Evidence map›Paper›PMID 42431843›Full record

ArticleInternational journal of cancer2026

Evaluation of Mutation Risk Using Patient-Derived Organoids in Patients With Lynch Syndrome.

Youmi Shin, Dong Keon Kim, Yoojeong Seo, Hyeon Hee Lee, Jihye Park, Soo Jung Park, Jae Jun Park, Jae Hee Cheon, Jongwon Oh, Sanghoo Lee and 1 more

Abstract read
In one paragraph

Article in International journal of cancer, 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

11 authors.

Youmi ShinDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Dong Keon KimDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Yoojeong SeoDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Hyeon Hee LeeDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Jihye ParkDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Soo Jung ParkDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Jae Jun ParkDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Jae Hee CheonDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Jongwon OhDepartment of Laboratory Medicine, Seoul Clinical Laboratories, Yongin-si, Gyeonggi-do, Korea.
Sanghoo LeeCompanion Biomarker Center, Seoul Clinical Laboratories Healthcare Inc, Yongin-si, Gyeonggi-do, Korea.
Tae Il KimDivision of Gastroenterology, Department of Internal Medicine and Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0003-4807-890X

Funding

Yonsei University College of Medicine 6-2022-0168Yonsei University College of Medicine 6-2024-0153
6 · The paper itself

Abstract

Lynch syndrome (LS) is a hereditary cancer predisposition syndrome caused by germline mutation of DNA mismatch repair (MMR) genes, most notably associated with colorectal cancer. Although LS patients face high risk of CRC, risk can vary even among those with the same pathogenic MMR germline mutations. We suggest a functional assay platform for assessing mutation risk using patient-derived organoid (PDOs). We measured organoid response to the cytotoxic effects of a methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) based on DNA damage-induced apoptosis. When normal (non-LS) colon organoids were used, treatment with MNNG and four passages of organoid culture led to decreased total growth (organoid area), but there was no significant change in number. To increase the effect of MNNG and induce apoptosis in normal colon organoids, we added O

Indexed as

Colorectal Neoplasms, Hereditary NonpolyposisOrganoidsApoptosisColonDNA DamageDNA Mismatch RepairFemaleGerm-Line MutationHumansMaleMethylnitronitrosoguanidineMiddle AgedMutationMethylnitronitrosoguanidinecolorectal cancerLynch syndromemutationorganoid

Identifiers

PMID42431843
PMCPMC13595499

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.