Evidence map›Paper›PMID 20615970›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Array comparative genomic hybridization-based characterization of genetic alterations in pulmonary neuroendocrine tumors.

Johannes Voortman, Jih-Hsiang Lee, Jonathan Keith Killian, Miia Suuriniemi, Yonghong Wang, Marco Lucchi, William I Smith, Paul Meltzer, Yisong Wang, Giuseppe Giaccone

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 128 citations in OpenAlex.

  1. Review
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  6. Carcinoid Syndrome: Preclinical Models and Future Therapeutic Strategies.International journal of molecular sciences · 2023
    Review
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  8. Article
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  10. Dual PET Imaging in Bronchial Neuroendocrine Neoplasms: The NETPET Score as a Prognostic Biomarker.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2021
    Article
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4 more citing papers are in PubMed but not listed here.

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 5 institutions in 2 countries.

Johannes VoortmanMedical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Jih-Hsiang Lee
Jonathan Keith Killian
Miia Suuriniemi
Yonghong Wang
Marco Lucchi
William I Smith
Paul Meltzer
Yisong Wang
Giuseppe Giaccone
Molecular Oncology (United States) · USNational Cancer Institute · USNational Institutes of Health · USSuburban Hospital · USUniversity of Pisa · IT

Funding

Molecular Profiling of Clinical SpecimensZICBC011040 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI EDELMAN, DANIEL · 2009 to 2020
$25.5M
Cancer Genomics Technology DevelopmentZIABC011091 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MELTZER, PAUL S. · 2009 to 2025
$16.9M
Thorarcic Cancer Research LaboratoryZIABC011269 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GIACCONE, GIUSEPPE · 2010 to 2013
$5.4M
6 · The paper itself

Abstract

The goal of this study was to characterize and classify pulmonary neuroendocrine tumors based on array comparative genomic hybridization (aCGH). Using aCGH, we performed karyotype analysis of 33 small cell lung cancer (SCLC) tumors, 13 SCLC cell lines, 19 bronchial carcinoids, and 9 gastrointestinal carcinoids. In contrast to the relatively conserved karyotypes of carcinoid tumors, the karyotypes of SCLC tumors and cell lines were highly aberrant. High copy number (CN) gains were detected in SCLC tumors and cell lines in cytogenetic bands encoding JAK2, FGFR1, and MYC family members. In some of those samples, the CN of these genes exceeded 100, suggesting that they could represent driver alterations and potential drug targets in subgroups of SCLC patients. In SCLC tumors, as well as bronchial carcinoids and carcinoids of gastrointestinal origin, recurrent CN alterations were observed in 203 genes, including the RB1 gene and 59 microRNAs of which 51 locate in the DLK1-DIO3 domain. These findings suggest the existence of partially shared CN alterations in these tumor types. In contrast, CN alterations of the TP53 gene and the MYC family members were predominantly observed in SCLC. Furthermore, we demonstrated that the aCGH profile of SCLC cell lines highly resembles that of clinical SCLC specimens. Finally, by analyzing potential drug targets, we provide a genomics-based rationale for targeting the AKT-mTOR and apoptosis pathways in SCLC.

Indexed as

Oligonucleotide Array Sequence AnalysisAdultAgedAged, 80 and overBronchial NeoplasmsCarcinoid TumorCell Line, TumorComparative Genomic HybridizationCytogenetic AnalysisDNA Copy Number VariationsFemaleGene DosageGene Expression Regulation, NeoplasticGenome, HumanHumansLung Neoplasms

Identifiers

PMID20615970
PMCPMC2919980
OpenAlexW1996883110

What OpenQuestion holds

Textmetadata
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.