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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with lymphomas are conventionally imaged with [67Ga]citrate for tumor detection and determination of dissemination. Fluorine-18-2-fluoro-2-deoxy-D-glucose [( 18F]FDG) is a radiopharmaceutical that accumulates into tissues where glucose utilization is enhanced, such as tumors. Six cancer patients (five non-Hodgkin's lymphomas, one endodermal retroperitoneal sinus carcinoma) were imaged with [18F]FDG and [67Ga]citrate whole-body scintigraphies in order to compare the sensitivities of these two tumor imaging radiopharmaceuticals. Among the five untreated lymphoma patients, two 67Ga scans and four [18F]FDG scans were positive; in the patient with the retroperitoneal carcinoma who had a positive [18F]FDG scan before treatment, both scans were negative after treatment. Fluorine-18 FDG may be a more sensitive tumor-detecting radiopharmaceutical for non-Hodgkin's lymphoma than [67Ga]citrate.
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PMID:Comparison of fluorine-18-2-fluorodeoxyglucose and gallium-67 citrate imaging for detection of lymphoma. 346 32

Glucose utilization by normal and neoplastic cerebral tissue can be measured in humans using positron emission tomography (PET) with fluorine-18-labeled 2-deoxy-D-glucose (FDG). Malignant gliomas are known to exhibit hypermetabolic glucose consumption compared to normal brain. Barbiturate-sensitive cerebral glucose utilization is coupled to neuronal activity, and lesions lacking neuronal activity should be relatively insensitive to barbiturate suppression of glucose utilization. In a study to examine this phenomenon, three patients with cerebral gliomas underwent FDG-PET while awake and during deep barbiturate coma. Cerebral glucose utilization was measured in normal brain, tumor, and a homologous, non-neoplastic control site in the contralateral hemisphere. A glucose utilization ratio for tumor/control tissue was calculated. The mean reduction of glucose utilization during barbiturate coma was: gray matter 67%, white matter 47%, basal ganglia 66%, thalamus 57%, cerebellar cortex 55%, tumor 32%, and the contralateral control site 64%. The mean tumor glucose utilization ratio was 1.48:1 in the awake state and 2.69:1 during barbiturate coma. The changes in gray matter, basal ganglia, thalamus, cerebellar cortex, and tumor/control tissue ratio were significant (p less than 0.05). In one patient, deep tumor invasion not evident on computerized tomography, magnetic resonance imaging, or baseline FDG-PET was apparent during barbiturate-enhanced FDG-PET scanning. The study findings suggest that gliomas resist suppression of glucose utilization by barbiturates; this supports the hypothesis that barbiturates reduce neuronal metabolism by blocking synaptic activity. This differential effect on normal brain and gliomas enhances the capability to assess the extent of neoplastic tissue in brain and may represent the basis for novel therapeutic strategies.
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PMID:Effect of barbiturate coma on glucose utilization in normal brain versus gliomas. Positron emission tomography studies. 349 28

Seventeen patients with intracranial meningiomas were studied with positron emission tomography and fluorine-18-2-fluorodeoxyglucose (PET-FDG) to assess the glucose utilization of these tumors. Four meningiomas followed for 3-5 years after PET-FDG and surgery showed no evidence of recurrence. These tumors had significantly lower glucose utilization rates (1.9 mg/dl/min +/- 1.0) than 11 recurrent or regrowing meningiomas (4.5 mg/dl/min +/- 1.96) (P less than .01). The glucose metabolic rates of meningiomas correlated with tumor growth, as estimated from changes in tumor size on repeated computed tomographic scans. Histopathologically, a syncytial (atypical) meningioma had the highest glucose utilization rate, followed by a papillary meningioma and an angioblastic meningioma. Individual transitional and syncytial (typical) meningiomas showed marked differences in glucose metabolism despite similar microscopic appearance. Glucose utilization rate appears to be at least as reliable as histologic classification and other proposed criteria for predicting the behavior and recurrence of intracranial meningiomas.
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PMID:Glucose utilization by intracranial meningiomas as an index of tumor aggressivity and probability of recurrence: a PET study. 349 26

We studied cerebellar metabolism in 118 subjects including young and elderly controls and patients suffering from stroke, supratentorial brain tumor and Alzheimer's disease using fluorine-18 fluorodeoxyglucose ([18F]FDG) and position emission tomography (PET). Alzheimer's disease and normal aging did not alter mean cerebellar metabolism. In stroke and tumor mean cerebellar metabolism was lower in the hemisphere contralateral to the supratentorial lesion. In tumor bilaterally significant reductions in absolute cerebellar metabolism also were noted, unlike stroke. Primary sensory stimulation did not alter absolute or relative cerebellar metabolism. These results show that absolute and relative values for cerebellar metabolism vary depending on the process under study. Thus analysis schemes employing normalization of regional metabolic data to cerebellar values may be subject to error.
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PMID:Cerebellar glucose consumption in normal and pathologic states using fluorine-FDG and PET. 349 90

Hemocirculatory and metabolic changes in tumor regions and the remote brain structure were analyzed using oxygen-15 and fluorine-18 positron emission tomography (PET) in eight patients with gliomas after radiation and chemotherapy of 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and N-(2-tetrahydrofuryl)-5-fluorouracil (FT-207). In the tumor regions after the radiochemotherapy, regional cerebral blood flow (rCBF) and cerebral blood volume (rCBV) varied widely and there was a tendency for oxygen consumption (rCMRO2) to fall. The change in glucose consumption (rCMRG1) was especially noteworthy with regard to clinical correlations. Six patients with decreased rCMRG1 values had 16% to 29% regressions in tumor size measured by X-ray computerized tomography (CT), and showed some period of clinical relief. In contrast, one patient with an increased rCMRG1 value had some progression of tumor growth, and there were no clinical amelioration. The hemocirculation and metabolism of the contralateral gray matter seem to fluctuate by various factors as intracranial pressure and the effectiveness of the therapy. In gliomas therapy, tumor rCMRG1 values can be a good indicator of therapeutic effectiveness.
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PMID:Positron emission tomographic evaluation of radiochemotherapeutic effect on regional cerebral hemocirculation and metabolism in patients with gliomas. 350 Feb 81

Hypoxic, non-functional, but viable, tissue may exist in heart and brain following an arterial occlusion. Identification of such tissue in vivo is crucial to the development of effective treatment strategies. It has been suggested that certain compounds capable of sensitizing hypoxic tumor cells to killing by x-rays (i.e., misonidazole) might serve as in vivo markers of hypoxic tissue in ischemic myocardium or brain if properly radiolabeled. To this end we have radiolabeled two fluorinated analogs of nitroimidazole based hypoxic cell sensitizers with the 110 minute half-lived positron-emitting fluorine-18. The ability of these tracers to quantitate the presence of hypoxic tissue has been studied in a gerbil stroke model. The in vivo uptake of one of these tracers [F-18]-fluoronormethyoxymisonidazole is dependent on the extent of tissue hypoxia, and thus, appears to have potential as a diagnostic indicator of non-functional but viable tissue when the tracer is used in conjunction with positron emission tomography.
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PMID:Radiolabeled hypoxic cell sensitizers: tracers for assessment of ischemia. 360 Jan 79

38 patients with locally advanced breast cancer, were treated with a program of cytotoxic chemotherapy including Adriamycin, Cyclophosphamide, 5 Fluoro-uracile and Prednisone. The concentration of hormonal receptors (Estrogen ER and Progesterone receptor PR) in the tumor were studied before starting the chemotherapy and after one to 9 courses of chemotherapy. This therapeutic response rate was not related to the initial level of ER and PR. After chemotherapy, we observed an increase of ER level in 14 cases out of 29 (59%), of PR level in 17 out of 32 cases (53%); A therapeutic response is observed in 11 cases out of 17 when the PR concentration is increased and in 3 cases out of 15 when the PR concentration was either stable or decreased. These observations let us to suppose a selective initial activity of chemotherapy on lesser differentiated tumor cells.
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PMID:[Breast cancer. Development of the concentration of hormonal receptors under cytotoxic chemotherapy]. 375 63

Misonidazole is a known hypoxic cell sensitizer that binds covalently in hypoxic cells. Its congeners labeled with 77Br, 75Br, or 18F, are likely candidates for imaging hypoxia. We have synthesized and tested [82Br]-4-bromomisonidazole, [3H]-4-bromomisonidazole, [3H]fluoromisonidazole and [3H]misonidazole as prototype radiopharmaceuticals and have compared their uptake in normal and malignant tissues. The higher lipophilicity of brominated misonidazole increased its concentration in the hypoxic portion of tumors at 2 hr, but high blood levels contributed to excessive background, incompatible with imaging. Hydrogen-3-fluoromisonidazole diffused into tumors at a slower rate than misonidazole but it also cleared from normal tissues so that after 2 hr tumor-to-blood ratios favorable for imaging were achieved. In the compounds that were studied, fluorine at the end of the alkyl chain is more stable in vivo than bromine on the imidazole ring. Our results indicate that [18F] fluoromisonidazole may be a useful tracer for imaging hypoxia at approximately 4 hr after injection.
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PMID:Synthesis and characterization of congeners of misonidazole for imaging hypoxia. 379 12

Several methylated analogs of fluorene were evaluated as mutagens in Salmonella typhimurium TA98 and TA100 in the presence and absence of microsomal activation. Among the methylated derivatives of fluorene assayed were 9-methylfluorene, 2-fluoro- and 2,7-difluoro-9-methylfluorene, 1,9-, 2,9-, 3,9- and 4,9-dimethylfluorene, 2,3,9-trimethylfluorene and 2,7,9-trimethylfluorene. Mutagenic activity was observed for several of these fluorene derivatives in the presence of rat liver homogenate. The data support a previous observation that a single methyl substituent in the 9-position of fluorene is associated with mutagenic activity within this series of compounds. Substitution with fluorine at both the 2- and 7-positions of 9-methylfluorene was not associated with a loss of mutagenic activity as evidenced by the similar mutagenic activity of 2,7-difluoro-9-methylfluorene and 9-methylfluorene. However, 2,7,9-trimethylfluorene was not mutagenic under these assay conditions. 9-Methylfluorene, 1,9-, 2,9-, 3,9- and 4,9-dimethylfluorene and 2,3,9-trimethylfluorene were active as mutagens in the presence of rat liver homogenate, but were inactive as tumor initiators when assayed on mouse skin.
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PMID:Studies on the mutagenicity and tumor-initiating activity of methylated fluorenes. 388 56

10-Fluoro-7,12-dimethylbenz(a)anthracene (10-F-DMBA) is a more potent skin tumor initiator in SENCAR mice when compared with the parent hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA). To elucidate the mechanism for this difference, the covalent binding of these two hydrocarbons to the DNA of mouse epidermal cells in vivo and in vitro was compared. The quantity of 10-F-DMBA covalently bound to mouse epidermal DNA in vivo was greater than that of DMBA at all doses tested over the range of 4 to 200 nmol/mouse. The magnitude of this binding difference between 10-F-DMBA and DMBA was greater at the higher doses (e.g., 1.5-fold at 4 nmol/mouse versus 3.4-fold at 200 nmol/mouse). These results correlated closely with the dose-response relationships for tumor initiation by the two hydrocarbons. Analysis of the isolated DNA samples by Servacel DHB chromatography revealed the relative proportion of syn-diol-epoxide:DNA adducts derived from DMBA increased dramatically as a function of dose (approximately 30% at 4 nmol/mouse versus approximately 55% at 200 nmol/mouse). Conversely, the relative proportion of syn-diol-epoxide adducts derived from 10-F-DMBA was low and remained essentially constant over the same dose range. High-pressure liquid chromatographic analyses of the DNA adducts derived from DMBA- and 10-F-DMBA-treated mice revealed qualitatively similar profiles. However, as expected, there was a marked reduction in the relative proportion of syn-diol-epoxide:DNA adducts in the profiles of epidermal samples from 10-F-DMBA-treated mice. The major syn-diol-epoxide:deoxy-adenosine adduct was present at a level only 30% that found in high-pressure liquid chromatographic profiles of DMBA samples. Similar results were obtained when primary cultures of mouse epidermal cells were treated with the hydrocarbons. The results suggest that the increased total binding and possibly the decreased proportion of syn-diol-epoxide:DNA adducts confer greater tumor-initiating potency on 10-F-DMBA.
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PMID:Covalent binding of 7,12-dimethylbenz(a)anthracene and 10-fluoro-7,12-dimethylbenz(a)anthracene to mouse epidermal DNA and its relationship to tumor-initiating activity. 391 51


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