Evidence map›Paper›PMID 41978784›Full record

ArticleSurgical case reports2026

Hyperprogression after Anti-Programmed Death-1 Therapy in a Case of Sigmoid Colon Cancer with Lynch Syndrome.

Ryota Miura, Gaku Ohira, Michihiro Maruyama, Toru Tochigi, Tetsuro Maruyama, Koichiro Okada, Atsushi Hirata, Hisahiro Matsubara

Abstract readCase Reports
In one paragraph

Article in Surgical case reports, 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

8 authors.

Ryota MiuraDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.
Gaku OhiraDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.
Michihiro MaruyamaDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.
Toru TochigiDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.
Tetsuro MaruyamaDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.
Koichiro OkadaDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.
Atsushi HirataDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.
Hisahiro MatsubaraDepartment of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Chiba, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionLynch syndrome is a hereditary condition caused by germline defects in mismatch repair (MMR) genes, resulting in microsatellite instability-high (MSI-H) tumors. Immune checkpoint inhibitors (ICIs) have demonstrated efficacy in the treatment of MSI-H advanced cancers. However, hyperprogressive disease (HPD) following ICI therapy is a rare and paradoxical phenomenon. We report a case of advanced sigmoid colon cancer associated with Lynch syndrome that developed HPD after pembrolizumab treatment. CASE PRESENTATION: A 51-year-old woman with advanced sigmoid colon cancer and a history of endometrial cancer presented with severe colonic stenosis, peritoneal dissemination, and suspected liver metastases, necessitating emergency colostomy. Immunohistochemistry revealed loss of MLH1 and PMS2 expression, consistent with suspected Lynch syndrome. Targeted molecular testing identified a

conclusionsThis case underscores the importance of early response evaluation in ICI-treated MSI-H tumors. Rapid disease progression requires prompt differentiation between HPD and pseudoprogression, emphasizing the necessity of timely therapeutic modification.

Indexed as

hyperprogressive diseaseimmune checkpoint inhibitorlynch syndromemicrosatellite instabilitypembrolizumab

Identifiers

PMID41978784
PMCPMC13070620

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