Abstract. Gene expression profiling of metastatic brain tumors from primary lung adenocarcinoma, using a 17k-expression array, revealed that 1561 genes were consistently altered. Further functional classification placed the genes into seven categories: cell cycle and DNA damage repair, apoptosis, signal transduction molecules, transcription factors, invasion and metastasis, adhesion, and angiogenesis. Genes involved in apoptosis, such as caspase 2 (CASP2), transforming growth factor-ß inducible early gene (TIEG), and neuroprotective heat shock protein 70 (Hsp70) were underexpressed in metastatic brain tumors. Alterations in Rho GTPases (ARHGAP26, ARHGAP1), as well as down-regulation of the metastasis suppressor gene KiSS-1 were noted, which may contribute to tumor aggression. Overexpression of the invasion-related gene neurofibromatosis 1 (NF1), and angiogenesis-related genes vascular endothelial growth factor-B (VEGF-B) and placental growth factor (PGF) was also evidenced. Brain-specific angiogenesis inhibitors 1 and 3 (BAI1 and BAI3) were underexpressed as well. Examination of cell-adhesion and migration-related genes revealed an increased expression of integrins and extracellular matrices collagen and laminin. The study also showed alterations in p53 protein-associated genes, among these increased gene expression of p53, up-regulation of Reprimo or candidate mediator of the p53-dependent G2-arrest, down-regulation of p53-regulated apoptosis-inducing protein 1 (p53AIP1), decreased expression of tumor protein inducible nuclear protein 1 (p53DINP1), and down-regulation of Mdm4 (MDMX). The results demonstrated that genes involved in adhesion, motility, and angiogenesis were consistently upregulated in metastatic brain tumors, while genes involved in apoptosis, neuroprotection, and suppression of angiogenesis were markedly down-regulated, collectively making these cancer cells prone to metastasis.
These results indicate that functional gap junction formation between human malignant glioma cells and VECs occurs. This communication appears to influence tumor angiogenesis. Targeting gap junction signaling may offer a potential mechanism for therapy in patients with these tumors.
Alternative causes of an encephalocele, including trauma, surgery, and congenital malformation, were ruled out in this patient. Histopathological analysis of the necrotic tissue and the absence of renal or pulmonary disease also indicated that the patient did not suffer from Wegener granulomatosis, a known cause of spontaneous intranasal lesions. To the best of our knowledge, this is the first report of an encephalocele likely induced solely by cocaine abuse.
Distal anterior inferior cerebellar artery (AICA) pseudoaneurysms are very rare lesions. Although cases have been previously reported, only a few have been reported as a result of vestibular schwannoma (VS) radiation, none have been reported as a result of VS resection, and only one has been reported as treated with parent vessel occlusion (PVO) with n-butyl cyanoacrylate (nBCA). We report a case of a 65-year-old man with a history of right-sided VS surgery and radiation who presented years later with a ruptured pseudoaneurysm of the distal right AICA and was treated with endovascular PVO using nBCA. The aneurysm was completely obliterated and the patient had no worsening of symptoms or neurological exam. The case illustrates a very rare complication of VS surgery and radiation as well as an effective treatment for distal AICA aneurysms.
The need for more accurate prediction of the biological behavior of brain tumors has lead to the use of immunohistochemical methods for assessment of proliferating cell nuclear antigens such as Ki-67. There is a variable association of glioma Ki-67 labeling index with patient survival. Brain invasion by individual tumor cells also defines biological aggressiveness, and can be assessed in vitro. Further, proliferation and migration seem to be mutually exclusive behaviors for a given cell at a point in time. We studied the relationship between Ki-67 labeling index and invasion rate in a group of 10 gliomas, and 2 meningiomas. Human tumor spheroids obtained from operative specimen were co-cultured with fetal rat brain aggregates, and invasion rate was measured by confocal microscopic observation. There was no correlation between two measures of invasion and Ki-67 labeling. This finding supports the dichotomous nature of glioma proliferation and invasion, and may in part explain the limited usefulness of proliferation marker labeling.
SUMMARYDistal anterior inferior cerebellar artery (AICA) pseudoaneurysms are very rare lesions. Although cases have been previously reported, only a few have been reported as a result of vestibular schwannoma (VS) radiation, none have been reported as a result of VS resection, and only one has been reported as treated with parent vessel occlusion (PVO) with n-butyl cyanoacrylate (nBCA). We report a case of a 65-year-old man with a history of right-sided VS surgery and radiation who presented years later with a ruptured pseudoaneurysm of the distal right AICA and was treated with endovascular PVO using nBCA. The aneurysm was completely obliterated and the patient had no worsening of symptoms or neurological exam. The case illustrates a very rare complication of VS surgery and radiation as well as an effective treatment for distal AICA aneurysms. BACKGROUND
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