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PubMed2002

Oligodendroglioma: pathology and molecular biology.

BACKGROUND: Recently, important new information has become available concerning the histologic recognition and molecular biology of oligodendrogliomas. This information, in turn, impacts the way neurosurgeons diagnose and treat patients with these tumors. The purpose of this paper is to review the pathology and basic science of oligodendroglioma, highlighting these developments. METHODS: Information for this review was obtained by a Medline search using the term "oligodendroglioma," and limiting the results to articles dealing with pathology. Chapters from standard textbooks were also used, and bibliographies were checked for additional key articles contributing to the understanding of the pathobiology of this disease. RESULTS: On histologic examination, oligodendrogliomas must be differentiated from tumors including the fibrillary astrocytoma, clear cell ependymoma, central neurocytoma, and dysembryoplastic neuroepithelial tumor (DNT). There is no specific immunocytochemical marker allowing for the recognition of human oligodendroglial tumor cells. A current simplified grading scheme separates these tumors into low grade (WHO grade II) and anaplastic (WHO grade III) oligodendrogliomas. New molecular and genetic markers may aid in grading oligodendrogliomas and identifying patients with a better prognosis or response to chemotherapy. Markers studied include Ki-67, PCNA, EGFr, VEGF, platelet-derived growth factor, p16, p18, p53, bcl-2, COX-1, and chromosomal deletions. The combination of allelic losses on chromosomes 1p and 19q has been statistically associated with a longer recurrence-free survival after chemotherapy. CONCLUSIONS: A patient with an oligodendroglioma may at times still present a diagnostic challenge for the neuropathologist. Yet making an accurate diagnosis is essential, since the clinical course and optimal therapeutic approach differs from that of other gliomas. In the near future, molecular characterization of oligodendrogliomas is expected to play an even greater clinical role.

Antibodies, Antinuclear↗

PubMed2000

Allelic loss of chromosome 1p and radiotherapy plus chemotherapy in patients with oligodendrogliomas.

INTRODUCTION: Allelic loss of the short arm of chromosome 1 predicts radiographic response to chemotherapy and long overall survival times in patients with anaplastic oligodendrogliomas. Using a database of patients with oligodendrogliomas in whom chromosome 1p status was known, we explored whether allelic loss of 1p also predicted longer duration of tumor control when radiotherapy was part of the initial treatment of these patients. MATERIALS AND METHODS: We measured progression-free survival following radiotherapy in a cohort of patients with World Health Organization (WHO) Grade II and WHO Grade III oligodendrogliomas. The effects on progression-free survival of patient age, Karnofsky performance score (KPS), tumor grade when irradiated and chromosome 1p status were examined by univariate and multivariate statistical analyses. For the subset of patients with newly diagnosed anaplastic oligodendrogliomas, relationships between use of chemotherapy, chromosome 1p status and progression-free survival were also examined. RESULTS: Fifty-five patients (29 male, 26 female; ages 18-75 years; median, 44 years; KPS 50-90, median 80) were irradiated for either a WHO Grade II (n = 19) or Grade III (n = 36) oligodendroglioma. Twenty-eight patients had chemotherapy immediately prior to radiotherapy, and 27 had chemotherapy at progression following radiotherapy. The median radiation dose was 54 Gy in 30 fractions. Loss of heterozygosity (LOH) at chromosome 1p was evident in 36 tumors and absent in 19. Overall median progression-free survival after radiotherapy was 40.4 months. Median progression-free survival was 55.0 months for patients whose tumors harbored 1p loss vs. 6.2 months for those patients whose tumors retained both copies of chromosome 1p (p < 0.001). On both univariate and multivariate analyses, chromosome lp loss was the principal independent predictor of longer progression-free survival for patients with Grade II and III oligodendrogliomas. For Grade III oligodendrogliomas, chemotherapy as an adjunct to radiotherapy prolonged tumor control for those patients whose tumors harbored allelic loss of chromosome 1p (p = 0.004). CONCLUSION: These data suggest allelic loss of chromosome 1p in patients with oligodendroglial neoplasms predicts longer progression-free survival among patients receiving radiotherapy +/- chemotherapy as part of their initial treatment. Chromosome 1p loss may be an important stratification variable in future therapeutic trials of oligodendroglioma.

Adolescent↗

PubMed2000

Diagnosis of human oligodendrogliomas with the help of the NeuroShell Easy Classifier neural network.

OBJECTIVE: To examine whether a suitable solution can be found concerning the ability to reproduce the histologic classification of human oligodendrogliomas with the assistance of the NeuroShell Easy Classifier neural network. STUDY DESIGN: Histologic sections of 449 human oligodendrogliomas were selected. The diagnostic task was given by differentiation of three oligodendroglioma types: 121 low grade oligodendrogliomas, World Health Organization grade 2; 180 low grade oligoastrocytomas; and 148 anaplastic oligodendrogliomas, grade 3. Age, sex and 50 histologic characteristics were examined in each case, describing the presence of a specific histologic feature on a scale of four (zero, absence of the feature; three, abundant presence). From each group, two-thirds of randomly selected tumors were available for the training set and one-third for the testing set. RESULTS: In the three-class problem, 98.88% of the tumors were correctly classified (testing set). Ninety-nine percent of new testing tumors were correctly classified with Easy Classifier as low grade and anaplastic oligodendrogliomas. In the case of low grade oligodendrogliomas versus low grade oligoastrocytomas, 99% of new tumors were correctly classified. CONCLUSION: The main conclusion from this study is that Easy Classifier was able to differentiate, with high accuracy, sensitivity and specificity, among the three types of oligodendrogliomas.

Brain Neoplasms↗

PubMed2005

Oligodendroglioma.

Surgery, radiotherapy, and chemotherapy are the standard treatment modalities for all primary brain tumors. Oligodendroglial tumors are uncommon primary brain tumors that typically are classified as low-grade or anaplastic based on their histologic appearance. A great deal of controversy has surrounded the diagnosis of an oligodendroglioma because no unique immunohistochemical marker exists to diagnose this tumor, forcing pathologists to render a diagnosis based on subjective microscopic features. Although once considered relatively rare, oligodendroglial tumors have been increasing in incidence because pathologists have become less rigorous about this diagnosis. However, recent advances in our understanding of the molecular genetic changes associated with brain tumors have identified loss of heterozygosity of chromosomes 1p and 19q as a unique genetic signature of most oligodendroglial tumors, an advance that has paved the way for pathologists to use molecular diagnostics to identify these tumors with improved reliability. These genetic derangements have significant clinical and therapeutic implications because they have been associated with a predictable and durable response to treatment, particularly chemotherapy, and an improved prognosis. The unique chemosensitivity of oligodendroglial tumors has been recognized by neurooncologists for at least 15 years, and various chemotherapeutic agents have been used to manage these diseases. However, the appropriate timing of chemotherapy, and the drugs of choice remain controversial. Increasingly, neurooncologists are reluctant to use radiotherapy as initial management for these diseases because of concerns surrounding the late neurocognitive sequelae of cranial irradiation. These toxicities are particularly important for patients with low-grade oligodendrogliomas in whom the prognosis often exceeds 10 years. Consequently, with the accumulating evidence supporting the chemosensitivity of low-grade and anaplastic oligodendrogliomas and the recent ability to use molecular diagnostics to identify a chemosensitive subset of oligodendrogliomas, neurooncologists are increasingly administering chemotherapy as the initial intervention for all oligodendroglial tumors that harbor favorable genetic derangements. Additionally, although immediate postoperative treatment is uniformly administered to patients with anaplastic oligodendrogliomas, there has been an increasing tendency to defer definitive therapy for those with low-grade oligodendrogliomas until evidence of progression. The development of temozolomide, an oral and well-tolerated alkylating agent that has activity against oligodendroglial tumors, has accelerated this trend to the extent that currently many patients with newly diagnosed low-grade and anaplastic oligodendrogliomas are offered this drug as initial treatment. This paper reviews the current management of oligodendrogliomas, with an emphasis on the expanding role of chemotherapy for these neoplasms.

Journal Article↗

PubMed2004

Bony metastases of anaplastic oligodendroglioma respond to temozolomide.

BACKGROUND: Fewer than 30 cases of oligodendroglioma or anaplastic oligodendroglioma metastatic to bone are reported in the literature. Prolonged survival even with therapy is uncommon. METHODS: We report a case of anaplastic oligodendroglioma metastatic to bone with a dramatic and durable response to temozolomide therapy. A retrospective case review, molecular analysis, and literature search were performed. RESULTS: The patient presented with a right frontal mass in 1990. Progression led to resection of the lesion in 1995. Histology revealed an anaplastic oligodendroglioma and the tumour was found to have allelic loss of heterozygosity (LOH) of chromosome 1p (1p-). He received standard radiation therapy. In 2000 he developed hip and pelvic pain. A bone scan showed multiple skeletal lesions. Magnetic resonance imaging of the brain showed stability of intracranial disease. Resection of one lesion found metastatic anaplastic oligodendroglioma with identical morphology to the patient's original tumour, including glial fibrillary acidic protein expression. The patient was started on standard temozolomide chemotherapy and celecoxib with prompt pain relief, and rapid normalization of serum alkaline phosphatase. He received a total of 12 cycles of combined therapy with no toxicity and no evidence of progression until increasing pain marked disease recurrence. The patient underwent palliative chemo- and radiation therapy but eventually succumbed. DISCUSSION: Loss of heterozygosity 1p- is associated with prolonged survival in anaplastic oligodendroglioma and may increase the cumulative risk for development of systemic metastases. We speculate that metastases from oligodendroglioma harbouring loss of heterozygosity at chromosome 1p- retain the chemosensitivity of the initial lesion.

Adult↗

PubMed2001

Losses of chromosomal arms 1p and 19q in the diagnosis of oligodendroglioma. A study of paraffin-embedded sections.

Comparative genomic hybridization (CGH), fluorescence in situ hybridization (FISH), polymerase chain reaction-based microsatellite analysis, and p53 sequencing were performed in paraffin-embedded material from 18 oligodendrogliomas and histologically similar astrocytomas. The study was undertaken because of evidence that concurrent loss of both the 1p and 19q chromosome arms is a specific marker for oligodendrogliomas. Of the six lesions with a review diagnosis of oligodendroglioma, all had the predicted loss of 1p and 19q seen by CGH, FISH, and polymerase chain reaction. Other lesions, including some considered oligodendroglioma or mixed glioma by the submitting institution, did not. There were no p53 mutations in any of the six oligodendrogliomas, whereas 5 of the 10 remaining, successfully studied cases did have p53 mutations. The results suggest that CGH and FISH performed on current or archival tissue can aid in classification of infiltrating gliomas such as oligodendrogliomas and astrocytomas. The results of the p53 studies are consistent with findings of previous investigations that such mutations are less common in oligodendrogliomas than they are in astrocytomas.

Adult↗

PubMed2003

Expression of cyclin A and topoisomerase IIalpha of oligodendrogliomas is correlated with tumour grade, MIB-1 labelling index and survival.

AIMS: This study was designed to investigate immunoexpression of cyclin A and D1, and topoisomerase IIalpha in oligodendrogliomas and to evaluate the correlation with MIB-1 (Ki67), tumour grade, and survival of the patients. METHODS AND RESULTS: Forty cases of oligodendrogliomas (20 high- and 20 low-grade) were studied immunohistochemically with the above-mentioned monoclonal antibodies. RESULTS: Normal brain tissues included in tumour sections did not express any of cyclin A, MIB-1 and topoisomerase IIalpha except cyclin D1, which was shown in perineuronal and interfascicular normal oligodendroglial cells. In low-grade and high-grade oligodendrogliomas, the mean cyclin A labelling index (LI) was 1.18 +/- 0.98% versus 4.65 +/- 1.99%, respectively; the mean topoisomerase IIalpha LI was 1.32 +/- 1.04% versus 6.63 +/- 4.31%, respectively; and the mean MIB-1 LI was 1.69 +/- 1.55% versus 9.46 +/- 4.66%, respectively. Interestingly, cyclin D1 was not expressed in any oligodendrogliomas. Both cyclin A and topoisomerase IIalpha LI showed a significant positive correlation with MIB-1 LI and histological grade of oligodendrogliomas (P < 0.01) and an inverse correlation with overall survival (P < 0.01). Univariate analysis showed that cyclin A and topoisomerase IIalpha LIs with a cut-off point at 3% were a significant prognostic factor (P: cyclin A = 0.0040, topoisomerase IIalpha = 0.0033). CONCLUSION: Cyclin A and topoisomerase IIalpha expression are closely correlated with anaplastic oligodendrogliomas and worse clinical outcomes. Cyclin D1 seems not to be involved in the tumorigenesis of oligodendrogliomas.

Adult↗

PubMed1999

CD44 expression in primary and recurrent oligodendrogliomas and in adjacent gliotic brain tissue.

CD44 expression was evaluated in 114 primary and recurrent oligodendrogliomas (46 primary oligodendrogliomas grade II and 15 recurrences grade II; 17 primary anaplastic oligodendrogliomas and nine recurrent oligodendrogliomas grade III; 14 glioblastomas with oligodendroglial growth pattern and 13 tumour recurrences grade IV). CD44 expression was found to correlate with tumour grading (P<0.001) and with survival (Kaplan-Meier Log Rank P<0.01, median survival 28 months in oligodendrogliomas with CD44 expression vs. 108 months in CD44-negative tumours). However, multivariate Cox regression analysis of grading and CD44 expression revealed that CD44 expression had no prognostic relevance independent of histological grading. Characterization of CD44 positive cells by double labelling with GFAP revealed that in addition to oligodendroglioma cells, reactive astrocytes within the tumour, at the invasive margin and along the pathways of oligodendroglioma invasion in the subpial matrix, and in the vicinity of vessels, frequently expressed CD44. It is suggested that in analogy to carcinoma invasion where a tumour-induced production of hyaluronan was found in fibroblasts at the invasive margin of the tumour, in the brain reactive astrocytes may produce hyaluronan which would facilitate the adhesion of new CD44-positive astrocytic processes but which would also promote tumour invasion.

Adult↗

PubMed2003

Tumour necrosis and microvascular proliferation are associated with 9p deletion and CDKN2A alterations in 1p/19q-deleted oligodendrogliomas.

A subset of oligodendrogliomas and oligoastrocytomas has been associated with 1p/19q deletion. Subsequently, this genetic alteration was linked to chemosensitivity and classic histology of oligodendrogliomas. Tumoural progression includes deletions of 9p, 10q and alterations of CDKN2A. However, these (epi)genetic changes have not been associated with specific histological features. In a series of 45 gliomas including oligodendrogliomas, oligoastrocytomas and astrocytomas, deletions of chromosomal regions implied in these tumours (1p, 9p, 10, 17p13, 19q and 22) were looked for by microsatellite analysis. Tumours that were deleted for 1p and 19q were selected. Subsequently, presence of deletions in the other studied regions, (epi)genetic changes in p14ARF, CDKN2A and CDKN2B, as well as histological features, were associated to these tumours. 1p/19q deletion was observed in 22 tumours. Twenty-one of them presented regions of classic histology of oligodendroglioma. A deletion of 9p was found in eight of them, always in association with tumour necrosis and/or microvascular proliferation. In addition, (epi)genetic alterations of CDKN2A were observed in 71% of these tumours. Presence of regions of classic histology of oligodendroglioma in a tumour sample is predictive of 1p/19q deletions. Necrosis and/or microvascular proliferation are signs of an additional 9p deletion. Finally, as CDKN2A (epi)genetic alterations were found in 71% of the 1p/19q/9p-deleted oligodendrogliomas, CDKN2A may have a role in oligodendroglioma-associated microvascular proliferation.

Central Nervous System Neoplasms↗

PubMed1998

Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas.

BACKGROUND/METHODS: Gliomas are common malignant neoplasms of the central nervous system. Among the major subtypes of gliomas, oligodendrogliomas are distinguished by their remarkable sensitivity to chemotherapy, with approximately two thirds of anaplastic (malignant) oligodendrogliomas responding dramatically to combination treatment with procarbazine, lomustine, and vincristine (termed PCV). Unfortunately, no clinical or pathologic feature of these tumors allows accurate prediction of their response to chemotherapy. Anaplastic oligodendrogliomas also are distinguished by a unique constellation of molecular genetic alterations, including coincident loss of chromosomal arms 1p and 19q in 50%-70% of tumors. We have hypothesized that these or other specific genetic changes might predict the response to chemotherapy and prognosis in patients with anaplastic oligodendrogliomas. Therefore, we have analyzed molecular genetic alterations involving chromosomes 1p, 10q, and 19q and the TP53 (on chromosome 17p) and CDKN2A (on chromosome 9p) genes, in addition to clinicopathologic features in 39 patients with anaplastic oligodendrogliomas for whom chemotherapeutic response and survival could be assessed. RESULTS/CONCLUSIONS: Allelic loss (or loss of heterozygosity) of chromosome 1p is a statistically significant predictor of chemosensitivity, and combined loss involving chromosomes 1p and 19q is statistically significantly associated with both chemosensitivity and longer recurrence-free survival after chemotherapy. Moreover, in both univariate and multivariate analyses, losses involving both chromosomes 1p and 19q were strongly associated with longer overall survival, whereas CDKN2A gene deletions and ring enhancement (i.e., contrast enhancement forming a rim around the tumor) on neuroimaging were associated with a significantly worse prognosis. The inverse relationship between CDKN2A gene deletions and losses of chromosomes 1p and 19q further implies that these differential clinical behaviors reflect two independent genetic subtypes of anaplastic oligodendroglioma. These results suggest that molecular genetic analysis may aid therapeutic decisions and predict outcome in patients with anaplastic oligodendrogliomas.

Adult↗

PubMed2001

Concurrent inactivation of RB1 and TP53 pathways in anaplastic oligodendrogliomas.

Oligodendrogliomas are characterized by frequent loss of heterozygosity (LOH) on chromosomes 1p and 19q, but additional genetic alterations are likely to be involved. In this study, we screened 28 oligodendrogliomas (WHO grade II) and 20 anaplastic oligodendrogliomas (WHO grade III) for alterations in the RB1/CDK4/p16INK4a/p15INK4b and TP53/p14ARF/MDM2 pathways. In oligodendrogliomas, hypermethylation of RB1 (1 case) and p14ARF (6 cases) were the only detectable genetic changes (7/28, 25%). In anaplastic oligodendrogliomas, the RB1/CDK4/p16INK4a/p15INK4b signaling pathway regulating the G1 -->3 S transition of the cell cycle was altered in 13/20 (65%) cases, by either RBI alteration, CDK4 amplification, or p16IN4a/p15INK4b homozygous deletion or promoter hypermethylation. Further, 50% (10/20) of anaplastic oligodendrogliomas showed alterations in the TP53 pathway through promoter hypermethylation or homozygous deletion of the p14ARF gene and, less frequently, through TP53 mutation or MDM2 amplification. Of 13 anaplastic astrocytomas with an altered RB1 pathway, 9 (69%) also showed a dysregulated TP53 pathway. Thus, simultaneous disruption of the RB1/CDK4/p16INK4a/p15INK4b and the TP53/p14ARF/MDM2 pathways occurs in 45% (9/20) of anaplastic oligodendrogliomas, suggesting that these phenomena contribute to their malignant phenotype.

Gene Deletion↗

PubMed2002

Oligodendrogliomas with neurocytic differentiation. A report of 4 cases with diagnostic and histogenetic implications.

Oligodendroglioma represents a distinct type of diffuse glioma with a relatively favorable prognosis. Although an O2A-like glial progenitor cell of origin has been suggested, a neuronal-oligodendroglial progenitor cell is also of interest, particularly because variable degrees of neuronal marker expression have been reported in typical oligodendrogliomas. We present 2 female and 2 male patients (ages 34-54) with frontal lobe oligodendrogliomas containing a) morphologically distinct collections of small round cells with hyperchromatic nuclei, b) well-formed Homer Wright-like and perivascular rosettes, and c) demonstrable neuronal differentiation by immunohistochemistry and/or electron microscopy in the rosette-associated regions. Unlike extraventricular neurocytomas, these cases featured an infiltrative growth pattern and a classic oligodendroglioma immunophenotype in non-rosette bearing portions of each tumor. FISH analysis demonstrated chromosome 1p and 19q codeletions in 3 (75%) cases, both in regions with and without rosettes. Recurrences were common, although all patients are currently alive 4 months to 13 yr from initial diagnosis. Based on clinicopathologic and genetic features, we diagnosed these tumors as oligodendrogliomas with neurocytic differentiation. However, it is unclear whether they represent a) gliomas with divergent neuronal differentiation, b) a distinctive form of glioneuronal neoplasm, or c) a reflection of glioneuronal histogenesis in oligodendrogliomas in general. In any case, their occurrence suggests a histogenetic overlap between oligodendroglioma and extraventricular neurocytoma not previously recognized.

Adult↗

PubMed1998

Expression of vascular endothelial growth factor and its receptors in the anaplastic progression of astrocytoma, oligodendroglioma, and ependymoma.

Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenic factor, which is known to be upregulated in most cases of glioblastoma multiforme (GBM). The expression of VEGF and its receptors in ependymomas, oligodendrogliomas, and particularly the expression during anaplastic progression of these three types of gliomas has not been studied extensively. Fifty-six gliomas, consisting of 10 ependymomas, 12 oligodendrogliomas, 3 anaplastic oligodendrogliomas, 6 astrocytomas grade II, 5 anaplastic astrocytomas, and 20 glioblastoma multiformes, were investigated for VEGF and receptor expression using in situ hybridization (ISH) and reverse transcription polymerase chain reaction (RT-PCR). Results showed that VEGF was moderately to strongly expressed in 8 of 10 ependymomas and in all anaplastic oligodendrogliomas and glioblastoma multiforme cases. These tumors displayed similar degrees of extensive necrosis and vascular proliferation, with VEGF expression consistently seen in tumor cells around necrotic areas. The VEGF expression, although present at a lower level, also was shown in 4 of 12 oligodendrogliomas, in 3 of 6 astrocytomas grade II, and in 2 of 5 anaplastic astrocytomas, with a regional rather than diffuse pattern of positive result. The findings from the in situ hybridization study correlated with the expression index, as determined by reverse transcription polymerase chain reaction. Expression of VEGF was correlated significantly with vascular proliferation (p < 10(-5)) and necrosis (p < 10(-5)), as well as with microvessel density (p = 0.002, rs = 0.41). The VEGF receptors, kinase domain region (KDR) and Fms-like-tyrosine kinase (Flt-1), also were upregulated in the tumor vasculature of glioblastoma multiforme, anaplastic oligodendrogliomas, and ependymomas with necrosis, whereas the astrocytomas grade II, anaplastic astrocytomas, and oligodendroglioma tumors tended to express a weak to nondetectable signal. Anaplastic progression in all three types of gliomas is heralded by the occurrence of small zones of VEGF-expressing cells and early vascular proliferation, followed by an accelerated phase of angiogenesis closely associated with VEGF induction around areas of necrosis and with the expression of VEGF receptors in the tumor vasculature.

Astrocytoma↗

PubMed1998

Magnetic resonance features of the enigmatic oligodendroglioma.

RATIONALE AND OBJECTIVES: The authors characterize magnetic resonance (MR) features of oligodendroglioma that permit diagnosis. These features may be used to guide MR stereotactic biopsies. METHODS: Fifteen patients with mixed oligodendroglioma and four with pure oligodendroglioma were studied on a 1.5-tesla MR unit with contrast and also by computed tomography (CT). All patients had their diagnosis confirmed by light and electron microscopy, and by immunohistochemical staining. RESULTS: The most characteristic finding was a honeycomb tumor matrix (4 of 19) in oligodendroglioma. The most common finding was an amorphous pattern (12 of 19) and the least common was a large cystic pattern (3 of 19). Contrast enhancement most commonly was minimal and dot-like or lacy in appearance (11 of 19), or absent (5 of 19). Calcification was present in the majority (11 of 19). CONCLUSIONS: The honeycomb and stippled amorphous patterns reflect the cytoarchitecture of oligodendroglioma and were the most characteristic MR features. The amorphous pattern was the most commonly encountered pattern. There was a wider range of imaging findings on MR compared with CT; the flocculent calcification on CT was typical, but it was not always detected on MR. Including these characteristic areas that appear along the path of the stereotactic biopsy may ensure a correct diagnosis of oligodendroglioma because it most often is seen with another tumor, usually of the astrocytic family. Identifying the oligodendrogliomatous portion of the tumor will influence the therapy. No differences could be found in the MR appearance or biologic behavior of pure versus mixed oligodendrogliomas.

Adolescent↗

PubMed2002

Current diagnosis and treatment of oligodendroglioma.

OBJECT: The strategies used to diagnose and treat oligodendroglial tumors have changed significantly over the past decade. The purpose of this paper is to review the topic of oligodendroglioma, emphasizing the new developments. METHODS: Information was obtained by conducting a Medline search in which the term oligodendroglioma was used. Recent editions of standard textbooks were also studied. Because of tools such as magnetic resonance imaging, oligodendrogliomas are being diagnosed earlier, and they are being recognized more frequently histologically than in the past. Seizures are common in these patients. Functional mapping and image-guided surgery may now allow for a safer and more complete resection, especially when tumors are located in difficult areas. Genetic analysis and positron emission tomography may provide data that supplement the standard diagnostic tools. Unlike other low-grade gliomas, patients in whom residual or recurrent oligodendroglioma (World Health Organization Grade II) is present may respond to chemotherapy. Although postoperative radiotherapy prolongs survival of the patient, increasingly this therapeutic modality is being delayed until tumor recurrence, especially if a gross-total tumor resection has been achieved. Oligodendrogliomas are the first type of brain tumor for which "molecular" characterization gives important information. The most significant finding is that allelic losses on chromosomes 1p and 19q indicate a favorable response to chemotherapy. CONCLUSIONS: Whereas surgery continues to be the primary treatment for oligodendroglioma, the scheme for postoperative therapy has shifted, primarily because of the lesion's relative chemosensitivity. Molecular characterization of oligodendrogliomas may become a standard practice in the near future.

Humans↗

PubMed2001

The prognostic significance of DNA topoisomerase II-alpha (Ki-S1), p21/Cip-1, and p27/Kip-1 protein immunoexpression in oligodendrogliomas.

OBJECTIVE: To evaluate a possible association between clinical outcome of patients with oligodendroglioma and expression of 2 cyclin-dependent kinase inhibitors, p21/Cip-1 (p21) and p27/Kip-1 (p27), and of DNA topoisomerase II-alpha (Ki-S1), which has been recently used as a marker of cellular proliferation. DESIGN: Ninety-one specially selected patients with cerebral oligodendrogliomas treated with surgery and radiotherapy were studied retrospectively. Tumor specimens were immunohistochemically examined with antibodies to p21, p27, and Ki-S1. A computerized color image analyzer was used to count immunostained nuclei. RESULTS: The mean Ki-S1 labeling index (LI) was found to be significantly prominent for World Health Organization (WHO) high-grade tumors (9.5% vs. 3.2% for WHO low-grade tumors). In contrast, the mean p27 LI was significantly higher for low-grade tumors (43.3% vs 25.7% for high-grade tumors). The number of p21-positive cases and the mean p21 LI were found to be relatively equal for low- and high-grade tumors. For low-grade oligodendrogliomas, the progression-free and overall survival times were found to be significantly shorter for tumors with p27 LIs less than 20%. For high-grade oligodendrogliomas, survival times were significantly reduced for tumors with Ki-S1 LIs greater than 10%. Regression-tree analysis identified 4 groups of oligodendrogliomas with distinctly different outcomes: (1) 32 patients with low-grade tumors and p27 LIs greater than 20%; (2) 14 patients with low-grade tumors and p27 LIs less than 20%; (3) 25 patients with high-grade tumors and Ki-S1 LIs less than 10%; and (4) 20 patients with high-grade tumors and Ki-S1 LIs greater than 10%. CONCLUSIONS: Immunoreactivity for Ki-S1 and p27 was found to be useful for further subdividing oligodendroglioma prognoses among low-grade and high-grade tumors. It seems unlikely that p21 immunohistochemistry will be of value for determining clinical outcomes for patients with oligodendrogliomas.

Adult↗

PubMedDate not supplied

Nitric oxide synthase expression of oligodendrogliomas.

In the central nervous system, nitric oxide (NO) has a variety of biological functions including vasorelaxation and neurotransmission. The synthesis of NO is catalyzed by NO synthases (NOS) existing in 3 isoforms, neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS). NO synthase has implications in the pathophysiology of primary glial brain tumors with enhanced expression of nNOS and eNOS in high-grade astrocytic tumors, WHO grades III and IV. Only minor groups of pure oligodendrogliomas have been investigated. The aim of the investigation was to study the expression of the 3 NOS isoforms in this genetically divergent group of primary gliomas and to correlate the findings with tumor grade and expression pattern for the major group of gliomas--the astrocytomas. We examined the NOS expression in 35 oligodendrogliomas, WHO grade II, and 7 anaplastic oligodendrogliomas, WHO grade III, by immunohistochemical methods using formalin-fixed paraffin-embedded material. We observed only a minor expression of nNOS and sparse expression of eNOS in the tumor cells, but a vivid expression of eNOS in the vascular endothelial cells in both the tumor and the surrounding tissue. The rich expression of eNOS in oligodendroglioma vessels independent of tumor grade may suggest that blood flow and angiogenesis in these richly vascularized tumors are modified by NO. Interestingly, enhanced expression of inducible NOS was observed in the oligodendroglial tumor cells in 19 of 35 oligodendrogliomas (54%) and in 2 of 7 anaplastic oligodendrogliomas (29%). This is diverging for iNOS expression in astroglial tumors and the data could be indicative of iNOS exerting anti-tumor activity which may protract the progression from low-grade oligodendrogliomas to more anaplastic types.

Brain Neoplasms↗

PubMedDate not supplied

Challenging diagnosis: oligodendroglioma versus extraventricular neurocytoma.

Diagnosis of oligodendroglioma from other clear cell neoplasms of central nervous system (CNS) is still challenging despite advances in neuroradiology and molecular diagnostic tools. Herein, we present a 44-year-old male patient who had a diagnosis of right parietal oligodendroglioma grade II in 1994 which recurred in 2002. He presented with intratumoral hemorrhage and he underwent radical resection of tumor in 2003. Histopathological examination of the recurrent tumor showed anaplastic progression with confusing immunohistochemical (IHC) results; the tumor was positive for NeuN and synaptophysin staining. The question arisen was whether the recurrent tumor was an oligodendroglioma with neuronal differentiation or an extraventricular neurocytoma initially misdiagnosed as oligodendroglioma. Repeated IHC staining showed negative results for NeuN and synaptophysin. Chromosomal analysis revealed 1p/19q deletion, which led to the diagnosis ofanaplastic oligodendroglioma grade III. Accurate diagnosis of oligodendroglioma is crucial due to recent advances and promises in its treatment. Current diagnostic methods of oligodendroglial tumors are discussed in context of differentiating oligodendrogliomas from other clear cell neoplasms of CNS, especially from extraventricular neurocytomas.

Adult↗