Evidence map›Paper›PMID 29103024›Full record

ArticleCancer biomarkers : section A of Disease markers2018

Long-term survivors of pancreatic adenocarcinoma show low rates of genetic alterations in KRAS, TP53 and SMAD4.

Michele Masetti, Giorgia Acquaviva, Michela Visani, Giovanni Tallini, Adele Fornelli, Moira Ragazzi, Francesco Vasuri, Daniela Grifoni, Simone Di Giacomo, Sirio Fiorino and 8 more

Abstract read
In one paragraph

Article in Cancer biomarkers : section A of Disease markers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  7. Genomic landscape of clinically advancedFrontiers in oncology · 2023
    Article
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  11. Highlights on the Role ofInternational journal of molecular sciences · 2021
    Review
  12. Review
  13. Molecular alterations in pancreatic tumors.World journal of gastroenterology · 2021
    Review
  14. 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

18 authors.

Michele MasettiSurgery Unit, Azienda USL-Maggiore Hospital, Bologna, Italy.
Giorgia AcquavivaDepartment of Medicine (Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale) - Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna School of Medicine, Bologna, Italy.
Michela VisaniDepartment of Medicine (Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale) - Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna School of Medicine, Bologna, Italy.
Giovanni TalliniDepartment of Medicine (Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale) - Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna School of Medicine, Bologna, Italy.
Adele FornelliAnatomic Pathology Unit, Azienda USL-Maggiore Hospital, Bologna, Italy.
Moira RagazziAnatomic Pathology Unit, Arcispedale Santa Maria Nuova - IRCCS, Reggio Emilia, Italy.
Francesco VasuriAnatomic Pathology Unit, "F. Addarii" Institute of Oncology and Transplantation Pathology, S. Orsola-Malpighi University Hospital, Bologna, Italy.
Daniela GrifoniDepartment of Pharmacy and Biotechnology (Dipartimento di Farmacia e Biotecnologie) - Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna, Bologna, Italy.
Simone Di GiacomoDepartment of Pharmacy and Biotechnology (Dipartimento di Farmacia e Biotecnologie) - Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna, Bologna, Italy.
Sirio FiorinoInternal Medicine Unit, Maggiore Hospital, Bologna, Italy.
Raffaele LombardiSurgery Unit, Azienda USL-Maggiore Hospital, Bologna, Italy.
David TuminatiSurgery Unit, Azienda USL-Maggiore Hospital, Bologna, Italy.
Matteo RavaioliDepartment of General Surgery and Transplantation, St. Orsola-Malpighi University Hospital, Bologna, Italy.
Carlo FabbriUnit of Gastroenterology and Digestive Endoscopy, AUSL Bologna Bellaria-Maggiore Hospital, Bologna, Italy.
Maria Letizia Bacchi-ReggianiDepartment of Medicine (Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale), Cardiology Unit, Policlinico S. Orsola-Malpighi, University of Bologna, Bologna, Italy.
Annalisa PessionDepartment of Pharmacy and Biotechnology (Dipartimento di Farmacia e Biotecnologie) - Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna, Bologna, Italy.
Elio JovineSurgery Unit, Azienda USL-Maggiore Hospital, Bologna, Italy.
Dario de BiaseDepartment of Pharmacy and Biotechnology (Dipartimento di Farmacia e Biotecnologie) - Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna, Bologna, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic adenocarcinoma (PDAC) is one of the deadliest human malignancies. Although surgery is currently the only effective treatment for PDAC, most patients survive less than 20 months after tumor resection.

objectiveThe primary goal was to investigate alterations in KRAS, TP53, SMAD4 and CDKN2A/p16 in tumors from patients with exceptionally long survival after surgery.

methodsTumors from 15 patients with PDAC that survived more than 55 months after surgery ("LS") were analyzed for KRAS, TP53, IDH1, NRAS and BRAF using next-generation sequencing. SMAD4 and CDKN2A/p16 was tested using immunohistochemistry. MGMT promoter methylation was investigated.

resultsTumors from "LS" have a lower prevalence of KRAS and TP53 mutations and had more frequently SMAD4 retained expression, if compared with that of patients died within 24 months from surgery. The survival of patients with wild-type KRAS and TP53 tumors was more than twice longer than that of patients bearing KRAS and TP53 mutations (90.2 vs. 41.1 months). Patients with KRAS wild-type tumors and that retained SMAD4 expression had a survival twice longer than cases with alterations in both genes (83.8 vs. 36.7 months). Eleven tumors (39.3%) showed MGMT methylation.

conclusionsOur data indicate that absence of KRAS, TP53 and SMAD4 genetic alterations may identify a subset of pancreatic carcinomas with better outcome.

Indexed as

AdenocarcinomaAgedCancer SurvivorsCarcinoma, Pancreatic DuctalFemaleHumansImmunohistochemistryMaleMiddle AgedMutationProto-Oncogene Proteins p21(ras)Smad4 ProteinTumor Suppressor Protein p53KRAS protein, humanProto-Oncogene Proteins p21(ras)Smad4 ProteinSMAD4 protein, humanTP53 protein, humanTumor Suppressor Protein p53KRASmutationPancreatic adenocarcinomaSMAD4TP53

Identifiers

PMID29103024
PMCPMC13078277

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