Loss of material from chromosome arm 1p during malignant progression of meningioma revealed by fluorescent in Situ hybridization

Abstract

BACKGROUND Atypical and anaplastic meningiomas tend to recur and to invade adjacent brain, bone, and skin. They also can metastasize to extracranial organs such as the lung, liver, or bone, causing death. Recent reports have indicated that allelic deletion of chromosome 1p is associated with malignant progression of meningiomas. METHODS Cytogenetic analysis of 37 meningiomas was performed using double‐target fluorescent in situ hybridization (FISH) and focusing on chromosome arm 1p. The meningioma series included 17 benign meningiomas, 11 atypical meningiomas, and 9 anaplastic meningiomas. FISH was performed with pericentromeric (1q12) and subtelomeric (1p36) DNA probes to cell nuclei prepared from surgically extirpated tumor samples. RESULTS A high incidence of deletion of at least part of 1p was observed in 60.0% of atypical and 85.7% of anaplastic meningiomas. Furthermore, statistically significant differences were found with respect to these data between benign versus atypical/anaplastic meningiomas. In four cases both primary and recurrent tumors from the same patient also were investigated for allelic status. CONCLUSIONS The results of the current study support the existence of tumor suppressor gene(s) on 1p associated with malignant progression of meningioma, and suggest that detection of the allelic status of chromosome 1p by FISH may assist physicians in predicting the clinical prognosis of patients affected by this type of brain tumor. Cancer 1998;83:360‐366. © 1998 American Cancer Society.

Narrowing of the regions of allelic losses of chromosome 1p36 in meningioma tissues by an improved SSCP analysis

“…8,34 Several studies have succeeded in narrowing down the critical regions on 1p that relate to tumorigenesis of meningiomas. [12][13][14]35,36 Several candidate genes on 1p have been discussed with regard to their relationship with meningioma tumorigenesis or progression, including TP73, CDKN2C (encoding p18 INK4c ), RAD54L and ALPL. [37][38][39][40] The roles of these genes, however, are still controversial.…”

“…[12][13][14] We finally defined a candidate common LOH region which might associate with meningioma. This region, located at 1p36.11, was considerably narrowed down when compared with a 19.3-Mbp candidate locus, R2, located at 1p36.21-p34.1 by Buckley et al 16 Genes located at this region are shown in Supplemental Table S3.…”

“…[9][10][11] Among them, chromosome 1p is considered to be one of the most probable regions in which a deletion is associated with the malignant progression of meningiomas and correlates with increased morbidity. 12,13 It has also been suggested that a putative area on chromosome 1p harbors tumor suppressor genes, which are yet to be identified; therefore, more detailed mapping of LOH regions is important to clarify the mechanism of meningioma progression. [14][15][16] In a previous study, we established a new LOH-detection method, named LOQUS (LOH Estimation by Quantitative singlestrand conformation polymorphism [SSCP] analysis), that can detect LOH at the single nucleotide polymorphism (SNP) level using a conventional capillary sequencer.…”

Incidence of numerical chromosome aberrations in meningioma tumors as revealed by fluorescence in situ hybridization using 10 chromosome‐specific probes

“…Loss of a sex Table 2 Correlation Between the Numerical Abnormalities Observed for Chromosomes 1,9,10,11,14,15,17,22 chromosome in somatic cells is a relatively frequent agerelated phenomenon, usually including loss of the Y chromosome in bone marrow cells from older male individuals (40). However, it was never found at the high frequencies reported here.…”

Gros1, a potential growth suppressor on chromosome 1: its identity to basement membrane-associated proteoglycan, leprecan

“…Loss of heterozygosity (LOH) for chromosome 1p is frequently observed in a variety of tumors. These include neuroblastomas (Ariyama et al, 1995;Cheng et al, 1995;White et al, 1997), meningiomas (Ishino et al, 1998), pheochromocytomas, medullary thyroid carcinomas and neuroendocrine carcinoma (Moley et al, 1992), T cell acute lymphoblastic leukemia (Iolascon et al, 1997), colorectal carcinoma (Bomme et al, 1998;Di Vinci et al, 1998;Praml et al, 1995), mesothelioma (Lee et al, 1996), hepatoma (Chen et al, 1996), endometrial carcinoma (Arlt et al, 1996) and breast carcinomas (Borg et al, 1992;Munn et al, 1995;Nagai et al, 1995;Tsukamoto et al, 1998). A unique category of germ cell tumors, childhood endodermal sinus tumors involving the testis and extragonadal region in children less than 4 years of age, show recurrent cytogenetic abnormalities including deletion of distal 1p region (Perlman et al, 1996).…”