Comparative genomic hybridization in pineal parenchymal tumors

Rickert, Christian H.; Simon, Ronald; Bergmann, Markus; Dockhorn‐Dworniczak, Barbara; Paulus, Werner

doi:10.1002/1098-2264(2000)9999:9999<::aid-gcc1067>3.0.co;2-c

Cited by 60 publications

(25 citation statements)

References 13 publications

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“…Despite pineal cysts being considered as non-neoplastic lesions, CGH analyses in the present study revealed gains of 16p. The cytogenetic spectrum of grade II PPTID is limited, revealing gains of 4q and 12q, and loss of chromosome 22 in two tumors each (1,26). One of the grade II PPTIDs in the present study did not reveal any chromosomal imbalances, while the other grade II PPTID, in addition to gains of 16p, showed a wide range of gains and losses.…”

Section: Discussioncontrasting

confidence: 59%

“…The tumors are most commonly found in children and infants, while only 1% occur during adulthood (1,2). The appropriate pathological classification and grading of the malignancy of tumors of the PR is essential for determining the clinical management and prognosis (3,4).…”

Section: Introductionmentioning

confidence: 99%

“…PPTs originating from the pineal gland itself account for 14-27% of PR tumors (1,(5)(6)(7). In addition to grade I pineocytoma and grade IV pineoblastoma, PPT of intermediate differentiation (PPTID) was recognized in the 2007 World Health Organization (WHO) classification as an intermediate-grade malignancy (II or III).…”

Section: Introductionmentioning

confidence: 99%

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Common molecularcytogenetic alterations in tumors originating from the pineal region

et al. 2015

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Abstract. Tumors of the pineal region (PR) are rare and can be subdivided into four main histomorphological groups: Pineal-parenchymal tumors (PPT), germ cell tumors (GCT), glial tumors and miscellaneous tumors. The appropriate pathological classification and grading of these malignancies is essential for determining the clinical management and prognosis. However, an early diagnosis is often delayed due to unspecific clinical symptoms, and histological support is not always decisive to identify the diversity of tumors of the PR. The present study aimed to characterize 18 tumors of the PR using comparative genomic hybridization. All the tumors were primarily surgically resected without any previous irradiation or chemotherapy. In addition to chromosomal aberrations in PPT and different GCTs of the PR, the present study described, for the first time, the chromosomal changes in a few rare entities (solitary-fibrous and neuroendocrine tumors) of the PR. The tumors in the study, regardless of histology and World Health Organization grade, were characterized by frequent gains at 7, 9q, 12q, 16p, 17 and 22q, and losses at 13q. While the detection of chromosomal aberrations in these tumors appears not to be indicative enough of histological entities and their grade of malignancy, the present data may be of use to select genes of interest for higher resolution genomic analyses.

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Section: Discussioncontrasting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

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Common molecularcytogenetic alterations in tumors originating from the pineal region

et al. 2015

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“…18,23 Of note, the genetic profiles of pineal germ cell tumors were different from pineal parenchymal tumors, which frequently showed gain of 12q and 22. 24 Considering these conflicting data, we have performed chromosomal CGH analysis of 19 tumors from representative histologic groups in order to define characteristic patterns of chromosomal imbalances in CNS-GCTs. In addition, we compared the CGH profiles of CNS-GCTs to those of 101 malignant germ cell tumors from gonadal and different extragonadal sites, including tumors of different age groups and all histologic entities.…”

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confidence: 99%

Molecular genetic analysis of central nervous system germ cell tumors with comparative genomic hybridization

et al. 2006

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The limited information available to date regarding the genetic alterations in germ cell tumors of the central nervous system has raised concerns about their biologic relationship to other germ cell tumor entities. We investigated fresh-frozen or archival tumor samples from 19 patients with central nervous system germ cell tumors (CNS-GCTs), including seven germinomas, eight malignant nongerminomatous germ cell tumors and four teratomas, using chromosomal comparative genomic hybridization to determine recurrent chromosomal imbalances. All 15 malignant CNS-GCTs and two of four teratomas showed multiple chromosomal imbalances. Chromosomal gains (median: 4 gains/tumor, range: 0-9 gains/tumor) were observed more frequently than losses (median: 1.6 losses/tumor, range: 0-6 losses/tumor). Gain of 12p, which is considered characteristic for germ cell tumors of the adult testis, was detected in 11 of 19 tumors and 10 of 15 malignant CNS-GCTs. In one tumor, gain of 12p was confined to an amplicon at 12p12, corresponding to the commonly amplified region on 12p. Other common gains were found on chromosome arms 1q and 8q (n ¼ 9, each). Among the chromosomal losses, parts of chromosome 11 (n ¼ 5), 18 (n ¼ 4), and 13 (n ¼ 3) were deleted most frequently. Notably, we observed no difference in the genetic profiles of germinomatous and nongerminomatous CNS-GCTs; however, the average number of imbalances was higher in the latter group. A meta-analysis comparing 116 malignant gonadal and extragonadal germ cell tumors revealed that the genomic alterations in CNS-GCTs are virtually indistinguishable from those found in their gonadal or other extragonadal counterparts of the corresponding age group. These data strongly argue in favor of common pathogenetic mechanisms in gonadal and extragonadal germ cell tumors. Keywords: germ cell tumor; central nervous system; extragonadal; chromosomal profile; isochromosome 12p; meta-analysis During childhood and adolescence, the majority of germ cell tumors arise outside of the gonads, and beyond early childhood, the central nervous system and the mediastinum constitute the most frequent sites of extragonadal germ cell tumors. 1 The vast majority of central nervous system germ cell tumors (CNS-GCTs) develop in the pineal gland or the suprasellar region, and approximately 10% of all CNS-GCTs present as bifocal tumors. 2,3 The extragonadal appearance of germ cell tumors is likely related to errors in germ cell migration during early embryonal development. Accordingly, imprinting studies of gonadal and extragonadal germ cell tumors show loss of the methylation imprint at imprinting control regions, correlating with the methylation status within early stages of primordial germ cell development. [4][5][6] However, the molecular mechanisms that interfere with normal homing of germ cells to the gonadal ridge and that allow for a

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“…Cytogenetic changes in PCs include loss of all or part of chromosome 22, partial deletion or loss of chromosomes 1 and 11, deletion in the distal 12q region [64,65], or losses of chromosomes 4, 5, 13, 14 and 15 and gain of chromosome 19 [66]. No chromosomal gains or losses were found in PCs by comparative genomic hybridization (CGH) [67].…”

Section: Biochemistry and Molecular/genetic Featuresmentioning

confidence: 99%

Histopathology of Tumors of the Pineal Region

et al. 2010

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Pineal region tumors are heterogeneous lesions and include mainly pineal parenchymal tumors (PPTs), papillary tumors of the pineal region (PTPRs) and germ cell tumors (GCTs). This article describes the cystic pineal gland compared with normal tissue and histopathological features of the most frequent pineal region tumors. PPTs are subdivided into pineocytoma (grade I), pineoblastoma (grade IV) and tumors with intermediate differentiation (PPTIDs; grades II-III). A grading system based on the number of mitoses and neurofilament protein expression distinguishes low- from high-grade PPTID. PTPR is a new tumoral entity thought to originate from the subcommissural organ. GCTs include germinoma, embryonal carcinoma, teratoma, yolk sac tumor and choriocarcinoma and are often of mixed histologic composition. New histogenetic data for GCTs are presented.

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Comparative genomic hybridization in pineal parenchymal tumors

Cited by 60 publications

References 13 publications

Common molecularcytogenetic alterations in tumors originating from the pineal region

Common molecularcytogenetic alterations in tumors originating from the pineal region

Molecular genetic analysis of central nervous system germ cell tumors with comparative genomic hybridization

Histopathology of Tumors of the Pineal Region

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