Evidence map›Paper›PMID 40734770›Full record

ArticleEJHaem2025

The Intersection of Lynch Syndrome and Hematological Malignancies: A Rare Short Report.

Tomomi Oka, Takeshi Nakajima, Makoto Iwasaki, June Takeda, Masako Torishima, Maki Sakurada, Takuya Shimizu, Takero Shindo, Masakazu Fujimoto, Shinya Otsuki and 9 more

Abstract read
In one paragraph

Article in EJHaem, 2025. 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

19 authors.

Tomomi OkaClinical Genetics Unit Kyoto University Hospital Kyoto Japan.ORCID https://orcid.org/0009-0008-8354-3604
Takeshi NakajimaClinical Genetics Unit Kyoto University Hospital Kyoto Japan.
Makoto IwasakiDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.
June TakedaDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.
Masako TorishimaClinical Genetics Unit Kyoto University Hospital Kyoto Japan.
Maki SakuradaDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.
Takuya ShimizuDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.
Takero ShindoDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.ORCID https://orcid.org/0000-0002-2085-6151
Masakazu FujimotoDepartment of Diagnostic Pathology Graduate School of Medicine Kyoto University Kyoto Japan.
Shinya OtsukiDepartment of Diagnostic Pathology Graduate School of Medicine Kyoto University Kyoto Japan.
Hironori HagaDepartment of Diagnostic Pathology Graduate School of Medicine Kyoto University Kyoto Japan.
Kokichi SuganoDivision of Clinical Genetics Sasaki Foundation, Kyoundo Hospital Tokyo Japan.
Miho AndoDivision of Clinical Genetics Sasaki Foundation, Kyoundo Hospital Tokyo Japan.
Chisaki MizumotoDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.
Junya KandaDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.ORCID https://orcid.org/0000-0002-6704-3633
Yasuhito NannyaDepartment of Pathology and Tumor Biology Graduate School of Medicine Kyoto University Kyoto Japan.
Seishi OgawaDepartment of Pathology and Tumor Biology Graduate School of Medicine Kyoto University Kyoto Japan.
Akifumi Takaori-KondoDepartment of Hematology Graduate School of Medicine Kyoto University Kyoto Japan.
Shinji KosugiClinical Genetics Unit Kyoto University Hospital Kyoto Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lynch syndrome (LS), which is an autosomal dominant disorder caused primarily by germline pathogenic variants of mismatch repair (MMR) genes, cases a number of malignancies. Hematologic malignancies are not included as related tumors of LS because it has not yet been established whether the carcinogenesis of hematologic malignancies is associated with MMR genes. A 75-year-old woman was admitted to our hospital with acute myeloid leukemia (AML) that had progressed from myelodysplastic syndrome (MDS). She had a history of multiple myeloma (MM) and multiple tumors associated with LS. Genetic testing revealed extensive homozygous deletions ranging from Exon 9 of

Identifiers

PMID40734770
PMCPMC12304074

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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.