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Published on: January 9, 2019
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High HMGA2 expression without gene rearrangement in meningiomas
Masaya Nagaishi1, Ryuta Nakae1, Yoshiyuki Matsumoto1
1Department of Neurosurgery, Dokkyo Medical University Saitama Medical Center, Koshigaya-shi, Saitama, Japan.
Summary
High mobility group AT-hook 2 (HMGA2) is often overexpressed in meningiomas, a common brain tumor. This increased HMGA2 expression, however, is not linked to chromosomal rearrangements or tumor cell proliferation.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- High mobility group AT-hook 2 (HMGA2) is a transcriptional regulator implicated in mesenchymal tumors.
- Aberrant HMGA2 expression and chromosomal rearrangements at 12q14 are noted in various mesenchymal tumors.
- Meningioma, a prevalent brain tumor of mesenchymal origin, warrants investigation into HMGA2's role.
Purpose of the Study:
- To analyze HMGA2 expression (full-length and truncated forms) in meningioma tissues.
- To investigate potential gene rearrangements involving HMGA2 at chromosomal region 12q14.
- To correlate HMGA2 expression with clinicopathological features and proliferation markers.
Main Methods:
- Analysis of 55 meningioma cases.
- Quantification of truncated and full-length HMGA2 expression.
- Fluorescence in situ hybridization (FISH) for gene rearrangements.
- 3'-rapid amplification of cDNA ends (3'-RACE) for transcript variants.
- Assessment of Ki-67 labeling index.
Main Results:
- 95% of meningiomas showed elevated HMGA2 expression compared to normal brain tissue.
- Truncated HMGA2 exceeded full-length HMGA2 expression by over two-fold in 14 cases.
- No chromosomal translocations involving 12q14 were detected.
- HMGA2 expression did not correlate with Ki-67 index or clinicopathological features.
Conclusions:
- Increased HMGA2 expression is a common finding in meningiomas, independent of 12q14 chromosomal rearrangements.
- The elevated HMGA2 expression in meningiomas is not associated with tumor cell proliferation.
- HMGA2's role in meningioma pathogenesis may differ from its role in other mesenchymal tumors.
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