Trisomy 7 in a lung carcinoid tumor: Precocious index of malignant transformation?

Teyssier, Jean-Raymond; Sadrin, R.; Nou, Jean-Marie; Bureau, G.; Adnet, J. J.; Bajolle, F; F, Pigeon

doi:10.1016/0165-4608(85)90171-2

Cited by 24 publications

(8 citation statements)

References 15 publications

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“…21 Our CGH results on TC and AC suggest that 3p deletions are rare events in these tumors (1 of 17 TCs and 1 of 6 ACs). Previous cytogenetic studies of a few pulmonary carcinoid tumors did not detect any 3p deletions, 23,24 except for that of Lai et al, 25 who reported chromosomal abnormalities of 3p in four of four pulmonary NETs.…”

Section: Discussionmentioning

confidence: 81%

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Typical and Atypical Carcinoid Tumors of the Lung Are Characterized by 11q Deletions as Detected by Comparative Genomic Hybridization

Walch¹,

Zitzelsberger²,

Aubele³

et al. 1998

The American Journal of Pathology

151

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Neuroendocrine tumors of the lung represent a wide spectrum of phenotypically distinct entities with different biological characteristics such as typical carcinoid tumor (TC), atypical carcinoid tumor (AC), large-cell neuroendocrine carcinoma (LCNEC), and small-cell lung carcinoma (SCLC). The histogenetic relationships between TC, AC, LCNEC, and SCLC are still unclear. This study was carried out to provide cytogenetic data about pulmonary neuroendocrine tumors and to evaluate their characteristic alterations and histogenetic relations for an improved understanding of the mechanisms of tumor development. Twenty-nine paraffin-embedded tumor samples of TC (n = 17), AC (n = 6), LCNEC (n = 3), and SCLC (n = 3) were selected for isolation of tumor DNA and subsequent comparative genomic hybridization (CGH) analysis. To confirm the comparative genomic hybridization results for characteristic chromosomal imbalances, selected cases were additionally investigated by loss of heterozygosity analysis. For statistical evaluation, we also used comparative genomic hybridization data from 45 published SCLC cases. DNA underrepresentations of 11q were the most frequent findings in TC (8 of 17) and AC (4 of 6), whereas these aberrations were rare in LCNEC (1 of 3) and SCLC (0 of 3). Furthermore, AC showed DNA underrepresentation of 10q (3 of 6) and 13q (3 of 6). In contrast, SCLC and LCNEC were characterized by a different pattern of DNA losses (3p-, 4q-, 5q-, 13q-, and 15q-) and gains (5p+, 17p+, and +20). Statistical analysis revealed significantly different occurrences of 11q deletions in TC/AC versus SCLC (45 published cases of SCLC and our 3 cases; P = 0.002; Fisher's exact test). Thus, TC and AC display frequent loss of 11q material including the MEN1 gene locus, which represents a characteristic genetic alteration in these tumors. Losses of 10q and 13q sequences allow a further cytogenetic differentiation between TC and AC. These additional changes might be responsible for the more aggressive behavior of AC. Three cases of LCNEC, the first to be analyzed by comparative genomic hybridization, exhibited similar complex abnormal patterns (4q-, 5q-, 10q-, 13q-, 15q-) to those of SCLC. Although neuroendocrine tumors of the lung share common phenotypic features, suggesting a genotypic relationship, they differ remarkably in their cytogenetic characteristics, highlighting an early fundamental molecular divergence during the development of these tumors.

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Section: Discussionmentioning

confidence: 81%

“…So far, only a few cell lines derived from TCs and ACs have been investigated by conventional cytogenetic analysis. [23][24][25] These studies, however, were limited to cell lines and did not detect any characteristic chromosomal abnormalities in these pulmonary NETs (Table 1). Until now, no CGH data from TC, AC, and LCNEC are available.…”

mentioning

confidence: 99%

Typical and Atypical Carcinoid Tumors of the Lung Are Characterized by 11q Deletions as Detected by Comparative Genomic Hybridization

Walch¹,

Zitzelsberger²,

Aubele³

et al. 1998

The American Journal of Pathology

151

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“…Data from other tumor types, including bladder (Hopman et al, 1991;Waldman et al, 1991) and malignant melanoma (Herlyn et al, 1985;Trent et al, 1990), support the association between gain of chromosome 7 and tumor progression, as does a study of 5 pleural fluids representing metastatic adenocarcinomas from different organ primaries (Cagle et al, 1989). However, abnormalities of chromosome 7 have also been described in normal bronchial epithelium from lung cancer patients (Lee et al, 1987;Sozzi et al, 1991), and in a benign carcinoid (Teyssier et al, 1985), suggesting this is an early change in malignant transformation.…”

Section: +3de1(3)(q2imentioning

confidence: 98%

Chromosome abnormalities in non‐small cell lung cancer pleural effusions: Cytogenetic indicators of disease subgroups

Lukeis¹,

Ball²,

Irving³

et al. 1993

Genes Chromosomes & Cancer

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A cytogenetic study of pleural effusions (PE) containing metastatic or invasive tumor cells from 11 patients with non-small cell lung cancer (NSCLC) (3 squamous cell carcinomas [SQC] and 8 adenocarcinomas [ADC] including 1 giant cell variant) was performed to identify non-random chromosome abnormalities. Numerical abnormalities seen in > or = 30% of cases included gain of chromosomes 7 and 20, and loss of chromosomes 4, 9, 10, 13, 15, 16, 18, 19, 21, and 22. The most frequent structural abnormality involved rearrangement in 1p with breakpoints clustering at 1p10-p13. Other recurrent breakpoint regions, seen in > or = 30% of cases, occurred in chromosome region 3p10-p21, 3q11-q25, 6p11-p25, 6q13-q23, 7q11-q36, 9q32-q34, 11p11-p13, 11q13-q24, 13p/14p and/or 15p, 17p and 19p, with, in particular, apparent loss of 6q21-q27, 3p21-p26, 7q21-q22, 9p22-p24 (shortest regions of common overlap) and 17p. There was also recurrent gain of 1q23-q44, 8q13-q24, and 11q13-q23. These abnormalities were not restricted to a particular histological subtype, with the exception of +8 and a breakpoint in 9q32-q34, which were seen only in ADC. The 9q32-q34 breakpoint observed in 4 ADC PE (including 1 giant cell variant) represents a new observation in NSCLC. These findings, when compared to those reported for primary NSCLC indicate cytogenetic differences between the two which may be associated with pleural invasion of NSCLC.

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“…Sixteen bronchopulmonary carcinoids, eight TC and eight ATC, were previously analyzed by classical cytogenetics (Teyssier et al, 1985;WhangPeng et al, 1991;Johansson et al, 1993;Lai et al, 1995;Sigl et al, 1999). Comparative genomic hybridization (CGH) studies were done in 23 cases (17 TC and 6 ATC) by Walch et al (1998), in 11 cases by Zhao et al (2000), and in seven carcinoids by our group (Ullmann et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

The position of pulmonary carcinoids within the spectrum of neuroendocrine tumors of the lung and other tissues

Ullmann¹,

Petzmann²,

Klemen³

et al. 2002

Genes Chromosomes & Cancer

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Bronchopulmonary carcinoids comprise 25% of all human carcinoids. The World Health Organization divides them into typical (TC) and atypical forms (ATC), distinguished by differences in mitotic counts lower or higher than 2/2 mm(2) and the presence or absence of necrosis. The reproducibility of this classification with respect to the borderline cases with 1-2 mitotic counts/2 mm(2) has been questioned. We have analyzed 15 TCs and 20 ATCs by comparative genomic hybridization. Loss of 11q was the most frequent aberration in ATC (55%), but was observed only twice in TC (13%). Deletions of 3p were seen only in ATC (25%). Meta-analysis of our data and data from 218 neuroendocrine tumors and 50 non-small-cell lung carcinomas obtained from the literature revealed differences between carcinoids and carcinomas. For example, loss of 5q is frequent in lung carcinomas (75%) but is rarely seen in carcinoids (1.4%). Deletions of 11q are less frequent in neuroendocrine lung carcinomas than in ATC. To obtain a more objective survey of the relationship of pulmonary carcinoids to other neuroendocrine tumors and lung carcinomas, we created a hierarchical clustering dendrogram. This statistical approach resulted in a clear separation of carcinoids and carcinomas, which both built up different clusters. In summary, this study demonstrates the benefit of chromosomal analysis supplementary to the diagnosis of bronchopulmonary carcinoids. We also identified the feasibility of hierarchical clustering to get some clues on relationship between different tumor types. This study further argues against a transition of ATC to high-grade neuroendocrine lung carcinoma.

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Trisomy 7 in a lung carcinoid tumor: Precocious index of malignant transformation?

Cited by 24 publications

References 15 publications

Typical and Atypical Carcinoid Tumors of the Lung Are Characterized by 11q Deletions as Detected by Comparative Genomic Hybridization

Typical and Atypical Carcinoid Tumors of the Lung Are Characterized by 11q Deletions as Detected by Comparative Genomic Hybridization

Chromosome abnormalities in non‐small cell lung cancer pleural effusions: Cytogenetic indicators of disease subgroups

The position of pulmonary carcinoids within the spectrum of neuroendocrine tumors of the lung and other tissues

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