Literature DB >> 9781656

Unbalanced chromosomal aberrations in neuroendocrine lung tumors as detected by comparative genomic hybridization.

R Ullmann1, A Schwendel, H Klemen, G Wolf, I Petersen, H H Popper.   

Abstract

Typical and atypical carcinoids (TC, ATC) and small (SCLC) and large cell neuroendocrine carcinomas (LCNEC) constitute the spectrum of neuroendocrine lung tumors. Chromosomal aberrations have not been studied in LCNEC and only rarely in carcinoids. Only SCLCs have been investigated frequently for chromosomal aberrations. We compared three typical and four atypical carcinoids, one atypical carcinoid/SCLC mixed type, three SCLC, and three LCNEC for chromosomal gains and losses using comparative genomic hybridization. Typical carcinoids showed either no changes or only few chromosomal gains. Atypical carcinoids appeared genetically heterogeneous: One case had no aberrations, and three cases had few aberrations; two of them showed a deletion of 11q. SCLC and LCNEC were characterized by many gains and losses, especially similar changes of 3p, 5q, 5p, and 13q. Although ATC resemble LCNEC morphologically, there were no similarities at the genetic level. We have found a reciprocal relationship of prognosis and the amount of aberrations. TCs and ATCs with few chromosomal changes have the best prognosis, whereas SCLCs and LCNECs were generally characterized by a great amount of aberrations and worst prognosis. There was no unbalanced aberration common in all types of neuroendocrine tumors of the lung.

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Year:  1998        PMID: 9781656     DOI: 10.1016/s0046-8177(98)90428-2

Source DB:  PubMed          Journal:  Hum Pathol        ISSN: 0046-8177            Impact factor:   3.466


  10 in total

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Review 2.  Neuroendocrine tumors of the thymus and mediastinum.

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

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

Authors:  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
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5.  DNA copy number aberrations in small-cell lung cancer reveal activation of the focal adhesion pathway.

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Journal:  Oncogene       Date:  2010-08-30       Impact factor: 9.867

6.  Analysis of chromosome-11 aberrations in pulmonary and gastrointestinal carcinoids: an array comparative genomic hybridization-based study.

Authors:  Susanna Petzmann; Reinhard Ullmann; Iris Halbwedl; Helmut H Popper
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7.  Genetics of a combined lung small cell carcinoma and large cell neuroendocrine carcinoma with adenocarcinoma.

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8.  PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours.

Authors:  Zixuan Zhang; Mengzhao Wang
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9.  Characterization of high-grade neuroendocrine tumors of the lung in relation to menin mutations.

Authors:  N Haruki; Y Yatabe; W D Travis; S Nomoto; H Osada; S Nakamura; A Nakao; Y Fujii; T Takahashi
Journal:  Jpn J Cancer Res       Date:  2000-03

10.  Molecular evidence for the bi-clonal origin of neuroendocrine tumor derived metastases.

Authors:  Beate Rinner; Birgit Gallè; Slave Trajanoski; Carina Fischer; Martina Hatz; Theresa Maierhofer; Gabriele Michelitsch; Farid Moinfar; Ingeborg Stelzer; Roswitha Pfragner; Christian Guelly
Journal:  BMC Genomics       Date:  2012-11-05       Impact factor: 3.969

  10 in total

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