Evidence map›Paper›PMID 38841798›Full record

ArticleHaematologica2024

Impact of genetic alterations on central nervous system progression of primary vitreoretinal lymphoma.

Kota Yoshifuji, Daichi Sadato, Takashi Toya, Yotaro Motomura, Chizuko Hirama, Hiroshi Takase, Kouhei Yamamoto, Yuka Harada, Takehiko Mori, Toshikage Nagao

Abstract read
In one paragraph

Article in Haematologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Decoding IGLL5 Mutation-Mediated BCR Signaling: A Novel Mechanism of CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Intraocular Lymphoma: A Review.Journal of ophthalmic & vision research · 2025
    Review
  9. Article
  10. 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

10 authors.

Kota YoshifujiDepartment of Hematology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo. yoshhema@tmd.ac.jp.
Daichi SadatoClinical Research Support Center, Tokyo Metropolitan Komagome Hospital, Tokyo.
Takashi ToyaHematology Division, Tokyo Metropolitan Komagome Hospital, Tokyo.
Yotaro MotomuraDepartment of Hematology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo.
Chizuko HiramaClinical Research Support Center, Tokyo Metropolitan Komagome Hospital, Tokyo.
Hiroshi TakaseDepartment of Ophthalmology and Visual Science, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo.
Kouhei YamamotoDepartment of Pathology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo.
Yuka HaradaClinical Laboratory, Tokyo Metropolitan Komagome Hospital, Tokyo.
Takehiko MoriDepartment of Hematology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo.
Toshikage NagaoDepartment of Hematology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary vitreoretinal lymphoma (PVRL) is a rare malignant lymphoma subtype with an unfavorable prognosis due to frequent central nervous system (CNS) progression. Thus, identifying factors associated with CNS progression is essential for improving the prognosis of PVRL patients. Accordingly, we conducted a comprehensive genetic analysis using archived vitreous humor samples of 36 PVRL patients diagnosed and treated at our institution and retrospectively examined the relationship between genetic alterations and CNS progression. Whole-exome sequencing (N=2) and amplicon sequencing using a custom panel of 107 lymphomagenesis-related genes (N=34) were performed to assess mutations and copy number alterations. The median number of pathogenic genetic alterations per case was 12 (range, 0-22). Pathogenic genetic alterations of CDKN2A, MYD88, CDKN2B, PRDM1, PIM1, ETV6, CD79B, and IGLL5, as well as aberrant somatic hypermutations, were frequently detected. The frequency of ETV6 loss and PRDM1 alteration (mutation and loss) was 23% and 49%, respectively. Multivariate analysis revealed ETV6 loss (hazard ratio [HR]=3.26, 95% confidence interval [CI]: 1.08-9.85) and PRDM1 alteration (HR=2.52, 95% CI: 1.03-6.16) as candidate risk factors associated with CNS progression of PVRL. Moreover, these two genetic factors defined slow-, intermediate-, and rapid-progression groups (0, 1, and 2 factors, respectively), and the median period to CNS progression differed significantly among them (52 vs. 33 vs. 20 months, respectively). Our findings suggest that genetic factors predict the CNS progression of PVRL effectively, and the genetics-based CNS progression model might lead to stratification of treatment.

Indexed as

Disease ProgressionMutationAdultAgedAged, 80 and overBiomarkers, TumorCentral Nervous System NeoplasmsDNA Copy Number VariationsExome SequencingFemaleHumansLymphomaMaleMiddle AgedPrognosisRetinal NeoplasmsBiomarkers, Tumor

Identifiers

PMID38841798
PMCPMC11532695

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.