Cytogenetic study of pituitary adenomas

Bettio, Daniela; Rizzi, Nicoletta; Giardino, Daniela; Persani, Luca; Pecori-Giraldi, Francesca; Losa, Marco; Larizza, Lidia

doi:10.1016/s0165-4608(96)00426-8

Cited by 31 publications

(23 citation statements)

References 10 publications

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“…32,35 Nevertheless, the pathogenetic importance of chromosome 19 for the development of pituitary tumors is emphasized by the findings of 1 cytogenetic study, where genetic aberrations including chromosome 19 were also frequently detected. 14 Similarly, gain of chromosomes 12, 7 and 9 identified in the our study are consistent with other published data 12,14,16,18,19,27,36 and should therefore be considered nonrandom in distribution. Extra copies of these chromosomes carrying 1 or more mutated genes might be of importance, since an increased expression of such genes could provide growth advantage to pituitary tumor cells.…”

Section: Resultssupporting

confidence: 90%

“…Because of their solid nature, these neoplasms grow poorly in culture media, 8,9 and cytogenetic studies 10 -19 have revealed chromosomal aberrations at a very low frequency, which may be due to the selective growth advantage of normal cells in the cell culture. 16 These limitations can be overcome by using comparative genomic hybridization (CGH), which allows tumor DNA to be used directly to search for imbalanced genetic material in tumor genomes. 20,21 CGH allows the detection of gain and loss of genetic material at a resolution of about 10 Mb, 22,23 and it has been used successfully to identify chromosomal imbalances in a variety of solid neoplasms, including pituitary tumors.…”

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confidence: 99%

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Chromosomal aberrations in sporadic pituitary tumors

et al. 2001

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Section: Resultssupporting

confidence: 90%

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confidence: 99%

Chromosomal aberrations in sporadic pituitary tumors

et al. 2001

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“…The primary pituitary cell cultures were set up as described elsewhere (Bettio et al 1997). The phytohemagglutinin (PHA)-stimulated peripheral blood cultures were set up according to standard procedure.…”

Section: Cell Cultures and Cytogenetic Analysismentioning

confidence: 99%

High-mobility group A2 gene expression is frequently induced in non-functioning pituitary adenomas (NFPAs), even in the absence of chromosome 12 polysomy

Pierantoni¹,

Finelli²,

Valtorta³

et al. 2005

Endocr Relat Cancer

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The high-mobility group A2 (HMGA2) gene has a critical role in benign tumors where it is frequently rearranged, and in malignant tumors, where it is overexpressed in the absence of structural modification of the HMGA2 locus. By previous fluorescence in situ hybridization (FISH) and reverse transcriptase PCR analyses on human prolactin-secreting pituitary adenomas we detected rearrangement of the HMGA2 gene and amplification of its native region associated with activated expression. These data indicated a role for the HMGA2 gene in the development of human pituitary prolactinomas, since they are consistent with the appearance of prolactin/growth hormone adenomas in transgenic mice overexpressing the HMGA2 gene. To assess a more general role for HMGA2 in pituitary oncogenesis, we investigated HMGA2 amplification and expression in a panel of non-functioning pituitary adenomas (NFPAs) which account for 25% of all pituitary adenomas. We provide evidence that out of 18 NFPA tumors tested, 12 expressed HMGA2, but, different from prolactinomas, only in two cases the upregulation of the gene could be associated with amplification and/or rearrangement of the HMGA2 locus. Increased dosage of chromosome 12 was found in the expressing and non-expressing NFPAs, confirming that this sole event is insufficient to drive up activation of the HMGA2 gene. A role for chromosome 12 polysomy to promote structural instability of HMGA2 is confirmed, but the mechanism via trisomy is less prevalent in the frequently diploid NFPAs than in the usually hyperdiploid prolactinomas. Micro-rearrangements of HMGA2 gene not detectable by FISH analysis and/or sequence alterations could contribute to upregulation of HMGA2 gene in pituitary adenomas of the NFPA subtype. However, it cannot be excluded that the HMGA2 overexpression may be due, in some NFPA patients, to the same, still mainly unknown, mechanisms responsible for HMGA2 overexpression in malignant neoplasias.

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“…In 10% of cases, gains of 9q34 were detected. Other gains were detected on regions of chromosomes 10,11,13,16,19,20, X, and Y. Koga, et al, 128 examined 50 cases of PNSTs; among them were 14 schwannomas, which revealed similar findings. Nevertheless, the authors noted that the schwannomas had losses of chromosomes 17 and 19 in less than 50% of cases, compared with other PNSTs.…”

Section: Tumors Of Cranial and Spinal Nervesmentioning

confidence: 91%

“…The CGAP site reports 48 cases of pituitary adenoma. 16,20,44,67,79,144,187,226 The karyotypes are largely diploid, showing frequent gains of chromosomes 4, 7, 8, 9, 12, and 20, and losses of chromosomes 10, 14, 19, and 22. Finelli and coworkers 79 conducted conventional cytogenetic and interphase FISH analyses on 53 specimens.…”

Section: Tumors Of the Sellar Regionmentioning

confidence: 99%

Molecular cytogenetic analysis in the study of brain tumors: findings and applications

Bayani¹,

Pandita²,

Squire³

2005

FOC

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Classic cytogenetics has evolved from black and white to technicolor images of chromosomes as a result of advances in fluorescence in situ hybridization (FISH) techniques, and is now called molecular cytogenetics. Improvements in the quality and diversity of probes suitable for FISH, coupled with advances in computerized image analysis, now permit the genome or tissue of interest to be analyzed in detail on a glass slide. It is evident that the growing list of options for cytogenetic analysis has improved the understanding of chromosomal changes in disease initiation, progression, and response to treatment. The contributions of classic and molecular cytogenetics to the study of brain tumors have provided scientists and clinicians alike with new avenues for investigation. In this review the authors summarize the contributions of molecular cytogenetics to the study of brain tumors, encompassing the findings of classic cytogenetics, interphase- and metaphase-based FISH studies, spectral karyotyping, and metaphase- and array-based comparative genomic hybridization. In addition, this review also details the role of molecular cytogenetic techniques in other aspects of understanding the pathogenesis of brain tumors, including xenograft, cancer stem cell, and telomere length studies.

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Cytogenetic study of pituitary adenomas

Cited by 31 publications

References 10 publications

Chromosomal aberrations in sporadic pituitary tumors

Chromosomal aberrations in sporadic pituitary tumors

High-mobility group A2 gene expression is frequently induced in non-functioning pituitary adenomas (NFPAs), even in the absence of chromosome 12 polysomy

Molecular cytogenetic analysis in the study of brain tumors: findings and applications

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