Evidence map›Paper›PMID 26673010›Full record

Trial reportOncotarget2016

Presence of sst5TMD4, a truncated splice variant of the somatostatin receptor subtype 5, is associated to features of increased aggressiveness in pancreatic neuroendocrine tumors.

Miguel Sampedro-Núñez, Raúl M Luque, Ana M Ramos-Levi, Manuel D Gahete, Ana Serrano-Somavilla, Alicia Villa-Osaba, Magdalena Adrados, Alejandro Ibáñez-Costa, Elena Martín-Pérez, Michael D Culler and 2 more

Open access · diamondAbstract readClinical Trial
In one paragraph

Trial report in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Somatostatin Receptor Splicing VariantInternational journal of molecular sciences · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Central somatostatin signaling and regulation of food intake.Annals of the New York Academy of Sciences · 2019
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Molecular Genetic Studies of Pancreatic Neuroendocrine Tumors: New Therapeutic Approaches.Endocrinology and metabolism clinics of North America · 2018
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

12 authors at 4 institutions in 1 country.

Miguel Sampedro-NúñezDepartment of Endocrinology and Nutrition, Hospital Universitario de la Princesa, Instituto de Investigación Princesa, Universidad Autónoma de Madrid, Madrid 28006, Spain.
Raúl M LuqueDepartment of Cell Biology, Physiology and Immunology, University of Cordoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofia, and CIBER Fisiopatología de la Obesidad y Nutrición, Córdoba 14014, Spain.
Ana M Ramos-LeviDepartment of Endocrinology and Nutrition, Hospital Universitario de la Princesa, Instituto de Investigación Princesa, Universidad Autónoma de Madrid, Madrid 28006, Spain.
Manuel D GaheteDepartment of Cell Biology, Physiology and Immunology, University of Cordoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofia, and CIBER Fisiopatología de la Obesidad y Nutrición, Córdoba 14014, Spain.
Ana Serrano-SomavillaDepartment of Endocrinology and Nutrition, Hospital Universitario de la Princesa, Instituto de Investigación Princesa, Universidad Autónoma de Madrid, Madrid 28006, Spain.
Alicia Villa-OsabaDepartment of Cell Biology, Physiology and Immunology, University of Cordoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofia, and CIBER Fisiopatología de la Obesidad y Nutrición, Córdoba 14014, Spain.
Magdalena AdradosDepartment of Endocrinology and Nutrition, Hospital Universitario de la Princesa, Instituto de Investigación Princesa, Universidad Autónoma de Madrid, Madrid 28006, Spain.
Alejandro Ibáñez-CostaDepartment of Cell Biology, Physiology and Immunology, University of Cordoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofia, and CIBER Fisiopatología de la Obesidad y Nutrición, Córdoba 14014, Spain.
Elena Martín-PérezDepartment of Endocrinology and Nutrition, Hospital Universitario de la Princesa, Instituto de Investigación Princesa, Universidad Autónoma de Madrid, Madrid 28006, Spain.
Michael D CullerIPSEN Bioscience, Cambridge, Massachusetts 02142, USA.
Mónica MarazuelaDepartment of Endocrinology and Nutrition, Hospital Universitario de la Princesa, Instituto de Investigación Princesa, Universidad Autónoma de Madrid, Madrid 28006, Spain.
Justo P CastañoDepartment of Cell Biology, Physiology and Immunology, University of Cordoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofia, and CIBER Fisiopatología de la Obesidad y Nutrición, Córdoba 14014, Spain.
Hospital Universitario de La Princesa · ESUniversity of Córdoba · ESInstituto Maimónides de Investigación Biomédica de Córdoba · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGastroenteropancreatic neuroendocrine tumors (GEP-NETs) are rare and heterogeneous tumors, and their biological behavior is not well known. We studied the presence and potential functional roles of somatostatin receptors (sst1-5), focusing particularly on the truncated variants (sst5TMD4, sst5TMD5) and on their relationships with the angiogenic system (Ang/Tie-2 and VEGF) in human GEP-NETs. EXPERIMENTAL

designWe evaluated 42 tumor tissue samples (26 primary/16 metastatic) from 26 patients with GEP-NETs, and 30 non-tumoral tissues (26 from adjacent non-tumor regions and 4 from normal controls) from a single center. Expression of sst1-5, sst5TMD4, sst5TMD5, Ang1-2, Tie-2 and VEGF was analyzed using real-time qPCR, immunofluorescence and immunohistochemistry. Expression levels were associated with tumor characteristics and clinical outcomes. Functional role of sst5TMD4 was analyzed in GEP-NET cell lines.

resultssst1 exhibited the highest expression in GEP-NET, whilst sst2 was the most frequently observed sst-subtype (90.2%). Expression levels of sst1, sst2, sst3, sst5TMD4, and sst5TMD5 were significantly higher in tumor tissues compared to their adjacent non-tumoral tissue. Lymph-node metastases expressed higher levels of sst5TMD4 than in its corresponding primary tumor tissue. sst5TMD4 was also significantly higher in intestinal tumor tissues from patients with residual disease of intestinal origin compared to those with non-residual disease. Functional assays demonstrated that the presence of sst5TMD4 was associated to enhanced malignant features in GEP-NET cells. Angiogenic markers correlated positively with sst5TMD4, which was confirmed by immunohistochemical/fluorescence studies.

conclusionssst5TMD4 is overexpressed in GEP-NETs and is associated to enhanced aggressiveness, suggesting its potential value as biomarker and target in GEP-NETs.

Indexed as

AdultAgedAged, 80 and overAngiogenic ProteinsApoptosisCell MovementCell ProliferationFemaleFluorescent Antibody TechniqueFollow-Up StudiesHumansImmunoenzyme TechniquesMaleMiddle AgedNeoplasm Recurrence, LocalNeoplasm StagingAngiogenic ProteinsReceptors, SomatostatinRNA, Messengersomatostatin receptor 5angiogenesisgastroenteropancreatic neuroendocrine tumorsneuroendocrine tumorssst5TMD4sst5TMD5

Identifiers

PMID26673010
PMCPMC4872735
OpenAlexW2276277878

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.