one paragraph

Trial report in International journal of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Koji IzutsuDepartment of Hematology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan. kizutsu@ncc.go.jp.ORCID http://orcid.org/0000-0001-9129-8057
Ayumi FujimotoDivision of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Shinya RaiDepartment of Hematology and Rheumatology, Faculty of Medicine, Kindai University, Sakai, Japan.
Dai MaruyamaDepartment of Hematology Oncology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Ken OhmachiDepartment of Hematology and Oncology, Tokai University Hospital, Isehara, Japan.
Akihiko YokohamaDepartment of Hematology, Gunma University Hospital, Maebashi, Japan.
Kunihiro TsukasakiDepartment of Hematology, International Medical Center, Saitama Medical University, Hidaka, Japan.
Toshiki UchidaDepartment of Hematology and Oncology, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan.
Junya KurodaDivision of Hematology and Oncology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Ilseung ChoiDepartment of Hematology and Cell Therapy, NHO Kyushu Cancer Center, Fukuoka, Japan.
Michihiro HidakaDepartment of Hematology, NHO Kumamoto Medical Center, Kumamoto, Japan.
Jun AndoDepartment of Hematology, Juntendo University School of Medicine, Tokyo, Japan.
Takashi SakamotoDepartment of Hematology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hisashi KatoDepartment of Hematology and Oncology, The University of Osaka Graduate School of Medicine, Suita, Japan.
Hironobu MinamiDivision of Medical Oncology and Hematology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Shinichiro YoshidaDepartment of Hematology, NHO Nagasaki Medical Center, Omura, Japan.
Matsuo YamamotoClinical Research Center, NHO Nagoya Medical Center, Nagoya, Japan.
Mireille GillingsHUYA BIO International, LLC, San Diego, CA, USA.
Hiroshi OnogiHuya Japan GK, Tokyo, Japan.
Kengo TakeuchiDivision of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T follicular helper (TFH)-derived peripheral T-cell lymphomas (PTCLs) harbor frequent mutations in epigenetic regulators and are sensitive to epigenetic therapies. The histone deacetylase inhibitor tucidinostat demonstrated efficacy in relapsed/refractory PTCL, especially angioimmunoblastic T-cell lymphoma (AITL), in a phase IIb trial; however, the lack of TFH phenotyping has prevented assessment of the predictive value of this phenotype across a broader PTCL spectrum. Therefore, we retrospectively analyzed patients originally diagnosed with AITL or PTCL not otherwise specified (NOS) based on 2008 World Health Organization criteria who participated in the aforementioned trial. TFH phenotype was defined as the expression of ≥ 2 TFH markers. Among the 23 evaluable patients, the TFH group (n = 17) included six with AITL and 11 with PTCL-NOS exhibiting TFH features, and the non-TFH group included six patients with PTCL-NOS. The objective response rate was numerically higher in the TFH group (12/17, 70.6%) than in the non-TFH group (2/6, 33.3%; P = 0.162). Three patients with the TFH phenotype maintained a progression-free survival exceeding 3 years. These findings highlight the potential long-term benefit of tucidinostat in patients with TFH-derived PTCL, supporting the distinct susceptibility of this subtype to epigenetic modulation.

Indexed as

Histone Deacetylase InhibitorsLymphoma, T-Cell, PeripheralT Follicular Helper CellsAdultAgedFemaleHumansMaleMiddle AgedPhenotypeRecurrenceRetrospective StudiesTreatment OutcomeHistone Deacetylase InhibitorsHistone deacetylase inhibitorPeripheral T-cell lymphomaPredictive biomarkerT follicular helper phenotypeTucidinostat

Identifiers

PMID42262647

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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.