Evidence map›Paper›PMID 40533677›Full record

ArticleVirchows Archiv : an international journal of pathology2025

Progression of dysplasia in sessile serrated lesions with proliferative zone redistribution: 'Top-down growth' as a marker of malignant potential.

Kaori Takamura, Yoichi Ajioka, Tatsuya Abé, Tatiana Gritcun, Saori Takashima, Shuhei Kondo, Yusuke Tani, Riuko Ohashi

Abstract read
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In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. 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

8 authors.

Kaori TakamuraDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan. takamura@med.niigata-u.ac.jp.ORCID http://orcid.org/0009-0001-0571-5780
Yoichi AjiokaDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Tatsuya AbéDivision of Oral Pathology, Faculty of Dentistry & Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.ORCID http://orcid.org/0000-0003-3166-6975
Tatiana GritcunDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Saori TakashimaDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Shuhei KondoDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Yusuke TaniDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Riuko OhashiDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.ORCID http://orcid.org/0000-0001-5820-7870

Funding

Japan Society for the Promotion of Science 22K15422
6 · The paper itself

Abstract

This study aimed to elucidate the morphological and proliferative progression of dysplasia in sessile serrated lesions (SSLs) to submucosal invasive carcinoma (SIC). Seventy-six SSLs with dysplasia, including 20 with SIC, were analysed. Each lesion was systematically partitioned into morphological units (MUs) based on cytological atypia (low/high) and gland pattern (serrated/tubular), resulting in 200 MUs: serrated-low (n = 76), serrated-high (n = 34), tubular-low (n = 26), and tubular-high (n = 64). These MUs were further categorised as SIC-related (n = 21) or -unrelated (n = 179). Ki67 immunostaining defined proliferative zones within each MU: lower (Ki67-L, n = 70), upper (Ki67-U, n = 40), diffuse (Ki67-D, n = 58), and other (n = 32, excluded from statistical analyses). Fisher's exact test was used in the following specific analyses. Significant associations between serrated-low MUs and SIC-unrelated MUs, and between tubular-high MUs and SIC-related MUs (p < 0.001, respectively) were observed. Moreover, Ki67-L patterns were absent in SIC-related MUs (0/70, 0%, p < 0.001), predominantly in serrated-low MUs (45/70, 64%, p < 0.001). Conversely, Ki67-D patterns were enriched in SIC-related (20/58, 34%, p < 0.001) and tubular-high MUs (39/58, 67%, p < 0.001). Furthermore, Ki67-U patterns exhibited intermediate frequencies between Ki67-L and Ki67-D patterns, with one (2.5%) in SIC-related MUs, six (15%) in serrated-low MUs, and 16 (40%) in tubular-high MUs. This study revealed a significant correlation between Ki67 expression patterns and morphological progression of dysplasia in SSLs. Additionally, the observed Ki67 redistribution, from lower to upper mucosa, followed by diffuse downward spread, mirrors the top-down growth pattern observed in conventional adenomas. Further molecular studies focusing on these proliferative zones are crucial for elucidating the underlying mechanisms of dysplasia progression in SSLs.

Indexed as

Biomarkers, TumorColonic PolypsColorectal NeoplasmsPrecancerous ConditionsAgedAged, 80 and overCell ProliferationDisease ProgressionFemaleHumansImmunohistochemistryKi-67 AntigenMaleMiddle AgedBiomarkers, TumorKi-67 AntigenMKI67 protein, humanDysplasiaKi67 immunohistochemistryProliferative zoneSerrated neoplasia pathwaySessile serrated lesionsTop-down growth

Identifiers

PMID40533677

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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.