Evidence map›Paper›PMID 34535012›Full record

ArticleBlood advances2021

Genetic profiles of subcutaneous panniculitis-like T-cell lymphoma and clinicopathological impact of HAVCR2 mutations.

Jiwon Koh, Insoon Jang, Seungchan Mun, Cheol Lee, Hee Jeong Cha, Young Ha Oh, Jin-Man Kim, Jae Ho Han, Jin Ho Paik, Junhun Cho and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. GermlineHaematologica · 2023
    Pooled it
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  11. Subcutaneous Panniculitis-Like T-Cell Lymphoma in Children: Two Case Reports.Clinical, cosmetic and investigational dermatology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 9 institutions in 1 country.

Jiwon KohDepartment of Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea.
Insoon JangDepartment of Data Science Research, Innovative Medical Technology Research Institute, Seoul National University Hospital, Seoul, Republic of Korea.ORCID 0000-0001-9542-6984
Seungchan MunSeoul National University Cancer Research Institute, Seoul, Republic of Korea.
Cheol LeeDepartment of Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-5098-8529
Hee Jeong ChaDepartment of Pathology, Ulsan University Hospital, Ulsan University College of Medicine, Ulsan, Republic of Korea.
Young Ha OhDepartment of Pathology, Hanyang University Guri Hospital, Hanyang University College of Medicine, Guri, Gyeonggi-do, Republic of Korea.ORCID 0000-0001-8750-9843
Jin-Man KimDepartment of Pathology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Jae Ho HanDepartment of Pathology, Ajou University School of Medicine, Suwon, Gyeonggi-do, Republic of Korea.
Jin Ho PaikDepartment of Pathology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Gyeonggi-do, Republic of Korea.
Junhun ChoDepartment of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Young Hyeh KoDepartment of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Chan-Sik ParkDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; and.
Heounjeong GoDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; and.ORCID 0000-0003-0412-8709
Jooryung HuhDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; and.
Kwangsoo KimDepartment of Data Science Research, Innovative Medical Technology Research Institute, Seoul National University Hospital, Seoul, Republic of Korea.
Yoon Kyung JeonDepartment of Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-8466-9681
Seoul National University Hospital · KRUlsan College · KRSamsung Medical Center · KRSeoul National University · KRAjou University · KRChungnam National University · KRHanyang University Guri Hospital · KRSeoul National University Bundang Hospital · KRUlsan University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies identified germline mutations in HAVCR2 (encoding T-cell immunoglobulin mucin 3) as a genetic factor that predisposes to subcutaneous panniculitis-like T-cell lymphoma (SPTCL). However, the differences between HAVCR2-mutated (HAVCR2MUT) and HAVCR2 wild-type (HAVCR2WT) SPTCLs remain unclear. A nationwide cohort of 53 patients with SPTCL diagnosed at 8 Korean institutions was established. Whole-exome sequencing and RNA-sequencing were performed on 8 patients in the discovery set. In the validation set, targeted gene sequencing or direct sequencing of HAVCR2 was performed. Of 49 patients with available HAVCR2 status, 25 (51.0%) were HAVCR2Y82C. HAVCR2Y82C was associated with younger age (P = .001), development of hemophagocytic lymphohistiocytosis or hemophagocytic lymphohistiocytosis-like systemic illness (P < .001), and short relapse-free survival (RFS) (P = .023). Most mutated genes in SPTCLs were involved in immune responses, epigenetic modifications, and cell signaling. Mutations in UNC13D, PIAS3, and KMT2D were more frequent in HAVCR2WT SPTCLs. At the gene expression level, HAVCR2Y82C SPTCLs were enriched in genes involved in IL6-JAK-STAT3 signaling and in tumor necrosis factor-α signaling via NF-κB. CCR4 was significantly upregulated in HAVCR2WT SPTCLs both at the messenger RNA level and at the protein level. We established a risk stratification system for SPTCL by integrating clinical and histopathological features, including age and HAVCR2 mutation status. This risk stratification system was strongly associated with RFS (P = .031). In conclusion, the HAVCR2Y82C mutation was common in Korean patients with SPTCL and was associated with unique clinicopathological and genetic features. Combining clinicopathological parameters could aid in predicting prognosis for patients with SPTCL.

Indexed as

Lymphoma, T-CellPanniculitisGenetic ProfileHepatitis A Virus Cellular Receptor 2HumansMembrane ProteinsMutationHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2Membrane ProteinsUNC13D protein, human

Identifiers

PMID34535012
PMCPMC8945616
OpenAlexW3200961547

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.