Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previously, we identified noscapine as a small molecule inhibitor of the hypoxia-inducible factor-1 pathway in hypoxic human glioma cells and human umbilical vein endothelial cells. Noscapine is a nontoxic ingredient in cough medicine currently used in clinical trials for patients with non-Hodgkin's lymphoma or chronic lymphocytic leukemia to assess antitumor efficacy. Here, we have evaluated the sensitivity of four human glioma cell lines to noscapine-induced apoptosis. Noscapine was a potent inhibitor of proliferation and inducer of apoptosis. Induction of apoptosis was associated with activation of the c-jun N-terminal kinase signaling pathway concomitant with inactivation of the extracellular signal regulated kinase signaling pathway and phosphorylation of the antiapoptotic protein Bcl-2. Noscapine-induced apoptosis was associated with the release of mitochondrial proteins apoptosis-inducing factor (AIF) and/or cytochrome c. In some glioma cell lines, only AIF release occurred without cytochrome c release or poly (ADP-ribose) polymerase cleavage. Knock-down of AIF decreased noscapine-induced apoptosis. Our results suggest the potential importance of noscapine as a novel agent for use in patients with glioblastoma owing to its low toxicity profile and its potent anticancer activity.
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PMID:Noscapine induces apoptosis in human glioma cells by an apoptosis-inducing factor-dependent pathway. 1852 14

In the realm of head and neck diseases, one particularly common clinical presentation is that of the patient with a cervical mass. In children, neck masses often prove to be developmental cysts; in adults, the recent onset of a neck mass can signal a metastasis from a head and neck squamous carcinoma. Less often, both adults and children may present with cervical masses caused by either non-Hodgkin's lymphoma or Hodgkin's disease. There are, of course, less frequently encountered differential diagnostic possibilities; one of the most uncommon of all is the possibility of metastasis from an intracranial tumor. Intracranial tumors rarely give rise to cervical node metastases. The present review examines the published experience with 128 tumors that gave rise to cervical node metastases in both adult and in pediatric patients. While it is presumed that the blood-brain barrier blocks the spread of most tumors beyond the intracranial locale, this is speculative. Although many of the cervical node metastases reported here arose after craniotomy (and, presumably, after breaching of the blood-brain barrier), some arose in the absence of any preceding surgical procedure. Cervical node metastases may arise from glial tumors (including glioblastoma multiforme, in both adult and pediatric patients) and non-glial tumors (such as medulloblastoma in pediatric patients). The history of a previous intracranial lesion is often the key to correct diagnosis, since, without prompting, neither the pathologist nor the radiologist is likely to think of a cervical node metastasis from a brain tumor when assessing a cervical mass of unknown etiology.
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PMID:A survey of metastatic central nervous system tumors to cervical lymph nodes. 2069 30

One of the most common type of primary brain tumors in adults is the glioblastoma multiforme (GBM) (World Health Organization grade IV astrocytoma). It is the most common malignant and aggressive form of glioma and it is among the most lethal ones. Poly (ADP-ribose) polymerase 1 (PARP-1) gene, located to 1q42, plays an important role for the efficient maintenance of genome integrity. PARP-1 protein is required for the apoptosis-inducing factor (AIF) translocation from the mitochondria to the nucleus. PARP-1 is proteolytically cleaved at the onset of apoptosis by caspase-3. Microarray analysis of PARP-1 gene expression in more than 8,000 samples revealed that PARP-1 is more highly expressed in several types of cancer compared with the equivalent normal tissues. Overall, the most differences in PARP-1 gene expression have been observed in breast, ovarian, endometrial, lung, and skin cancers, and non-Hodgkin's lymphoma. We evaluated the expression of PARP-1 protein in normal brain tissues and primary GBM by immunohistochemistry. Positive nuclear PARP-1 staining was found in all samples with GBM, but not in normal neurons from controls (n=4) and GBM patients (n=27). No cytoplasmic staining was observed in any sample. In conclusion, PARP-1 gene is expressed in GBM. This finding may be envisioned as an attempt to trigger apoptosis in this tumor, as well as in many other malignancies. The presence of the protein exclusively at the nucleus further support the function played by this gene in genome integrity maintenance and apoptosis. Finally, PARP-1 staining may be used as GBM cell marker.
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PMID:PARP-1 protein expression in glioblastoma multiforme. 2247 97

CNS involvement in the setting of lymphoid neoplasia is a clinical situation that requires specific diagnosis due to the disparate treatment regimens recommended for neoplasms of specific lymphoid cell types. Cerebrospinal fluid (CSF) sampling may provide sufficient information to determine the presence of abnormal lymphoid cells but may not be able to further specify the malignant cellular population. In cases where abnormal clinical or radiographic features are present, accurate tissue diagnosis is essential. In this report, we define a rare case of primary CNS intramedullary Hodgkin's lymphoma without leptomeningeal dissemination diagnosed via resectional biopsy of a conus medullaris lesion. The patient received post-resection radiation therapy and subsequently demonstrated radiographic and clinical improvement. Lymphoid neoplasia within the CNS comprises a diverse group with varying response and survival rates. Treatment hinges upon accurate diagnosis as chemotherapy varies widely among Hodgkin's and non-Hodgkin's lymphoma. While CSF sampling may yield a positive result with sufficiency to diagnose an abnormal lymphoid cell population, tissue is necessary for further defining cellular pathology. In this report, we define a rare case of primary CNS intramedullary Hodgkin's lymphoma without leptomeningeal dissemination via resectional biopsy of a conus medullaris lesion. In cases where abnormal enhancement is found in eloquent CNS regions and lymphoid neoplasia is suspected, management often entails either stereotactic biopsy or CSF sampling. While CSF analysis may differentiate malignancy at a low rate, tissue diagnosis via paraffin block immunohistochemistry is necessary to further classify malignancy as primary or peripheral, Hodgkin's or non-Hodgkin's lymphoma, or other such as metastatic leptomeningeal dissemination and glioma. Within the subtypes of lymphoid neoplasms, treatment regimens vastly differ and thus accurate tissue diagnosis is paramount. We therefore present a rare case of primary CNS intramedullary Hodgkin's lymphoma without leptomeningeal disease in the setting of immunocompromise diagnosed via open resectional biopsy of the conus medullaris.
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PMID:Isolated CNS Hodgkin's lymphoma: implications for tissue diagnosis. 2543 9

Neurofibromatosis type 1 (NF1) is an autosomal dominant hereditary neurocutaneous syndrome characterized by multi-system involvement and an increased incidence of both benign and malignant tumors. In this study, we evaluated the clinical presentation and prognosis of NF1 and malignancy. Between 1975 and 2013, 26 (5%) of the 473 patients with NF1 at our center developed non-neurofibroma neoplasms. The patient files of 26 subjects with tumors, other than optic glioma, were analyzed retrospectively to evaluate clinical features and treatment results. The age at diagnosis of NF1 ranged from 3 months to 16 years (median 5.5 years). The age range at tumor diagnosis was 1.5-33 years (median 8 years) in these 26 patients. The tumor histological subtypes included the following: 12 soft-tissue tumors (6 malignant peripheral nerve sheath tumors (MPNST), 5 rhabdomyosarcomas (RMS) and 1 malignant fibrous histiocytoma), 11 brain tumors (6 low-grade gliomas, 3 high-grade gliomas, and 2 medulloblastoma), 2 neuroblastomas and 1 non-Hodgkin's lymphoma. Twelve of 26 patients were alive at the time of the study. Although benign brain tumors with NF1 are more common, high-grade brain tumors also occur. Thus, careful and regular follow-up is crucial for early detection of malignancy in NF1 patients.
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PMID:Neurofibromatosis type 1 and malignancy in childhood. 2607 32

IL-6 is critical for tumorigenesis. However, previous studies on the association of IL-6 promoter polymorphisms with predisposition to different cancer types are somewhat contradictory. Therefore, we performed this meta-analysis regarding the relationship between IL-6 promoter single nucleotide polymorphisms and cancer susceptibility and prognosis. Up to April 2017, 97 original publications were identified covering three IL-6 promoter SNPs. Our results showed statistically significant association between IL-6 promoter and cancer risk and prognosis. Subgroup analysis indicated that rs1800795 was significantly associated with increased risk of cervical cancer, colorectal cancer, breast cancer, prostate cancer, lung cancer, glioma, non-Hodgkin's lymphoma and Hodgkin's lymphoma but not gastric cancer and multiple myeloma. Furthermore, rs1800796 was significantly associated with increased risk of lung cancer, prostate cancer and colorectal cancer but not gastric cancer. Additionally, rs1800797 was significantly association with breast cancer, non-Hodgkin's lymphoma, B-cell lymphoma and diffuse large B-cell lymphoma but not gastric cancer. Simultaneously, rs1800795 and rs1800796 were associated with a significantly higher risk of cancer in Asia and Caucasian, rs1800797 was associated with a significantly risk of cancer in Caucasian but not in Asia. Furthermore, IL-6 promoter polymorphisms were significantly associated with the prognosis of cancer. Considering these promising results, IL-6 promoter including rs1800795, rs1800796 and rs1800797 may be a tumor marker for cancer therapy.
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PMID:Genetic polymorphisms of IL-6 promoter in cancer susceptibility and prognosis: a meta-analysis. 2955 16


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