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      PROX1 is a predictor of survival for gliomas WHO grade II

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          Abstract

          Background:

          The clinical course of World Health Organisation grade II gliomas remains variable and their time point of transformation into a more malignant phenotype is unpredictable. Identification of biological markers that can predict prognosis in individual patients is of great clinical value. PROX1 is a transcription factor that has a critical role in the development of various organs. PROX1 has been ascribed both oncogenic and tumour suppressive functions in human cancers. We have recently shown that PROX1 may act as a diagnostic marker for high-grade gliomas. The aim of this study was to address the prognostic value of PROX1 in grade II gliomas.

          Methods:

          A total of 116 samples were evaluated for the presence of PROX1 protein. The number of immunopositive cells was used as a variable in survival analysis, together with established prognostic factors for this patient group.

          Results:

          Higher PROX1 protein was associated with poor outcome. In the multivariate analysis, PROX1 was identified as an independent factor for survival ( P=0.024), together with the presence of mutated isocitrate dehydrogenase 1 R132H protein, and with combined losses of chromosomal arms 1p/19q in oligodendrocytic tumours.

          Conclusion:

          PROX1 is a novel predictor of survival for grade II gliomas.

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          Most cited references22

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          Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas.

          Hiroko Ohgaki, Paul Kleihues (2005)
          Published data on prognostic and predictive factors in patients with gliomas are largely based on clinical trials and hospital-based studies. This review summarizes data on incidence rates, survival, and genetic alterations from population-based studies of astrocytic and oligodendrogliomas that were carried out in the Canton of Zurich, Switzerland (approximately 1.16 million inhabitants). A total of 987 cases were diagnosed between 1980 and 1994 and patients were followed up at least until 1999. While survival rates for pilocytic astrocytomas were excellent (96% at 10 years), the prognosis of diffusely infiltrating gliomas was poorer, with median survival times (MST) of 5.6 years for low-grade astrocytoma WHO grade II, 1.6 years for anaplastic astrocytoma grade III, and 0.4 years for glioblastoma. For oligodendrogliomas the MSTwas 11.6 years for grade II and 3.5 years for grade III. TP53 mutations were most frequent in gemistocytic astrocytomas (88%), followed by fibrillary astrocytomas (53%) and oligoastrocytomas (44%), but infrequent (13%) in oligodendrogliomas. LOH 1p/19q typically occurred in tumors without TP53 mutations and were most frequent in oligodendrogliomas (69%), followed by oligoastrocytomas (45%), but were rare in fibrillary astrocytomas (7%) and absent in gemistocytic astrocytomas. Glioblastomas were most frequent (3.55 cases per 100,000 persons per year) adjusted to the European Standard Population, amounting to 69% of total incident cases. Observed survival rates were 42.4% at 6 months, 17.7% at one year, and 3.3% at 2 years. For all age groups, survival was inversely correlated with age, ranging from an MST of 8.8 months ( 80 years). In glioblastomas, LOH 10q was the most frequent genetic alteration (69%), followed by EGFR amplification (34%), TP53 mutations (31%), p16INK4a deletion (31%), and PTEN mutations (24%). LOH 10q occurred in association with any of the other genetic alterations, and was the only alteration associated with shorter survival of glioblastoma patients. Primary (de novo) glioblastomas prevailed (95%), while secondary glioblastomas that progressed from low-grade or anaplastic gliomas were rare (5%). Secondary glioblastomas were characterized by frequent LOH 10q (63%) and TP53 mutations (65%). Of the TP53 mutations in secondary glioblastomas, 57% were in hot-spot codons 248 and 273, while in primary glioblastomas, mutations were more evenly distributed. G:C-->A:T mutations at CpG sites were more frequent in secondary than primary glioblastomas, suggesting that the acquisition of TP53 mutations in these glioblastoma subtypes may occur through different mechanisms.
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            Monoclonal antibody specific for IDH1 R132H mutation.

            Jörg Balss, David Capper, A Deimling … (2009)
            IDH1 R132H mutations occur in approximately 70% of astrocytomas and oligodendroglial tumors. We developed a mouse monoclonal antibody targeting the IDH1 R132H mutation. Here, we show the high specificity and sensitivity of this antibody on Western blots and tissue sections from formalin fixed paraffin embedded tumor specimens. This antibody is highly useful for tumor classification, in detecting single infiltrating tumor cells and for the characterization of the cellular role of mutant IDH1 protein.
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              Continuous growth of mean tumor diameter in a subset of grade II gliomas.

              Marie-Laure Tanguy, Hugues Duffau, K Swanson … (2003)
              Serial magnetic resonance images of 27 patients with untreated World Health Organization grade II oligodendrogliomas or mixed gliomas were reviewed retrospectively to study the kinetics of tumor growth before anaplastic transformation. Analysis of the mean tumor diameters over time showed constant growth. Linear regression, using a mixed model, found an average slope of 4.1mm per year (95% confidence interval, 3.8-4.4mm/year). Untreated low-grade oligodendrogliomas or mixed gliomas grow continuously during their premalignant phase, and their pattern of growth can be predicted within a relatively narrow range. These findings could be of interest to optimize patients management and follow-up.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Br J Cancer
                Title: British Journal of Cancer
                Publisher: Nature Publishing Group
                ISSN (Print): 0007-0920
                ISSN (Electronic): 1532-1827
                Publication date (Print): 24 May 2011
                Publication date (Electronic): 10 May 2011
                Volume: 104
                Issue: 11
                Pages: 1747-1754
                Affiliations
                [1 ]simpleDepartment of Oncology-Pathology, Karolinska Institutet, CCK R8:05, Karolinska University Hospital , S-17176 Stockholm, Sweden
                [2 ]simpleDepartment of Neuroscience, Neurology, Uppsala University , S-75185 Uppsala, Sweden
                [3 ]simpleNational Board of Forensic Medicine , S-75140 Uppsala, Sweden
                [4 ]simpleDepartment of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, and Clinical Cooperation Unit Neuropathology, German Cancer Research Center , 69120 Heidelberg, Germany
                Author notes
                [5]

                Current address: Department of Neurosurgery, 2nd Affiliated Hospital, Suzhou University, Suzhou 215004, China

                [6]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: bjc2011162
                DOI: 10.1038/bjc.2011.162
                PMC ID: 3111172
                PubMed ID: 21559010
                SO-VID: 5f1294d3-c371-4ca9-99fc-9b079ff7dd32
                Copyright © Copyright © 2011 Cancer Research UK
                History
                Date received : 07 March 2011
                Date revision received : 14 April 2011
                Date accepted : 17 April 2011
                Categories
                Subject: Molecular Diagnostics

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: prox1,oligodendroglioma,low-grade glioma,prognosis,astrocytoma,survival
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: prox1, oligodendroglioma, low-grade glioma, prognosis, astrocytoma, survival

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