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PubMed2006

Differentiation of recurrent brain tumor versus radiation injury using diffusion tensor imaging in patients with new contrast-enhancing lesions.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the use of diffusion tensor imaging (DTI) in the evaluation of new contrast-enhancing lesions and perilesional edema in patients previously treated for brain neoplasm in the differentiation of recurrent neoplasm from treatment-related injury. METHODS: Twenty-eight patients with new contrast-enhancing lesions and perilesional edema at the site of previously treated brain neoplasms were retrospectively reviewed. Nine directional echoplanar DTIs with b=1000 s/mm(2) were obtained using a single-shot spin-echo echoplanar imaging. Standardized regions of interest were manually drawn in several regions. Mean apparent diffusion coefficient (ADC), fractional anisotropy (FA) and eigenvalue indices (lambda( parallel) and lambda( perpendicular)) and their ratios relative to the contralateral side were compared in patients with recurrent neoplasm versus patients with radiation injury, as established by histological examination or by clinical course, including long-term imaging studies and magnetic resonance spectroscopy. RESULTS: The ADC values in the contrast-enhancing lesions were significantly higher (P=.01) for the recurrence group (range=1.01 x 10(-3) to 1.66 x 10(-3) mm(2)/s; mean+/-S.D.=1.27+/-0.15) than for the nonrecurrence group (range=0.9 x 10(-3) to 1.31 x 10(-3) mm(2)/s; mean+/-S.D.=1.12+/-0.14). The ADC ratios in the white matter tracts in perilesional edema trended higher (P=.09) in treatment-related injury than in recurrent neoplasm (mean+/-S.D.=1.85+/-0.30 vs. 1.60+/-0.27, respectively). FA ratios were significantly higher in normal-appearing white matter (NAWM) tracts adjacent to the edema in the nonrecurrence group (mean+/-S.D.=0.89+/-0.15) than in those in the recurrence group (mean+/-S.D.=0.74+/-0.14; P=.03). Both eigenvalue indices lambda( parallel) and lambda( perpendicular) were significantly higher in contrast-enhancing lesions in the recurrence group than in those in the nonrecurrence group (P=.02). As well, both eigenvalue indices lambda( parallel) and lambda( perpendicular) were significantly higher in perilesional edema than in normal white matter (P<.01 and P<.001, respectively) in both groups. CONCLUSION: The assessment of diffusion properties, especially ADC values and ADC ratios, in contrast-enhancing lesions, perilesional edema and NAWM adjacent to the edema in the follow-up of new contrast-enhancing lesions at the site of previously treated brain neoplasms may add to the information obtained by other imaging techniques in the differentiation of radiation injury from tumor recurrence.

Adolescent↗

PubMed2000

[Radiotherapy for brain stem neoplasms in children].

The immediate and short-term results of radiotherapy of brain stem tumors in 24 children were evaluated. All the patients were able to sustain treatment due to adjuvant support with dehydrating and hormonal drugs, and beneficial clinical effect was recorded in 80%. However, MRT showed no decrease in tumor size. Tumor growth relapsed 3-8 months after radiotherapy. Although total dose ranged 60-72 Gy in 19 patients, there was clinical evidence of radiation injury.

Adolescent↗

PubMed1998

The significance of lack of MR contrast enhancement of supratentorial brain tumors in adults: histopathological evaluation of a series.

BACKGROUND: To correlate magnetic resonance imaging (MRI) findings of non-enhancement of supratentorial brain neoplasms in adults with histopathologic findings. METHODS: Forty adult patients whose preoperative MRI studies demonstrated a non-enhancing supratentorial brain neoplasm were identified retrospectively. Biopsy material for all patients was then reviewed by a board-certified neuropathologist. RESULTS: Histopathologic examination identified 24 (60%) low-grade gliomas: 4 (10%) low-grade astrocytomas, 10 (25%) low-grade gliomas (not further classified), 8 (20%) low-grade oligodendrogliomas, and 2 (5%) low-grade mixed oligoastrocytomas. However, 16 (40%) nonenhancing lesions were classified as anaplastic gliomas: 12 (30%) anaplastic astrocytomas, 1 (2.5%) anaplastic mixed oligoastrocytoma, 1 (2.5%) anaplastic oligodendroglioma, and 2 (5%) anaplastic infiltrating gliomas of indeterminate subtype. CONCLUSION: Non-enhancement of supratentorial brain neoplasms in adults does not equate with low-grade malignancy. This fact should be taken into account when biopsy and treatment are being planned in patients with nonenhancing brain tumors. More aggressive and/or surgical therapy might be indicated for such lesions, particularly those in the nondominant hemisphere or nonmotor areas.

Adult↗

PubMed1992

Renal transplacental carcinogenicity of 3,3-dimethyl-1-phenyltriazene in rats: relationship of renal mesenchymal tumor to congenital mesoblastic nephroma and intralobar nephrogenic rests.

Exposure of rat embryos to 3,3-dimethyl-1-phenyltriazene (DMPT) results in numerous malformations, but the urogenital system is not affected. In contrast, exposure of rat fetuses to DMPT has been reported to result in renal neoplasms, which were not further classified. To better understand this discrepancy in organotropism of the teratogenic and transplacental carcinogenic processes, the present study was undertaken to characterize the neoplasms induced in rat fetuses exposed to DMPT in utero. Renal neoplasms and persistent mesenchyme were observed in 19.2 and 11.5%, respectively, of the offspring of rats treated with 1 mg DMPT/kg body weight intraperitoneally on gestation days 16, 18, and 20. The majority of these renal lesions were observed in females. The renal neoplasms were mixtures of various types of mesenchymal tissue derivatives including smooth muscle and fibrous connective tissue. These neoplasms would be classified as renal mesenchymal tumors in rats. Brain neoplasms (numerous types), compound odontomas, and micrognathism were observed predominantly in male offspring from the same group. This treatment also resulted in decreased body weights, increased incidence of sudden loss of body weight, tremors and ataxia, and hypoplastic testes. Exposure to single intraperitoneal doses of DMPT on gestation day 20 did not produce a classic dose-response pattern: Minimal effects were observed with 10 mg DMPT/kg (occasional renal mesenchymal tumors and brain neoplasms), marked effects were observed with 30 mg DMPT/kg (lower incidence rate of most of the alterations observed with 1 mg/kg on gestation days 16, 18, and 20), and no effects were observed with 60 mg DMPT/kg. DMPT administered intraperitoneally at 1 mg/kg body weight on gestation days 16, 18, and 20 is an animal model of transplacental chemically induced renal neoplasms, which provide lesions with similarities to both intralobar nephrogenic rests and congenital mesoblastic nephroma of humans. Why the kidney is a carcinogenic target and not a teratogenic target remains unknown.

Animals↗

PubMed1991

Transthyretin immunoreactivity in choroid plexus neoplasms and brain metastases.

Although choroid plexus papillomas (CPP) and primary choroid plexus carcinomas (CPC) are rare neoplasms of the central nervous system, they have been the subject of a number of immunohistochemical studies. To date, no unique or specific marker for these neoplasms has been found, however. Normal choroid plexus is a major site of transthyretin (TTR) synthesis, and recently this protein has been proposed as a possible specific marker of choroid plexus differentiation in tumors. In this study, we performed immunohistochemistry for TTR on 13 choroid plexus tumors (six CPP and seven CPC) and on 23 carcinomas metastatic to the brain, four of which had a papillary architecture. We also included four ovarian teratomas that contained choroid plexus elements. Two of the CPP had diffuse staining for TTR, while the four others stained only focally. Five of the CPC stained only focally and less intensely than the control, while one case was negative. Only one CPC stained as strongly and diffusely as normal choroid plexus. Two of the papillary and six of the nonpapillary metastases had focal staining similar to that seen in the five focally positive CPC. The choroid plexus elements of the ovarian teratomas stained as strongly as the positive control. These findings indicate that TTR immunoreactivity is not restricted to primary choroid plexus tumors. Furthermore, most choroid plexus carcinomas stain only weakly or not at all. This limits the usefulness of TTR immunohistochemistry in the diagnosis of primary choroid plexus neoplasms and in the distinction of CPC from metastatic carcinoma.

Adenocarcinoma↗

PubMed1990

Descriptive epidemiology of malignant brain tumors in the Swiss Canton of Vaud.

Incidence registration and survival data from brain neoplasms have been analyzed from the population-based system of the Cancer Registry of the Swiss Canton of Vaud, which has been operating in a particularly favorable environment for surveillance and using an integrated and homogeneous system of cancer registration. Between 1974 and 1987, a total of 401 cases was registered, corresponding to an age-adjusted rate for all malignant histotypes of 5.3/100,000 (world standard) for the period 1975-1980 and 5.0 for 1981-1987 in males, and of 3.9 and 3.7, respectively, in females. Thus, no increase in brain neoplasm incidence has taken place in this population, and indeed some decline has been observed in males, particularly for gliomas (from 2.7 to 2.0). During the most recent calendar period, incidence rates were 2.0 in males and 1.5 in females for gliomas, 0.9 in both sexes for astrocytomas, 0.4 in males and 0.1 in females for oligodendrogliomas, and 1.7 in males and 1.2 in females for other or unspecified histotypes. For both gliomas, astrocytomas and total brain neoplasms, the peak rate was observed in the age group 55-74, and some flattening of rates was registered above age 75. Overall 5-year survival was 16%. While there was no difference between sexes, survival rates were substantially lower at older (greater than or equal to 60 years, 3%) than at younger (less than 60 years, 26%) age, and for gliomas (7% at 5 years) than for other histological types. However, the histotype distribution could not explain the major difference in survival by age, since similar differences were observed for various histotypes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2003

MR spectroscopy of brain tumors.

MR spectroscopy is a non-invasive technique for measuring tissue metabolites. Changes in tissue metabolites may be useful for diagnosing or characterizing primary and other brain neoplasms, planning treatment, and assessing the results of treatment. Ongoing improvements in equipment and pulse sequence design may make full brain spectroscopy clinically practical in the near future. The authors review the basic concepts of MR spectroscopy and its use in clinical management of brain neoplasms.

Aspartic Acid↗

PubMed1982

Intracerebral chemotherapy: chronic microinfusion of cisplatin.

Cisplatin, a chemotherapeutic agent used to treat tumors in many parts of the body, does not reach brain tissue during systemic injection because of the blood-brain barrier and protein binding in the blood. To allow hydrophilic drugs, such as cisplatin, to reach brain neoplasms with minimal body toxicity, we tested chronic intracerebral microperfusion into the extracellular space of the brain in normal rats. Small stainless steel cannulas connected to osmotic minipumps were stereotactically placed in the midline cerebellum or frontal cortex, and cisplatin was pumped into the brain at the rate of 0.9 microgram/hour for periods of up to 7 days. Brain tissue was then analyzed for the total platinum content, at 1-mm intervals from the cannula tip, using atomic absorption spectroscopy. The results of the animal studies show that a platinum concentration of 2 ng/mg of tissue, wet weight, can be maintained over a 1-cm region of brain. If all of the extracellular platinum has remained in the active cisplatin form, then this would be equivalent to a drug concentration of 10 microM. Cisplatin at this constant level has been shown to have a therapeutic effect against various tumor lines in vitro. To extend these results to human brain neoplasms, we estimate that one cannula would be sufficient to treat a 1-cm tumor or a larger tumor that could be surgically reduced. For inoperable tumors of up to 2 cm in diameter, a multiple cannula system would be required to yield the 10 microM concentration throughout. For larger inoperable tumors, local infusion will not produce high enough drug levels. In conclusion, chronic intracerebral microinfusion can be used to produce adequate and sustained therapeutic drug levels over a considerable region of tissue without the problem of systemic toxicity.

Animals↗

PubMed1994

Endothelial cell implantation and survival within experimental gliomas.

The delivery of therapeutic genes to primary brain neoplasms opens new opportunities for treating these frequently fatal tumors. Efficient gene delivery to tissues remains an important obstacle to therapy, and this problem has unique characteristics in brain tumors due to the blood-brain and blood-tumor barriers. The presence of endothelial mitogens and vessel proliferation within solid tumors suggests that genetically modified endothelial cells might efficiently transplant to brain tumors. Rat brain endothelial cells immortalized with the adenovirus E1A gene and further modified to express the beta-galactosidase reporter were examined for their ability to survive implantation to experimental rat gliomas. Rats received 9L, F98, or C6 glioma cells in combination with endothelial cells intracranially to caudate/putamen or subcutaneously to flank. Implanted endothelial cells were identified by beta-galactosidase histochemistry or by polymerase chain reaction in all tumors up to 35 days postimplantation, the latest time examined. Implanted endothelial cells appeared to cooperate in tumor vessel formation and expressed the brain-specific endothelial glucose transporter type 1 as identified by immunohistochemistry. The proliferation of implanted endothelial cells was supported by their increased number within tumors between postimplantation days 14 and 21 (P = 0.015) and by their expression of the proliferation antigen Ki67. These findings establish that genetically modified endothelial cells can be stably engrafted to growing gliomas and suggest that endothelial cell implantation may provide a means of delivering therapeutic genes to brain neoplasms and other solid tumors. In addition, endothelial implantation to brain may be useful for defining mechanisms of brain-specific endothelial differentiation.

Adenovirus E1A Proteins↗

PubMed1997

Primary central nervous system lymphoma in patients with AIDS.

Primary central nervous system lymphoma (PCNSL), once considered a rare brain neoplasm, has been steadily increasing in incidence mainly due to an enlarging population of immunosuppressed patients. PCNSL has become the second most common brain space occupying lesion in patients with the acquired immunodeficiency syndrome. A rapid diagnosis of this entity may represent weeks to months of survival to immunosuppressed HIV-positive patients. The radiologist now plays an important role in the noninvasive diagnosis and management of this condition through the accurate interpretation of imaging findings provided by CT, MR, and brain SPECT studies. This article focuses on the pathogenesis, clinical manifestations, neuropathology, and imaging characteristics of this brain neoplasm. New accurate imaging algorithms combining the diagnostic information provided by CT, MR, and T1-201 brain SPECT are discussed.

Brain↗

PubMed2001

Aspects of intracranial and spinal tumors in patients with Down syndrome and report of a rapidly progressing Grade 2 astrocytoma.

BACKGROUND: Brain tumors in patients with Down syndrome (DS) rarely are reported, and their behavior is not well known. METHODS: The authors report on a male patient age 19 years who had DS with diffuse astrocytoma (World Health Organization Grade 2) that recurred twice despite treatment, leading to a glioblastoma and, finally, to death in just over 2 years. The literature on brain tumors in patients with DS is reviewed. RESULTS: Although brain neoplasms were suspected to be in excess in patients with DS, the authors found only 36 patients with brain neoplasms and 2 spinal tumors. An unusual distribution of histologic tumor types, with an over-representation of germ cell and mesenchymal tumors and a lack of embryonal tumors, was observed, in agreement with what is known currently about the tumor profile of patients with DS. CONCLUSIONS: Cerebral tumors in patients with DS have a specific distribution and may behave differently compared with the general population. These features may be related to the gene dosage effect of oncogenes, antioncogenes, and genes involved in cerebral development due to the supernumerary chromosome 21.

Adult↗

PubMed2006

Pitfalls in the diagnosis of brain tumours.

Establishing the diagnosis of a brain tumour is not always a straightforward process. Many non-neoplastic neurological diseases can mimic brain neoplasms on neuroimaging or on histological examination, including multiple sclerosis, stroke, pyogenic abscess, toxoplasmosis, tuberculosis, cysticercosis, fungal infections, syphilis, sarcoidosis, Behçet disease, radiation necrosis, venous thrombosis, and others. Conversely, several types of brain neoplasms, such as glioblastomas, low-grade gliomas, CNS lymphomas, and brain metastases, can present in the absence of typical tumefactive lesions, posing significant diagnostic challenges. In this Review, we discuss the process of accurately establishing the diagnosis of brain tumours, focusing on pitfalls commonly encountered in clinical practice. We also discuss the rational use and limitations of new diagnostic techniques, such as diffusion-weighted MRI, perfusion-weighted MRI, magnetic resonance spectroscopy, single-photon emission tomography, and positron emission tomography, as well as new tools for histological examination, such as immunohistochemistry and molecular genetics analysis.

Brain Diseases↗

PubMed1994

Purine and pyrimidine metabolism in human gliomas: relation to chromosomal aberrations.

Chromosomal aberrations in human gliomas are principally numerical. In tumours of low malignancy, karyotypes are frequently normal, but occasionally an excess of chromosome 7 and a loss of sex chromosome are observed. In highly malignant tumours, the most frequent aberrations are gain of chromosome 7, loss of chromosome 10 and less frequently losses or deletions of chromosomes 9, 22, 6, 13 and 14 or gains of chromosomes 19 and 20. To understand the meaning of these chromosome imbalances, the relationships between chromosome abnormalities and metabolic disturbances were studied. The losses or deletions observed affected principally chromosomes carrying genes encoding enzymes involved in purine metabolism. The activities of ten enzymes were measured: adenosine kinase, adenine phosphoribosyltransferase, adenylate kinase, methylthioadenosine phosphorylase, hypoxanthine phosphoribosyltransferase, adenylosuccinate lyase, inosine monophosphate dehydrogenase, adenosine deaminase, nucleoside phosphorylase and adenosine monophosphate deaminase. In parallel, two enzymes involved in pyrimidine metabolism, thymidine kinase and thymidylate synthase (TS), were studied. The activities of all these enzymes were measured on samples from 30 human primary glial tumours with low or high malignancy, six xenografted tumours at different passages, four portions of normal brain tissue and four non-glial brain neoplasms. As suggested by cytogenetic data, the enzymatic results showed a relatively low activity of purine metabolism in glial tumours when compared with normal brain and non-glial brain neoplasms. Considering the two enzymes involved in pyrimidine metabolism, only TS had higher activity in glial tumours of high malignancy than in normal brain. In comparison with normal brain, the balance between salvage and de novo pathways changes in gliomas, and even more in grafted tumours, in favour of de novo synthesis. The relation between chromosomes and metabolic imbalances does not correspond to a simple gene dosage effect in these tumours. These data suggest that the decrease of adenosine metabolism occurs before chromosomal aberrations appear, since it is observed in tumours of low malignancy when most karyotypes are still normal, and that the de novo pathway increases with tumour progression.

Adolescent↗

PubMed2004

Glioblastoma multiforme in three baboons (Papio spp).

Glioblastoma multiforme is the most malignant astrocytic neoplasm and the most common brain neoplasm of humans. Spontaneous neoplasms of the brain are rare in nonhuman primates. This report describes three glioblastomas in adult captive-reared baboons. The animals exhibited a range of clinical signs, including depression, weight loss, weakness, and blindness. All three neoplasms were located in the cerebrum, with extension into the pons in one case. Histologically, the tumors were similar and were characterized by cellular pleomorphism, multinucleated cells, areas of necrosis, microvascular proliferation (glomeruloid bodies), and palisading of neoplastic cells around blood vessels and areas of necrosis. Two baboons exhibited gemistocytic differentiation, and in one baboon, the neoplastic cells were predominantly spindle shaped with a fascicular growth pattern. Immunohistochemical staining for glial fibrillary acidic protein, vimentin, and S-100 protein was positive, whereas immunostaining for synaptophysin and chromogranin A was negative. Positive staining for the cell proliferation marker Ki67 ranged from 8.2% to 13.9%. Terminal deoxynucleotidyl transferase mediated dVTPnick end labeling (TUNEL) staining ranged from 1.8% to 5.7%. These baboon glioblastomas share many features with those of humans.

Animals↗

PubMed1999

Intracranial inflammatory tumors: a survey of their various etiologies by presentation of 5 cases.

Due to similar clinical and neuroradiological features, intracranial inflammatory tumors (IITs) are frequently misdiagnosed as brain neoplasms, from which they notably differ in respect to therapy and prognosis. In this article, five cases of such tumors are presented. Three of the patients with brain tumors (cases 3, 4 and 5) presented a history of 'pararheumatic' syndromes but no diagnosis of defined immunopathies. On the basis of radiological findings, all processes were classified as genuine brain neoplasms, but histology showed reactive inflammatory features. The possible etiologies of these 'tumors' are discussed on the basis of all clinical and histological data of the patients. The spectrum of diseases potentially leading to the manifestation of an IIT is reviewed. Additionally, the presentation of case 5, who developed a highly malignant B-cell-lymphoma 6 months after the removal of an IIT without any histological signs of atypia, shows that this differential diagnosis always has to be kept in mind.

Adult↗

PubMed2002

Functional magnetic resonance imaging - basics and applications in oncology.

Functional MR imaging (F-MRI) permits to visualize active processes evolving in the human brain. The shifts in blood oxygenation following local neuronal activation are used for generating an MR signal. Specific procedural problems have to be solved when using F-MRI in patients with brain neoplasms. The relationship between perirolandic tumors and the adjacent motor areas has been studied most intensively. When the resection of tumors in the motor area is considered, functional imaging can help the surgeon to avoid or at least to minimize postoperative functional deficits. Overall, F-MRI study results are useful in at least one crucial preoperative decision step for about 90% of brain tumor patients. Experience with functional imaging in radiotherapy of brain neoplasms is still limited. Presently, F-MRI cannot yet replace intraoperative brain mapping.

Brain↗

PubMed1993

Cytokine gene expression in primary brain tumours, metastases and meningiomas suggests specific transcription patterns.

To obtain an insight into the network of cytokine gene transcription in the brain tumour microenvironment, we investigated the expression of genes encoding for interleukin (IL)-1 alpha, IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, interferon (IFN)-gamma, granulocyte-macrophage colony-stimulating factor, tumour necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta 1, -beta 2 and -beta 3 in freshly excised brain tumour samples and autologous peripheral blood mononuclear cells. Tissue specimens from 15 primary brain tumours, three brain metastases, five meningiomas, autologous peripheral blood mononuclear cells (PBMC) and three brain tumour cell lines were tested by reverse polymerase chain reaction. Despite the presence of T-lymphocytes, cytokine gene transcripts typically detectable upon T cell receptor triggering could not be observed in central nervous system tumours of diverse histology. In primary brain neoplasms, transcription of genes encoding for the inhibitory cytokines TGF-beta and IL-10 was detectable in more than 50% of samples. IL-6 transcripts could only be detected in malignant gliomas. In brain metastases, virtually no cytokine gene transcripts could be observed. Surprisingly, TGF-beta transcripts were also detected in all meningiomas. Thus, transcription of genes encoding for inhibitory factors appears to prevail in primary brain neoplasms.

Adolescent↗

PubMed2005

Microglia function in brain tumors.

Microglia play an important role in inflammatory diseases of the central nervous system (CNS). These cells have also been identified in brain neoplasms; however, as of yet their function largely remains unclear. More recent studies designed to characterize further tumor-associated microglia suggest that the immune effector function of these cells may be suppressed in CNS tumors. Furthermore, microglia and macrophages can secrete various cytokines and growth factors that may contribute to the successful immune evasion, growth, and invasion of brain neoplasms. A better understanding of microglia and macrophage function is essential for the development of immune-based treatment strategies against malignant brain tumors.

Animals↗