Javascript must be enabled to continue!
Enhanced expression of the sis and c-myc oncogenes in human meningiomas
View through CrossRef
✓ In 19 human meningiomas (14 primary and four recurrent tumors and one tumor transplanted into athymic nude mice), oncogene expression, amplification, and rearrangement, and loss of heterozygosity on chromosome 22 were examined. Compared to nontumor brain tissue, there was greater than a fivefold expression of the sis oncogene in six (40%) of 15 tumors studied and of the c-myc oncogene in 12 (63%) of the total 19 tumors. Expression of the sis gene was lower in the recurrent tumors than in the primary cases, and there was no detectable expression in anaplastic meningioma cells. Rearrangement of the sis gene was found in one meningioma. Loss of heterozygosity on chromosome 22 was detected in two of the five informative heterozygous cases. Expression of the c-myc gene was higher in cases with loss of heterozygosity than in those without. These results suggest that the sis and c-myc oncogenes are associated with tumorigenicity and that c-myc may induce meningiomas through loss of the putative tumor suppressor gene.
Journal of Neurosurgery Publishing Group (JNSPG)
Title: Enhanced expression of the sis and c-myc oncogenes in human meningiomas
Description:
✓ In 19 human meningiomas (14 primary and four recurrent tumors and one tumor transplanted into athymic nude mice), oncogene expression, amplification, and rearrangement, and loss of heterozygosity on chromosome 22 were examined.
Compared to nontumor brain tissue, there was greater than a fivefold expression of the sis oncogene in six (40%) of 15 tumors studied and of the c-myc oncogene in 12 (63%) of the total 19 tumors.
Expression of the sis gene was lower in the recurrent tumors than in the primary cases, and there was no detectable expression in anaplastic meningioma cells.
Rearrangement of the sis gene was found in one meningioma.
Loss of heterozygosity on chromosome 22 was detected in two of the five informative heterozygous cases.
Expression of the c-myc gene was higher in cases with loss of heterozygosity than in those without.
These results suggest that the sis and c-myc oncogenes are associated with tumorigenicity and that c-myc may induce meningiomas through loss of the putative tumor suppressor gene.
Related Results
<i>MYC</i> rearrangement but not extra <i>MYC</i> copies is an independent prognostic factor in patients with mantle cell lymphoma
<i>MYC</i> rearrangement but not extra <i>MYC</i> copies is an independent prognostic factor in patients with mantle cell lymphoma
Mantle cell lymphoma (MCL) with MYC rearrangement (MYC-R) is rare and little is known about the importance of MYC extra copies (EC) in the absence of MYC-R in MCL patients. This st...
Improving immunotherapy in high-grade B-cell lymphoma
Improving immunotherapy in high-grade B-cell lymphoma
MYC is a transcription factor that upon deregulation acts as an oncogene. Cancer patients with MYC overexpression face significant worse outcomes to treatment with (immuno)chemothe...
Abstract 5833: Targeting the transcription co-activator TAZ inhibits MYC-driven medulloblastoma
Abstract 5833: Targeting the transcription co-activator TAZ inhibits MYC-driven medulloblastoma
Abstract
Medulloblastoma (MB), the most common malignant pediatric brain tumor, results in significant neurological, intellectual and physical disability or death. F...
Abstract 1872: Targeting MYC-driven medulloblastoma using inhibitors of glutamine metabolism.
Abstract 1872: Targeting MYC-driven medulloblastoma using inhibitors of glutamine metabolism.
Abstract
Medulloblastoma is the most common malignant brain tumor in children. Currently, treatment consists of surgical resection, chemotherapy, and whole brain and...
Abstract PO-037: Machine learning-enabled transomics identifies three therapeutic targets for MYC-driven diffuse large B cell lymphoma
Abstract PO-037: Machine learning-enabled transomics identifies three therapeutic targets for MYC-driven diffuse large B cell lymphoma
Abstract
MYC activation and dysregulation is a powerful oncogenic driver in multiple cancers, including diffuse large B cell lymphoma (DLBCL). There is a known corre...
Abstract 3333: Cancer stem cell-mediated regulation of Myc overexpressing medulloblastoma cells on proliferation, migration and invasion
Abstract 3333: Cancer stem cell-mediated regulation of Myc overexpressing medulloblastoma cells on proliferation, migration and invasion
Abstract
Medulloblastoma (MB) is the most common and malignant pediatric brain tumor. Myc amplification was frequently shown in the tumor. Hereby cancer stem cells a...
Abstract 1592: Pulsatile Myc expression as a source of Myc heterogeneity in cancer cells
Abstract 1592: Pulsatile Myc expression as a source of Myc heterogeneity in cancer cells
Abstract
Myc is the most commonly amplified oncogene, and is known to play critical roles in cancer establishment and maintenance. Myc expression heterogeneity has a...
Abstract 1275: MK591 (Quiflapon) downregulates c-Myc oncogenic signaling and induces apoptosis in enzalutamide-resistant prostate cancer cells
Abstract 1275: MK591 (Quiflapon) downregulates c-Myc oncogenic signaling and induces apoptosis in enzalutamide-resistant prostate cancer cells
Abstract
Background: Enzalutamide is an FDA-approved drug commonly prescribed for advanced prostate cancer. Enzalutamide slows down prostate tumor growth but resista...

