Trisomy 8 as a recurrent clonal abnormality in breast cancer?

Bullerdiek, Jörn; Leuschner, Elke; Taquia, Elena; Bonk, U; Bartnitzke, Sabine

doi:10.1016/0165-4608(93)90060-y

Cited by 46 publications

(19 citation statements)

References 10 publications

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“…34 Trisomy 8 frequently occurs in myelocytic malignancies 35 and breast cancers. 36,37 Multiplication of 8q has also been described in cancers of the breast and the liver. 38,39 The candidate oncogene on 8q includes c-myc, which has yet to be investigated in thymic neuroendocrine tumors.…”

Section: Discussionmentioning

confidence: 99%

Comparative genomic hybridization analysis of thymic neuroendocrine tumors

Pan

Jong²,

Chen

2005

Modern Pathology

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Thymic neuroendocrine (carcinoid) tumors are a rare neoplasm of the anterior mediastinum. The tumors frequently exhibit a wide spectrum of histology and appear to follow a more aggressive behavior than their nonthymic counterparts. Given the differing clinicopathologic manifestations, thymic neuroendocrine tumors may also possess different cytogenetic abnormalities from those that occur in foregut carcinoid tumors. In this study, we employed comparative genomic hybridization to detect genomic instability in 10 sporadic thymic neuroendocrine tumors and one multiple endocrine neoplasia type 1 (MEN1)-associated case. Gross chromosomal imbalances were found in nine cases, including gains of chromosomal material on regions X, 8, 18 and 20p and losses on 3, 6, 9q, 13q and 11q. We did not observe deletion at locus 11q13 where the MEN1 gene is located. These findings were essentially dissimilar to those reported in sporadic and MEN1-associated foregut carcinoid tumors. Consequently, we consider that a distinctive cytogenetic mechanism is at work in the development of thymic neuroendocrine tumors, which is different from that of foregut carcinoid tumors. The term thymic carcinoid tumor was first introduced by Rosai and Higa 1 to denote a group of thymic neoplasms that histologically resemble the carcinoid tumors of other systems. Later series of studies demonstrated that this group of neoplasms frequently displays a diversity of morphologic features ranging from typical carcinoid as those seen in the bronchopulmonary and digestive tracts, to poorly differentiated small-cell carcinoma. In addition, many such tumors behave more aggressively than the conventional nonthymic carcinoid tumors. Reportedly around half of the cases invaded the surrounding mediastinal structures, and 30-40% metastasized.2-4 Consequently, Moran and Suster 3 proposed to designate the entity as thymic neuroendocrine carcinoma with a threetiered (low, intermediate and high) grading system, which is roughly equivalent to the classic carcinoid, atypical carcinoid and small-cell undifferentiated carcinoma of the World Health Organization (WHO) classification. 5Owing to differing pathologic and clinical presentation, we postulate a different cytogenetic oncogenesis between the thymic and foregut neuroendocrine tumors. Nevertheless, few cytogenetic studies specifically addressing the thymic neuroendocrine tumors are available. So far, only a total of 12 cases in three reports of multiple endocrine neoplasia type 1 syndrome (MEN1)-associated thymic neuroendocrine tumors were examined by using loss of heterozygosity (LOH) study at the 11q13 locus where MEN1 gene is located.6-8 The cytogenetic and molecular events underlying the development of thymic neuroendocrine tumor remain largely unknown. In this study, we aim to characterize the chromosomal aberrances in thymic neuroendocrine tumors with comparative genomic hybridization (CGH) analysis and compare our findings with those of previous reports. Materials and methods Case SelectionWe retrieved 11 cases of ...

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Section: Discussionmentioning

confidence: 99%

Comparative genomic hybridization analysis of thymic neuroendocrine tumors

Pan

Jong²,

Chen

2005

Modern Pathology

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“…Trisomy of chromosome 8, detected in 4/15 invasive ductal carcinomas, has been found by other authors in studies on the same type of pathology (BULLERDIEK et al 1993;ROHEN et al 1995). BULLERDIEK et al (1993) reported trisomy 8 in 2 of 16 cases which presented lymph node involvement and were positive for estrogen and progesterone receptors.…”

Section: Discussionmentioning

confidence: 68%

“…Differences were detected in the karyotypic profile according to the cell culture method used. However, the chromosomes more frequently involved regardless of the methods used, were chromosomes 1, 6, 8, 1 1, 3, 7, 16, 17, and 18, which are reported in the majority of cytogenetic studies on breast tumors (TRENT 1985;HILL et al 1987;DUTRILLAUX et al 1990;HAINSWORTH and GARSON 1990;MITCHELL and SANTIBANEZ-KOREF 1990;BULLERDIEK et al 1993;Lu et al 1993;PANDIS et al 1993PANDIS et al , 1995THOMPSON et al 1993;TRENT et al 1993;ROHEN et al 1995;STEINARSD~TTIR et al 1995). In the present study, we found the nonrandom involvement of the same chromosomes as described above in addition to abnormalities involving chromosomes X, 19, 20, and 22.…”

Section: Discussionmentioning

confidence: 99%

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Cytogenetic Evaluation of 20 Primary Breast Carcinomas

et al. 2004

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Chromosome analysis was performed on samples from 20 Brazilian patients with breast cancer. All the samples were from untreated patients who presented the clinical symptoms for months or years before surgical intervention. Six cases showed axillary lymph node metastases. Clonal chromosome abnormalities were detected in all cases. The numerical alterations most frequently observed involved the loss of chromosomes X, 19, 20, and 22 followed by gain of chromosomes 9 and 8. Among the structural anomalies observed, there was preferential involvement of chromosomes 11, 6, I , 7, 3, and 12, supporting previous reports that these chromosomes may harbour genes of importance in the development of breast tumors. Two cases with a family history of breast cancer had in common total or partial trisomy 1.

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“…Iso 8q and trisomy 8 are common chromosomal changes in cancers. [7][8][9][10][11][12][13] Thus, AI can detect genes involved in tumorigenesis either because of gains of activity or loss of function, but would not distinguish between 8p loss, 8 gain (trisomy), or iso 8q because of the nature of this assay.…”

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confidence: 99%

Allelic Imbalance of 8p Indicates Poor Survival in Gastric Cancer

French

Petroni

Thibideau

et al. 2004

The Journal of Molecular Diagnostics

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Gastric cancer is a common tumor worldwide and a tremendous health burden. However, the underlying mechanisms of tumorigenesis in this cancer's development are primarily undefined. Allelic imbalance (AI) of 8p has been reported in many cancers, yet, the target(s) of alteration and the importance of allelic imbalance on this chromosomal arm in gastric carcinoma development remained to be characterized. Our findings confirmed a high rate of AI on 8p in gastric cancers. Moreover, we demonstrated that AI on 8p, either overall or at marker D8S560, was associated with poorer survival in patients with gastric cancer. Finally, gastric cancers with a high rate of microsatellite instability were significantly associated with noncardia tumors and with female gender.

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Trisomy 8 as a recurrent clonal abnormality in breast cancer?

Cited by 46 publications

References 10 publications

Comparative genomic hybridization analysis of thymic neuroendocrine tumors

Comparative genomic hybridization analysis of thymic neuroendocrine tumors

Cytogenetic Evaluation of 20 Primary Breast Carcinomas

Allelic Imbalance of 8p Indicates Poor Survival in Gastric Cancer

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