Evidence map›Paper›PMID 27430658›Full record

ArticleInternational journal of molecular medicine2016

Serrated polyposis associated with a family history of colorectal cancer and/or polyps: The preferential location of polyps in the colon and rectum defines two molecular entities.

Patrícia Silva, Cristina Albuquerque, Pedro Lage, Vanessa Fontes, Ricardo Fonseca, Inês Vitoriano, Bruno Filipe, Paula Rodrigues, Susana Moita, Sara Ferreira and 5 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 32% of its field
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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
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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

15 authors at 1 institution in 1 country.

Patrícia SilvaMolecular Pathobiology Research Unit (UIPM), Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Cristina AlbuquerqueMolecular Pathobiology Research Unit (UIPM), Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Pedro LageGastroenterology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Vanessa FontesMolecular Pathobiology Research Unit (UIPM), Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Ricardo FonsecaPathology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Inês VitorianoMolecular Pathobiology Research Unit (UIPM), Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Bruno FilipeMolecular Pathobiology Research Unit (UIPM), Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Paula RodriguesFamilial Cancer Risk Clinic, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Susana MoitaMolecular Pathobiology Research Unit (UIPM), Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Sara FerreiraGastroenterology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Rita SousaGastroenterology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Isabel ClaroGastroenterology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Carlos Nobre LeitãoGastroenterology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Paula ChavesPathology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
António Dias PereiraGastroenterology Service, Portuguese Institute of Oncology of Lisbon Francisco Gentil, E.P.E. (IPOLFG, EPE), Lisbon, Portugal.
Instituto Português de Oncologia Francisco Gentil · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serrated polyposis (SPP) is characterized by the development of multiple serrated polyps and an increased predisposition to colorectal cancer (CRC). In the present study, we aimed to characterize, at a clinical and molecular level, a cohort of SPP patients with or without a family history of SPP and/or polyps/CRC (SPP-FHP/CRC). Sixty-two lesions from 12 patients with SPP-FHP/CRC and 6 patients with sporadic SPP were included. The patients with SPP-FHP/CRC presented with an older mean age at diagnosis (p=0.027) and a more heterogeneous histological pattern of lesions (p=0.032) than the patients with sporadic SPP. We identified two molecular forms of SPP-FHP/CRC, according to the preferential location of the lesions: proximal/whole-colon or distal colon. Mismatch repair (MMR) gene methylation [mutS homolog 6 (MSH6)/mutS homolog 3 (MSH3)] or loss of heterozygosity (LOH) of D2S123 (flanking MSH6) were detected exclusively in the former (p=3.0x10-7), in most early lesions. Proximal/whole‑colon SPP-FHP/CRC presented a higher frequency of O-6-methylguanine-DNA methyltransferase (MGMT) methylation/LOH, microsatellite instability (MSI) and Wnt mutations (19/29 vs. 7/17; 16/23 vs. 1/14, p=2.2x10-4; 15/26 vs. 2/15, p=0.006; 14/26 vs. 4/20, p=0.02) but a lower frequency of B-raf proto-oncogene, serine/threonine kinase (BRAF) mutations (7/30 vs. 12/20, p=0.0089) than the distal form. CRC was more frequent in cases of Kirsten rat sarcoma viral oncogene homolog (KRAS)-associated proximal/whole-colon SPP-FHP/CRC than in the remaining cases (4/4 vs. 1/8, p=0.01). Thus, SPP-FHP/CRC appears to be a specific entity, presenting two forms, proximal/whole-colon and distal, which differ in the underlying tumor initiation pathways. Early MGMT and MMR gene deficiency in the former may underlie an inherited susceptibility to genotoxic stress.

Indexed as

AdultAgedAged, 80 and overColonColonic PolypsColorectal NeoplasmsDNA-Binding ProteinsDNA MethylationDNA Modification MethylasesDNA Repair EnzymesFamily HealthFemaleHumansMaleMicrosatellite InstabilityMiddle AgedBRAF protein, humanDNA-Binding ProteinsDNA Modification MethylasesDNA Repair EnzymesG-T mismatch-binding proteinKRAS protein, humanMAS1 protein, humanMGMT protein, humanMSH3 protein, humanMutS Homolog 3 ProteinProto-Oncogene MasProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Tumor Suppressor Proteins

Identifiers

PMID27430658
PMCPMC4990292
OpenAlexW2471573307

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.