Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transcription factor nuclear factor-kappaB (NF-kappaB) is a key regulator of stress-induced transcriptional activation and has been implicated in mediating primary or acquired apoptosis resistance in various cancers. In the present study, we therefore investigated the role of NF-kappaB in regulating apoptosis in malignant glioma, a prototypic tumor refractory to current treatment approaches. Here, we report that constitutive NF-kappaB DNA-binding activity was low or moderate in eight different glioblastoma cell lines compared to Hodgkin's lymphoma cells, known to harbor aberrant constitutive NF-kappaB activity. Specific inhibition of NF-kappaB by overexpression of inhibitor of kappaB (IkappaB)alpha superrepressor did not enhance spontaneous apoptosis of glioblastoma cells. Also, overexpression of IkappaBalpha superrepressor had no significant impact on apoptosis induced by two prototypic classes of apoptotic stimuli, that is, chemotherapeutic drugs or death-inducing ligands such as TNF-related apoptosis inducing ligand (TRAIL), which are known to trigger NF-kappaB activation as part of a cellular stress response. Similarly, inhibition of NF-kappaB by the proteasome inhibitor MG132 did not increase doxorubicin (Doxo)-induced apoptosis of glioblastoma cells, although it prevented DNA binding of NF-kappaB complexes in response to Doxo. Interestingly, proteasome inhibition significantly sensitized glioblastoma cells for TRAIL-induced apoptosis. These findings indicate that the characteristic antiapoptotic function of NF-kappaB reported for many cancers is not a primary feature of glioblastoma and thus, specific NF-kappaB inhibition may not be effective for chemosensitization of glioblastoma. Instead, proteasome inhibitors, which enhanced TRAIL-induced apoptosis in an NF-kappaB-independent manner, may open new perspectives to increase the efficacy of TRAIL-based regimens in glioblastoma, which warrants further investigation.
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PMID:NF-kappaB-independent sensitization of glioblastoma cells for TRAIL-induced apoptosis by proteasome inhibition. 1690 19

A critical event in tumor growth and progression is the upregulation of angiogenesis. Thus, targeting angiogenesis has become an attractive treatment modality in cancer medicine. Our study analyzed various solid tumor types for the expression of Dkk-3, a cystein-rich, N-glycosylated secreted member of the Dickkopf protein family that has been proposed as a tumor suppressor gene. Tissue microarrays of gliomas (n = 30), high-grade non-Hodgkin's lymphomas (NHL, n = 80), colorectal cancer (n = 35) and melanoma (n = 30) were immunohistochemically analyzed for Dkk-3 and CD31 expression. Moreover, the effects of Dkk-3 were studied in vitro in primary endothelial colony-forming cells (ECFC) and in vivo in a mouse melanoma model. In comparison to normal tissue, the number of blood vessels expressing Dkk-3 was increased in glioma, high-grade NHL, melanoma and colorectal carcinoma. Confocal laser scanning microscopy revealed that Dkk-3 vesicles localized also in Weibel Palade bodies. In vitro cell proliferation and migration of ECFC was not significantly affected by adenoviral overexpression or siRNA-mediated downregulation of Dkk-3. Interestingly, tube formation in matrigel decreased after downregulation of Dkk-3 and increased after adenoviral overexpression. Stable overexpression of murine Dkk-3 in B16F10 cells significantly increased microvessel density in the C57/BL6 melanoma model. Thus, we postulate a novel function of Dkk-3 in endothelial cells as a differentiation factor involved in remodeling the tumor vasculature.
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PMID:The Dickkopf-homolog 3 is expressed in tumor endothelial cells and supports capillary formation. 1803 87

A 72-year-old previously healthy man developed rapidly progressive visual loss, and brain imaging showed features suggestive of a malignant glioma of the anterior visual pathway. Biopsy of one optic nerve yielded a diagnosis of lymphoma. There was no evidence of an extracranial non-Hodgkin lymphoma, so the conclusion was that this represented a primary central nervous system lymphoma (PCNSL). PCNSL isolated to the optic chiasm has been described only once in an immunocompetent patient. Our patient is unusual in that the lymphoma involved the optic nerve, chiasm, and tract in an immunocompetent patient.
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PMID:Isolated lymphoma of the anterior visual pathway diagnosed by optic nerve biopsy. 1834 57

In order to explore the possibility of identifying toxins based on their effect on the shape of action potentials, we created a computer model of the action potential generation in NG108-15 cells (a neuroblastoma/glioma hybrid cell line). To generate the experimental data for model validation, voltage-dependent sodium, potassium, and high-threshold calcium currents, as well as action potentials, were recorded from NG108-15 cells with conventional whole-cell patch-clamp methods. Based on the classic Hodgkin-Huxley formalism and the linear thermodynamic description of the rate constants, ion channel parameters were estimated using an automatic fitting method. Utilizing the established parameters, action potentials were generated using the Hodgkin-Huxley formalism and were fitted to the recorded action potentials. To demonstrate the applicability of the method for toxin detection and discrimination, the effect of tetrodotoxin (a sodium channel blocker) and tefluthrin (a pyrethroid that is a sodium channel opener) was studied. The two toxins affected the shape of the action potentials differently, and their respective effects were identified based on the predicted changes in the fitted parameters.
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PMID:Modeling of action potential generation in NG108-15 cells. 1882 94

Malignant peripheral nerve sheath tumors (MPNSTs) arising from cranial nerves or their branches are very uncommon. The literature consists mainly of isolated case reports and small series. We identified 17 such cases in 14 males and 3 females. With one exception, the tumors affected adults (age range 5 to 69 y, mean 39, median 32). Sites of involvement included vestibular nerves (n=6), vagal nerves (n=4), facial nerves (n=3) (1 centered in the geniculate ganglion), and 2 unspecified cranial nerves in the posterior fossa. In addition, 1 tumor involved the optic chiasm (n=1). Only 1 tumor arose in brain parenchyma of (frontal lobe). All but 3 lesions were intracranial. Five tumors arose in patients who satisfied clinical criteria for neurofibromatosis type 1 (NF1). One patient with a vestibular tumor and presumed NF2 had previously undergone resection of a contralateral vestibular cellular schwannoma. One posterior fossa tumor was a malignant melanotic schwannoma. Four patients had postirradiation malignant peripheral nerve sheath tumors, 2 having been treated for optic chiasm glioma, both being NF1 affected. One patient was irradiated for hypothalamic pilocytic astrocytoma and another for cervical Hodgkin disease. Identifiable precursor lesions included schwannoma (n=4), plexiform neurofibroma (n=2), and solitary intraneural neurofibroma (n=2). All tumors were histologically high grade (6 grade III and 10 grade IV). Three tumors showed heterologous elements, 2 osseous, and 1 rhabdomyoblastic. More often scattered than diffuse, S-100 protein staining was noted in 11 of 16 tumors and variable collagen IV staining in 10 of the 16. Immunoreactivity for p53 protein was diffuse and strong in 7 of 11 tumors. Twelve patients died within 17 months to 3 years of diagnosis, 1 was lost to follow-up, 2 are very recent cases, and 2 patients are currently alive, 1 after 2 recurrences, and another with spinal leptomeningeal metastases. Malignant cranial nerve sheath tumors are rare and are associated with the same poor prognosis as those of spinal nerves at other sites.
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PMID:Malignant peripheral nerve sheath tumors of cranial nerves and intracranial contents: a clinicopathologic study of 17 cases. 1906 5

During recent years there has been increasing public concern on potential cancer risks from microwave emissions from wireless phones. We evaluated the scientific evidence for long-term mobile phone use and the association with certain tumors in case-control studies, mostly from the Hardell group in Sweden and the Interphone study group. Regarding brain tumors the meta-analysis yielded for glioma odds ratio (OR)=1.0, 95% confidence interval (CI)=0.9-1.1. OR increased to 1.3, 95% CI=1.1-1.6 with 10 year latency period, with highest risk for ipsilateral exposure (same side as the tumor localisation), OR=1.9, 95% CI=1.4-2.4, lower for contralateral exposure (opposite side) OR=1.2, 95% CI=0.9-1.7. Regarding acoustic neuroma OR=1.0, 95% CI=0.8-1.1 was calculated increasing to OR=1.3, 95% CI=0.97-1.9 with 10 year latency period. For ipsilateral exposure OR=1.6, 95% CI=1.1-2.4, and for contralateral exposure OR=1.2, 95% CI=0.8-1.9 were found. Regarding meningioma no consistent pattern of an increased risk was found. Concerning age, highest risk was found in the age group <20 years at time of first use of wireless phones in the studies from the Hardell group. For salivary gland tumors, non-Hodgkin lymphoma and testicular cancer no consistent pattern of an association with use of wireless phones was found. One study on uveal melanoma yielded for probable/certain mobile phone use OR=4.2, 95% CI=1.2-14.5. One study on intratemporal facial nerve tumor was not possible to evaluate due to methodological shortcomings. In summary our review yielded a consistent pattern of an increased risk for glioma and acoustic neuroma after >10 year mobile phone use. We conclude that current standard for exposure to microwaves during mobile phone use is not safe for long-term exposure and needs to be revised.
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PMID:Epidemiological evidence for an association between use of wireless phones and tumor diseases. 1926 51

Intussusceptive microvascular growth (IMG), which occurs by splitting of the existing vasculature by transluminal pillars or transendothelial bridges, has been demonstrated in several tumors such as colon and mammary carcinomas, melanoma and B-cell non-Hodgkin's lymphomas. In this study, we have correlated in human glioma the extent of angiogenesis, evaluated as microvascular density, the immunoreactivity of tumor cells to vascular endothelial growth factor (VEGF), vessel diameter and IMG to the tumor stage. Results demonstrate for the first time a relationship in human glioma progression between angiogenesis, VEGF immunoreactivity of tumor cells, vessel diameter and the number of connections of intraluminal tissue folds with the opposite vascular wall, expression of IMG and suggest that IMG could be a mechanism of compensatory vascular growth occurring in human glioma. The advantages are that (1) blood vessels are generated more rapidly; (2) it is energetically and metabolically more economic; (3) the capillaries thereby formed are less leaky.
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PMID:Intussusceptive microvascular growth in human glioma. 1988 13

The experimental infectivity and excellent tolerance of some rodent autonomous parvoviruses in humans, together with their oncosuppressive effects in preclinical models, speak for the inclusion of these agents in the arsenal of oncolytic viruses under consideration for cancer therapy. In particular, wild-type parvovirus H-1PV can achieve a complete cure of various tumors in animal models and kill tumor cells that resist conventional anticancer treatments. There is growing evidence that H-1PV oncosuppression involves an immune component in addition to the direct viral oncolytic effect. This article summarizes the recent assessment of H-1PV antineoplastic activity in glioma, pancreatic ductal adenocarcinoma, and non-Hodgkin lymphoma models, laying the foundation for the present launch of a first phase I/IIa clinical trial on glioma patients.
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PMID:Oncolytic parvoviruses as cancer therapeutics. 2021 77

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

Fluorodeoxyglucose positron emission tomography (FDG-PET) plays an increasingly important role in radiotherapy, beyond staging and selection of patients. Especially for non-small cell lung cancer, FDG-PET has, in the majority of the patients, led to the safe decrease of radiotherapy volumes, enabling radiation dose escalation and, experimentally, redistribution of radiation doses within the tumor. In limited-disease small cell lung cancer, the role of FDG-PET is emerging. For primary brain tumors, PET based on amino acid tracers is currently the best choice, including high-grade glioma. This is especially true for low-grade gliomas, where most data are available for the use of (11)C-MET (methionine) in radiation treatment planning. For esophageal cancer, the main advantage of FDG-PET is the detection of otherwise unrecognized lymph node metastases. In Hodgkin's disease, FDG-PET is essential for involved-node irradiation and leads to decreased irradiation volumes while also decreasing geographic miss. FDG-PET's major role in the treatment of cervical cancer with radiation lies in the detection of para-aortic nodes that can be encompassed in radiation fields. Besides for staging purposes, FDG-PET is not recommended for routine radiotherapy delineation purposes. It should be emphasized that using PET is only safe when adhering to strictly standardized protocols.
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PMID:The use of FDG-PET to target tumors by radiotherapy. 2081 58


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