[Brainlife] Newsletter, Vol.4 No.43

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BRAINLIFE NEWSLETTER

Volume 4, Number 43 - 18 October 2005	Volume 4 Archive

1: AJNR Am J Neuroradiol. 2005 Oct;26(9):2187-99.

Assessment of Diagnostic Accuracy of Perfusion MR Imaging in Primary and Metastatic Solitary Malignant Brain Tumors.

Bulakbasi N, Kocaoglu M, Farzaliyev A, Tayfun C, Ucoz T, Somuncu I.

Department of Radiology, Gulhane Military Medical School, Ankara, Turkey.

PURPOSE: The purpose of this study was to estimate the diagnostic accuracy of relative cerebral blood volume (rCBV) measurement in preoperative grading and differentiation of solitary intra-axial malignant brain tumors. METHODS: Thirty-six low-grade glial tumors (LGGTs), 22 high-grade glial tumors (HGGTs), and 17 metastases (METs) were prospectively evaluated by MR imaging and standard dynamic susceptibility contrast-enhanced gradient echo, echoplanar imaging during first pass of a bolus injection of contrast material. Normalized rCBV values from tumoral (rCBV(T)) and peritumoral (rCBV(P)) areas were calculated by standard software and statistically tested independently. RESULTS: The mean differences of rCBV(T) and rCBV(P) values between LGGT (2.30 +/- 1.12 and 1.18 +/- 0.24) and HGGT (5.42 +/- 1.52 and 2.17 +/- 0.82) (P < .001); HGGTs and METs (3.21 +/- 0.98 and 0.97 +/- 0.09) (P < .001); and LGGTs and METs (P < .05 and P < .001, respectively) were significant. No clear cutoff value was present. A clear rCBV(T) cutoff value of 2.6 was detected for differentiation of low- (1.75 +/- 0.38; LGA) versus high-grade (4.78 +/- 0.99; HGA) astrocytomas when nonastrocytic glial tumors were excluded. The rCBV(T) values were linearly correlated with degree of malignancy (r = 0.869; P < .001). Cutoff rCBV(P) values of 1.1 and 1.2 were quite effective in differentiation of METs from LGGTs and HGGTs, respectively. The overall efficacy of rCBV was higher in grading than in differentiation. CONCLUSION: The diagnostic accuracy of rCBV measurement is higher in grading of glial brain tumors than in differentiation of HGGTs from solitary intra-axial METs. The astrocytic and nonastrocytic glial tumors have to be evaluated separately for precise grading.

PMID: 16219821 [PubMed - in process]

2: AJNR Am J Neuroradiol. 2005 Oct;26(9):2183-6.: Fiber density index correlates with reduced fractional anisotropy in white matter of patients with glioblastoma.

Roberts TP, Liu F, Kassner A, Mori S, Guha A.

Department of Medical Imaging, University of Toronto, Toronto, Canada.

A quantitative description of white matter fiber attenuation, the fiber density index (FDi) is described. This measure is derived from quantitative analysis of diffusion tensor imaging and reveals an index of the number of fiber paths traversing a region of interest. In this report, FDi is computed in 10 patients with glioblastoma multiforme, in white matter that is peritumoral and contralateral. FDi is shown to correlate significantly with fractional anisotropy.

PMID: 16219820 [PubMed - in process]

3: AJNR Am J Neuroradiol. 2005 Oct;26(9):2178-82.: Brain Compression without Global Neuronal Loss in Meningiomas: Whole-Brain Proton MR Spectroscopy Report of 2 Cases.

Cohen BA, Knopp EA, Rusinek H, Liu S, Gonen O.

Department of Radiology, New York University School of Medicine, New York, NY.

We report the findings from whole-brain proton MR spectroscopy, quantifying the neuronal marker N-acetylaspartate (NAA), for 2 presurgical meningioma patients and 10 healthy controls. The patients' whole-brain NAA (WBNAA) concentrations were considerably elevated (3+ SDs) compared with healthy controls when excluding the tumors from brain volume; WBNAA levels normalized following correction to approximate "preneoplastic" brain size. These results suggest global neuronal preservation in these 2 patients while their brains were compressed by large, slowly growing, extra-axial masses.

PMID: 16219819 [PubMed - in process]

4: Cancer. 2005 Oct 11; [Epub ahead of print]

Primary pediatric brain tumors.

Wong TT, Ho DM, Chang KP, Yen SH, Guo WY, Chang FC, Liang ML, Pan HC, Chung WY.

Department of Neurosurgery, Neurological Institute, Taipei Veterans General Hospital and National Yang Ming University, School of Medicine, Taiwan, Republic of China.

BACKGROUND: The purpose of the current study was to investigate a hospital series of 986 cases of primary pediatric brain tumors in Taiwan. METHODS: The authors reviewed the database of primary pediatric brain tumors in patients < 18 years of age collected in Taipei Veterans General Hospital (Taipei VGH) from 1975 to May 2004. Age and gender distribution, location, and classification of brain tumors were analyzed. Intracranial tumors with diagnostic imaging were included. Nontumoral lesions, cysts, and vascular malformations were excluded. RESULTS: The mean age of these 986 patients was 7.8 years, and the male to female ratio was 1.4:1. Supratentorial (including pineal-quadrigeminal) located tumors (58.3%) was predominant to infratentorial tumors (41.1%). In these series, 886 patients had either histologic diagnosis (842 patients) or clinical diagnosis (44 patients). The most common 5 categories of tumors were astrocytic tumors (31.1%), germ cell tumors (14.0%), medulloblastomas (13.3%), craniopharyngiomas (8.3%), and ependymal tumors (5.8%). Atypical teratoid/rhabdoid tumors (AT/RTs), a rare but highly malignant tumor, were 2.1%. The high incidence of primary intracranial germ cell tumors correlated with reported series from Japan and Korea. For the remaining 100 patients without diagnostic classifications, the majority were most likely astrocytic tumors in brain stem. CONCLUSIONS: The authors analyzed a large hospital series of primary brain tumors in children. Both histologically verified and unverified tumors were recruited to avoid selective bias. Although it was not a study of a population-based brain tumor registry, it could still be representative of primary pediatric brain tumors in Taiwan. Cancer 2005. (c) 2005 American Cancer Society.

PMID: 16220552 [PubMed - as supplied by publisher]

5: Cancer Genet Cytogenet. 2005 Oct 15;162(2):135-9.: Inactivation patterns of NF2 and DAL-1/4.1B (EPB41L3) in sporadic meningioma.

Nunes F, Shen Y, Niida Y, Beauchamp R, Stemmer-Rachamimov AO, Ramesh V, Gusella J, Maccollin M.

Department of Neurology, Massachusetts General Hospital, Building 149, 13th Street, Charlestown, MA 02129.

The molecular basis of tumorigenesis and tumor progression in meningiomas is not fully understood. The neurofibromatosis 2 (NF2) locus is inactivated in 50-60% of sporadic meningiomas, but the genetic basis of sporadic meningiomas not inactivated at the NF2 locus remains unclear. Specifically, there is conflicting data regarding the role of the tumor suppressor gene DAL-1/4.1B. Using microsatellite markers, we studied 63 sporadic meningiomas to determine loss of heterozygosity (LOH) at the NF2 and DAL-1/4.1B loci. Array comparative genomic hybridization analysis of 52 of these tumors was performed to determine copy number changes on chromosomes 18 and 22. Forty-one of 62 informative tumors showed LOH at the NF2 locus (66%) while only 12 of 62 informative tumors (19%) showed LOH of DAL-1/4.1B. Eleven of 12 (92%) tumors with DAL-1/4.1B LOH also had NF2 LOH. Monosomy or large deletions of chromosomes 18 and 22 were the main mechanism for LOH in these tumors. These studies implicate the DAL-1/4.1B locus in sporadic meningiomas less commonly than reported previously, and suggest that it is a progression rather than an initiation locus. Furthermore, we found the majority of meningiomas developed monosomy rather than isodisomy at the NF2 and DAL-1/4.1B loci as the mechanism for LOH.

PMID: 16213361 [PubMed - in process]

6: Int J Cancer. 2005 Oct 10; [Epub ahead of print]: Cigarette smoking and risk of glioma: A prospective cohort study.

Silvera SA, Miller AB, Rohan TE.

Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA.

The etiology of glioma, the most commonly diagnosed malignant brain tumor among adults in the United States, is poorly understood. N-nitroso compounds are known carcinogens, which are found in cigarette smoke and can induce gliomas in rats. On this basis, it has been hypothesized that cigarette smoking may be associated with an increased risk of glioma. We investigated the association between cigarette smoking and glioma risk in the National Breast Screening Study, which included 89,835 Canadian women aged 40-59 years at recruitment between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths from all causes, respectively, with follow-up ending between 1998 and 2000. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between cigarette smoking and risk of glioma. During a mean of 16.4 years of follow-up, we observed 120 incident glioma cases. Among ever smokers, women who reported having quit smoking had a 51% increase in risk of glioma compared with never smokers (HR = 1.51, 95% CI = 0.97-2.34), while current smokers did not appear to have an increase in risk. When the association with former smokers was further examined by years since quitting, women who had quit smoking >10 years before baseline were at a decreased risk of glioma compared with women who had quit within the 10 years prior to baseline (HR = 0.55, 95% CI = 0.29-1.07), indicating that the association between former smokers and glioma may be driven by women, who recently quit smoking. Compared with nonsmokers, duration of cigarette smoking, number of cigarettes smoked per day and pack-years of smoking were associated with increased glioma risk, although the increases in risk were relatively modest. The present study provides some support for a positive association between cigarette smoking and risk of glioma. (c) 2005 Wiley-Liss, Inc.

PMID: 16217772 [PubMed - as supplied by publisher]...

7: Int J Cancer. 2005 Oct 10; [Epub ahead of print]: Immune stimulatory effects of CD70 override CD70-mediated immune cell apoptosis in rodent glioma models and confer long-lasting antiglioma immunity in vivo.

Aulwurm S, Wischhusen J, Friese M, Borst J, Weller M.

Laboratory of Molecular Neuro-Oncology, Department of General Neurology, Hertie Institute for Clinical Brain Research, School of Medicine, University of Tubingen, Tubingen, Germany.

CD70 (CD27 ligand) promotes the expansion of primed lymphocytes by enhancing cell survival. Surprisingly, we previously observed that CD70 aberrantly expressed on human glioma cells promoted immune cell apoptosis and inhibited alloreactive lysis. Here we report that ectopic expression of CD70 in mouse glioma cells enhances apoptosis of T, B and NK cells in coculture, but nevertheless promotes glioma cell lysis by NK cells in vitro. In nude mice, CD70 expression in SMA-560 gliomas delays the glioma growth upon subcutaneous (s.c.) or intracerebral (i.c.) inoculation, suggesting a role for CD70/CD27-dependent NK cell activity in tumor surveillance. In syngeneic immunocompetent VM/Dk mice, CD70 allows the rejection of s.c. and i.c. implanted SMA-560 tumors. The tumorigenicity of CD70-expressing glioma cells is abrogated when TGF-beta signaling is blocked. Moreover, mice surviving the s.c. CD70 glioma challenge subsequently also reject wild-type glioma cells administered i.c. Similarly, CD70-expressing GL-261 gliomas are rejected in syngeneic C57BL/6 mice, while glioma growth is restored in C57BL/6 CD27(-/-) mice, suggesting that the CD70/CD27 interaction recruits a tumor-specific T-cell repertoire and induces tumor-specific memory. Altogether, these observations indicate that the net effect of aberrant CD70 expression in gliomas is immune stimulatory rather than immune paralytic and encourage its application in tumor immunotherapy. (c) 2005 Wiley-Liss, Inc.

PMID: 16217761 [PubMed - as supplied by publisher]

8: Int J Cancer. 2005 Oct 10; [Epub ahead of print]: The pro-cell death Bcl-2 family member, BNIP3, is localized to the nucleus of human glial cells: Implications for glioblastoma multiforme tumor cell survival under hypoxia.

Burton TR, Henson ES, Baijal P, Eisenstat DD, Gibson SB.

Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, MB, Canada.

The Bcl-2 nineteen kilodalton interacting protein 3 (BNIP3) is a hypoxia-inducible proapoptotic member of the Bcl-2 family that induces cell death by associating with the mitochondria. Under normal conditions, BNIP3 is expressed in skeletal muscle and in the brain at low levels. In many human solid tumors, BNIP3 is upregulated in hypoxic regions but paradoxically, this BNIP3 expression fails to induce cell death. Herein, we have determined that BNIP3 is primarily localized to the nucleus of glial cells of the normal human brain, as well as in the malignant glioma cell line U251. Upon exposure of U251 cells to hypoxia, BNIP3 expression in the cytoplasm increases and localizes with the mitochondria, contributing to induction of cell death. In contrast, when BNIP3 is forcibly over expressed in the nucleus, it fails to induce cell death. Expression of N-terminal BNIP3 (lacking the transmembrane and conserved domains) in U251 cells blocks hypoxia-induced cell death acting as a dominant negative protein by binding to wild-type BNIP3 and blocking its association with the mitochondria. In glioblastoma multiforme (GBM) tumors, BNIP3 expression is increased in hypoxic regions of the tumor and is primarily localized to the nucleus in approximately 80% of tumors. Hence, BNIP3 is sequestered in the nucleus within the brain but under hypoxic conditions, BNIP3 becomes primarily cytoplasmic, promoting cell death. In GBMs, BNIP3 expression is increased but it remains sequestered in the nucleus in hypoxic regions, thereby blocking BNIP3's ability to associate with the mitochondria, providing tumor cells with a possible survival advantage. (c) 2005 Wiley-Liss, Inc.

PMID: 16217754 [PubMed - as supplied by publisher]

9: Int J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):91-100.: Long-term survival and functional status of patients with low-grade astrocytoma of spinal cord.

Robinson CG, Prayson RA, Hahn JF, Kalfas IH, Whitfield MD, Lee SY, Suh JH.

Department of Radiation Oncology, Brain Tumor Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.

PURPOSE: To determine survival and changes in neurologic function and Karnofsky performance status (KPS) in a series of patients treated for low-grade astrocytoma of the spinal cord during the past two decades. METHODS: This study consisted of 14 patients with pathologically confirmed low-grade astrocytoma of the spinal cord who were treated between 1980 and 2003. All patients underwent decompressive laminectomy followed by biopsy (n = 7), subtotal resection (n = 6), or gross total resection (n = 1). Ten patients underwent postoperative radiotherapy (median total dose 50 Gy in 28 fractions). The overall survival, progression-free survival, and changes in neurologic function and KPS were measured. RESULTS: The overall survival rate at 5, 10, and 20 years was 100%, 75%, and 60%, respectively. The progression-free survival rate at 5, 10, and 20 years was 93%, 80%, and 60%, respectively. Neither overall survival nor progression-free survival was clearly correlated with any patient, tumor, or treatment factors. Neurologic function and KPS worsened after surgery in 8 (57%) of 14 and 9 (69%) of 13 patients, respectively. At a mean follow-up of 10.2 years, neurologic function had stabilized or improved in 8 (73%) of 11 remaining patients, but the KPS had worsened in 5 (50%) of 10. Most patients who were employed before surgery were working at last follow-up. CONCLUSION: Patients who undergo gross total resection of their tumor may be followed closely. Patients who undergo limited resection should continue to receive postoperative RT (50.4 Gy in 1.8-Gy fractions). The functional measures should be routinely evaluated to appreciate the treatment outcomes.

PMID: 16111576 [PubMed - indexed for MEDLINE]

10: J Neurooncol. 2005 Oct;75(1):31-42.: Radiotherapy and chemotherapy of brain metastases.

Soffietti R, Costanza A, Laguzzi E, Nobile M, Ruda R.

Neuro-Oncology Service, Department of Neuroscience, University and San Giovanni Battista Hospital, Via Cherasco 15, 10126, Torino, Italy, riccardo.soffietti@unito.it.

The authors have reviewed the results, the indications and the controversies regarding radiotherapy and chemotherapy of patients with newly diagnosed and recurrent brain metastases. Whole-brain radiotherapy, radiosurgery, hypofractionated stereotactic radiotherapy, brachytherapy and chemotherapy are the available options. New radiosensitizers and cytotoxic or cytostatic agents are being investigated. Adjuvant whole brain radiotherapy, either after surgery or radiosurgery, and prophylactic cranial irradiation in small-cell lung cancer are discussed, taking into account local control, survival, and risk of late neurotoxicity. Increasingly, the different treatments are tailored to the different prognostic subgroups, as defined by Radiation Therapy Oncology Group RPA Classes.

PMID: 16215814 [PubMed - in process]

11: J Neurooncol. 2005 Oct;75(1):21-9.: Surgery of brain metastases - Is there still a place for it?

Modha A, Shepard SR, Gutin PH.

Neurosurgery Service, Memorial Sloan-Kettering Cancer Center and the Department of Neurological Surgery, Weill Medical College of Cornell University, New York, NY, gutinp@mskcc.org.

The role of surgery in the treatment of metastatic brain tumors has always been a source of controversy. It was only in the early 1990s that two randomized prospective trials demonstrated that surgery plus radiation therapy improved survival in patients with single metastatic brain tumors vs. radiation therapy alone. This paper reviews these articles as well as other evidence outlining management options for multiple brain metastases. An attempt has been made to better define the role of surgery in brain metastases. The prognostic factors for brain metastases after surgery are also reviewed and the data comparing stereotactic radiosurgery to surgery is examined. A short description of surgical planning, operative techniques and tools, followed by a discussion on complication avoidance before, during, and after surgery is included.

PMID: 16215813 [PubMed - in process]

12: J Neurooncol. 2005 Oct;75(1):15-20.: Symptomatic management and imaging of brain metastases.

Kaal EC, Taphoorn MJ, Vecht CJ.

Department of Neurology, Medical Center Haaglanden, P.O. Box 432, 2501, CK, The Hague, Netherlands, c.vecht@mchaaglanden.nl.

Brain metastasis is the most common malignancy of the nervous system. Survival is short and the majority of patients die within 5 months after diagnosis. In this review, clinical and pathophysiological aspects of brain metastases are described, including novel radiological methods as triple-dose gadolinium-enhanced MRI. Recursive partitioning analysis is a powerful tool to analyse prognosis, and recent studies contribute to subgroup division. Subsequently, treatment choices can be made, based on prognostic characteristics of the individual patient. Commonly, symptomatic therapy starts with the administration of corticosteroids, often resulting in improvement of neurological deficit. Anticonvulsants are administered in patients with symptomatic epilepsy. The risk on vascular complications in patients with brain metastases is increased and needs special attention. Treatment of psychiatric complications e.g. delirium or depression may also improve quality of life.

PMID: 16215812 [PubMed - in process]

13: J Neurooncol. 2005 Oct;75(1):5-14.: Brain metastases: epidemiology and pathophysiology.

Gavrilovic IT, Posner JB.

Department of Neurology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY, 10021, USA, posnerj@mskcc.org.

Metastases are the most common tumors of the central nervous system (CNS), but cancer databases are often incomplete leading to underestimation of the incidence of even symptomatic brain metastases. Brain imaging studies are not routinely performed on neurologically asymptomatic cancer patients and autopsy studies are outdated. Furthermore, while incidence rates for cancers are stable and mortality is decreasing due to earlier detection and better therapy, the incidence of brain metastases appears to be increasing. The pathophysiology of brain metastases is a complex multistage process, mediated by molecular mechanisms; from the primary organ, cancer cells must transform, grow and be transported to the CNS where they can lay dormant for various lengths of time before invading and growing further. Understanding the pathophysiology of brain metastases is of great importance, because it may lead to the development of more efficient therapies to combat brain tumor growth or to possibly make the CNS an undesirable environment for tumor progression.

PMID: 16215811 [PubMed - in process]

14: J Neuropathol Exp Neurol. 2005 Oct;64(10):875-881.: Monomorphous Angiocentric Glioma: A Distinctive Epileptogenic Neoplasm With Features of Infiltrating Astrocytoma and Ependymoma.

Wang M, Tihan T, Rojiani AM, Bodhireddy SR, Prayson RA, Iacuone JJ, Alles AJ, Donahue DJ, Hessler RB, Kim JH, Haas M, Rosenblum MK, Burger PC.

From the Department of Pathology and Laboratory Medicine (MW), University of Texas Health Science Center at Houston, Medical School, Houston, Texas; Department of Pathology (TT), University of California at San Francisco, San Francisco, California; Departments of Pathology and Oncology (AR), Moffitt Cancer Center at University of South Florida, Tampa, Florida; Department of Pathology (SRB), Covenant Medical Center, Lubbock, Texas; Department of Pathology (RAP), The Cleveland Clinic Foundation, Cleveland, Ohio; Department of Hematology/Oncology (JJI), Covenant Children's Hospital, Lubbock, Texas; Department of Pathology and Laboratory Medicine (AJA), Cook Children's Medical Center, Fort Worth, Texas; Department of Neurosurgery (DJD), Cook Children's Medical Center, Fort Worth, Texas; Section of Anatomic Pathology (RBH), Medical College of Georgia, Augusta, Georgia; Department of Pathology (YHK), Yale University School of Medicine, New Haven, Connecticut; Department of Pathology (MKR), Memorial-Sloan Kettering Cancer Center, New York, NY; and Department of Pathology (MH, PCB), The Johns Hopkins University School of Medicine, Baltimore, Maryland.

We present 8 examples of a neoplasm with features of both astrocytoma and ependymoma that may represent a distinct clinicopathologic entity. The cerebral hemispheric tumors occurred in patients that were 3, 4, 12, 14, 15, 26, 30, and 37 years of age. All presented with seizures that, with the exception of 2, began in childhood. Magnetic resonance imaging studies showed ill-defined, T2-hyperintense, generally noncontrast-enhancing lesions that, although centered on the cortex or amygdala, extended into the underlying white matter for a short distance. Histologically, the variably infiltrative tumors were distinctively angiocentric with well-developed perivascular pseudorosettes in some cases. Longitudinal and/or circumferential orientations of perivascular cells were common also. The cells were uniform in their cytologic features from case to case and were bipolar in all but one case. A glial nature was inferred from immunoreactivity for GFAP, and ependymal differentiation was suggested by positivity for EMA in three cases and ultrastructural features in one. Overall, the tumors were biologically indolent except for one that recurred and ultimately proved fatal.

PMID: 16215459 [PubMed - as supplied by publisher]

15: J Neuropathol Exp Neurol. 2005 Oct;64(10):869-874.: Anaplasia Is Rare and Does Not Influence Prognosis in Adult Medulloblastoma.

Giordana MT, D'agostino C, Pollo B, Silvani A, Ferracini R, Paiolo A, Ghiglione P, Chio A.

From the Department of Neuroscience (MTG, CD, PG, AC), University of Torino, Torino, Italy; Department of Neuropathology and Neurology (BP, AS), Istituto Nazionale Neurologico C. Besta, Milan, Italy; and Departments of Pathology and Oncology (RF, AP), University of Bologna, Bologna, Italy.

Histopathologic grading based on increasing anaplasia predicts clinical behavior of pediatric medulloblastomas. The present study was aimed at grading 86 medulloblastomas of adult patients (aged 18 and older) by anaplasia and analyzing the predictive power. Nodularity, desmoplasia, nuclear size, nuclear pleomorphism, necrosis, and endothelial proliferations have been evaluated. Morphometric analysis of nuclear size was performed using the Eclipse Net program. Patients treated with standard postoperative radiotherapy (35 Gy to craniospinal axis and 50 Gy to posterior fossa) were considered for correlation with survival. Pathologic data and total survival were compared by Kaplan-Meier and logrank analysis. No correlation was found between total survival duration and individual pathologic features. Cooccurrence of nuclear pleomorphism, large nuclear diameter, microvascular proliferations, and necroses did not predict outcome. Severe nuclear pleomorphism was found in 4 of 86 cases; the only large-cell medulloblastoma was from an 18-year-old patient. Histopathologic factors have no clinical use for stratification of patients in risk groups. The histologic spectrum of medulloblastoma in adults is different from that in children.

PMID: 16215458 [PubMed - as supplied by publisher]

16: J Neurosurg. 2005 Mar;102(2 Suppl):172-8.: Surveillance imaging strategies following surgery and/or radiotherapy for childhood cerebellar low-grade astrocytoma.

Saunders DE, Phipps KP, Wade AM, Hayward RD.

Department of Neuroradiology, Great Ormond Street Hospital, London, United Kingdom. SaundD@gosh.nhs.uk

OBJECT: The authors sought to evaluate surveillance strategies for the detection and monitoring of residual and recurrent disease in children with cerebellar low-grade astrocytomas (CLGAs) treated surgically or with radiotherapy. Patients were divided into three groups: (1) those in whom a "complete" resection was achieved; (2) those with residual disease with no immediate adjuvant therapy; and (3) those who received radiotherapy for residual/recurrent disease. METHODS: Magnetic resonance (MR) imaging studies and clinical data obtained in children with CLGA who presented between January 1988 and September 1998 were reviewed. Eighty-four children were followed for a mean period of 73 months (range 2-159 months). One child died. Of the 70 children in whom a complete resection was achieved, nine (13%) developed a recurrence detected by surveillance imaging at 6, 8, 9, 9, 13, 27, 39, 44, and 47 months, respectively. Following an incomplete resection, radiologically detected tumor progression leading to further treatment was detected at 7, 9, 12, 13, and 20 months, respectively, and an additional six tumors regressed or stablized. In 11 of 12 children treated with radiotherapy, stabilization/regression occurred radiologically at a mean of 14.9 months. CONCLUSIONS: The authors recommend surveillance MR imaging in children treated for CLGA at 6 months and 1, 2, 3.5, and 5 years following a complete resection and after radiotherapy performed either initially or following recurrence. For follow up of residual tumor, 6-month interval imaging for at least 3 years, yearly images for another 2 years, and subsequent 2-year imaging is recommended.

PMID: 16156227 [PubMed - indexed for MEDLINE]