Evidence map›Paper›PMID 27661019›Full record

Observational studyMedicine2016

Gastrointestinal stromal tumors (GISTs) and second malignancies: A novel "sentinel tumor"? A monoinstitutional, STROBE-compliant observational analysis.

Maria Grazia Rodriquenz, Sabrina Rossi, Riccardo Ricci, Maurizio Martini, Mario Larocca, Angelo Dipasquale, Michela Quirino, Giovanni Schinzari, Michele Basso, Ettore D'Argento and 3 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Additional malignancies in patients with gastrointestinal stromal tumors (GIST): incidence, pathology and prognosis according to a time of occurrence-based classification.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    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

13 authors at 4 institutions in 3 countries.

Maria Grazia RodriquenzDepartment of Medical Oncology, Istituto Oncologico Veneto, Padova Department of Medical Oncology, Humanitas Clinical and Research Center, Rozzano (MI) Department of Pathology, Catholic University of Sacred Heart, Rome Department of Medical Oncology, Catholic University of Sacred Heart, Rome, Italy.
Sabrina Rossi
Riccardo Ricci
Maurizio Martini
Mario Larocca
Angelo Dipasquale
Michela Quirino
Giovanni Schinzari
Michele Basso
Ettore D'Argento
Antonia Strippoli
Carlo Barone
Alessandra Cassano
Università Cattolica del Sacro Cuore · ITIstituto Oncologico Veneto · ITPontifícia Universidade Católica de São Paulo · BRUniversity of the Sacred Heart · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several evidences showed that patients with gastrointestinal stromal tumors (GISTs) develop additional malignancies. However, thorough incidence of second tumors remains uncertain as the possibility of a common molecular pathogenesis.A retrospective series of 128 patients with histologically proven GIST treated at our institution was evaluated. Molecular analysis of KIT and PDGFR-α genes was performed in all patients. Following the involvement of KRAS mutation in many tumors' pathogenesis, analysis of KRAS was performed in patients with also second neoplasms.Forty-six out of 128 GIST patients (35.9%) had a second neoplasm. Most second tumors (52%) raised from gastrointestinal tract and 19.6% from genitourinary tract. Benign neoplasms were also included (21.7%). Molecular analysis was available for 29/46 patients with a second tumor: wild-type GISTs (n. 5), exon 11 (n. 16), exon 13 (n. 1), exon 9 (n. 1) KIT mutations, exon 14 PDGFR-α mutation (n. 2) and exon 18 PDGFR-α mutation (n. 4). KIT exon 11 mutations were more frequent between patients who developed a second tumor (P = 0.0003). Mutational analysis of KRAS showed a wild-type sequence in all cases. In metachronous cases, the median time interval between GIST and second tumor was 21.5 months.The high frequency of second tumors suggests that an unknown common molecular mechanism might play a role, but it is not likely that KRAS is involved in this common pathogenesis. The short interval between GIST diagnosis and the onset of second neoplasms asks for a careful follow-up, particularly in the first 3 years after diagnosis.

Indexed as

AdultAgedAged, 80 and overDNA Mutational AnalysisExonsFemaleGastrointestinal NeoplasmsGastrointestinal Stromal TumorsHumansImmunohistochemistryIncidenceMaleMiddle AgedMutationNeoplasms, Second PrimaryPolymerase Chain ReactionKRAS protein, humanProto-Oncogene Proteins c-kitProto-Oncogene Proteins p21(ras)Receptor, Platelet-Derived Growth Factor alpha

Identifiers

PMID27661019
PMCPMC5044889
OpenAlexW2521929627

What OpenQuestion holds

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LicenceCC BY-ND
Read underepoch 390

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.