Evidence map›Paper›PMID 35457279›Full record

ReviewInternational journal of molecular sciences2022

Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis.

Martino Mezzapesa, Giuseppe Losurdo, Francesca Celiberto, Salvatore Rizzi, Antonio d'Amati, Domenico Piscitelli, Enzo Ierardi, Alfredo Di Leo

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 4 pooled it
–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

49 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  19. Embryonic Signaling Pathways Shape Colorectal Cancer Subtypes: Linking Gut Development to Tumor Biology.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
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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.

Martino MezzapesaSection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.
Giuseppe LosurdoSection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.ORCID 0000-0001-7038-3287
Francesca CelibertoSection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.
Salvatore RizziSection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.
Antonio d'AmatiSection of Pathology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.ORCID 0000-0002-4810-1201
Domenico PiscitelliSection of Pathology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.
Enzo IerardiSection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.ORCID 0000-0001-7275-5080
Alfredo Di LeoSection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Until 2010, colorectal serrated lesions were generally considered as harmless lesions and reported as hyperplastic polyps (HPs) by pathologists and gastroenterologists. However, recent evidence showed that they may bear the potential to develop into colorectal carcinoma (CRC). Therefore, the World Health Organization (WHO) classification has identified four categories of serrated lesions: hyperplastic polyps (HPs), sessile serrated lesions (SSLs), traditional serrated adenoma (TSAs) and unclassified serrated adenomas. SSLs with dysplasia and TSAs are the most common precursors of CRC. CRCs arising from serrated lesions originate via two different molecular pathways, namely sporadic microsatellite instability (MSI) and the CpG island methylator phenotype (CIMP), the latter being considered as the major mechanism that drives the serrated pathway towards CRC. Unlike CRCs arising through the adenoma-carcinoma pathway, APC-inactivating mutations are rarely shown in the serrated neoplasia pathway.

Indexed as

AdenomaColonic PolypsColorectal NeoplasmsHumansMicrosatellite InstabilityMutationProto-Oncogene Proteins B-rafProto-Oncogene Proteins B-rafcolorectal cancercolorectal serrated lesionsCpG island methylator phenotypemicrosatellite instabilitymolecular pathwaysserrated pathwaysessile serrated lesions

Identifiers

PMID35457279
PMCPMC9032676

What OpenQuestion holds

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Registered trials

None linked

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.