Evidence map›Paper›PMID 11073802›Full record

ArticleThe American journal of pathology2000

Genomic alterations in well-differentiated gastrointestinal and bronchial neuroendocrine tumors (carcinoids): marked differences indicating diversity in molecular pathogenesis.

J Zhao, R R de Krijger, D Meier, E J Speel, P Saremaslani, S Muletta-Feurer, C Matter, J Roth, P U Heitz, P Komminoth

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 106 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Genomic dissection of gastrointestinal and lung neuroendocrine neoplasm.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2019
    Article
  6. Review
  7. Neuroendocrine tumors of the thymus and mediastinum.Journal of thoracic disease · 2017
    Review
  8. Article
  9. Article
  10. Genomic landscape of pancreatic neuroendocrine tumors.World journal of gastroenterology · 2014
    Article
  11. Second primary malignancies in patients with neuroendocrine tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Array comparative genomic hybridization-based characterization of genetic alterations in pulmonary neuroendocrine tumors.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  19. Article
  20. Molecular profiles of gastroenteropancreatic endocrine tumors.Virchows Archiv : an international journal of pathology · 2007
    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

10 authors at 2 institutions in 2 countries.

J ZhaoDepartment of Pathology, University of Zurich, Zurich, Switzerland.
R R de Krijger
D Meier
E J Speel
P Saremaslani
S Muletta-Feurer
C Matter
J Roth
P U Heitz
P Komminoth
University of Zurich · CHRotterdam University of Applied Sciences · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroendocrine tumors (carcinoids) are a heterogeneous group of neoplasms arising from the diffuse neuroendocrine system. Genetic changes underlying their tumorigenesis are primarily unknown. We used comparative genomic hybridization to screen 32 well-differentiated neuroendocrine tumors (21 gastrointestinal and 11 bronchial) and three associated metastases for genomic alterations. There were striking differences of genomic imbalances between the two subgroups of neuroendocrine tumors. Losses of chromosome 18q and 18p were shown in eight (38%) and seven (33%), respectively, out of 21 gastrointestinal tumors and in none of the 11 bronchial tumors. Conversely, deletions of 11q occurred in four of 11 (36%) bronchial tumors but only in one gastrointestinal tumor. These comparative genomic hybridization findings were confirmed by interphase cytogenetics. Our data indicate that neuroendocrine tumors of the two subgroups develop via different molecular pathways. Inactivation of one or several tumor suppressor genes on chromosome 18 may be important for the biological behavior of gastrointestinal tumors, whereas gene inactivation on 11q seems to be associated with tumor development of the bronchi.

Indexed as

GenomeAdultAgedBronchial NeoplasmsCarcinoid TumorChromosome DeletionChromosome MappingChromosomes, Human, Pair 11Chromosomes, Human, Pair 18DNAFemaleGastrointestinal NeoplasmsGene DosageGene FrequencyHumansIn Situ Hybridization, FluorescenceDNA

Identifiers

PMID11073802
PMCPMC1885722
OpenAlexW161611109

What OpenQuestion holds

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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.