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Emerging Concepts in Glioma Biology: Implications for Clinical Protocols and Rational Treatment Strategies

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Emerging Concepts in Glioma Biology: Implications for Clinical Protocols and Rational Treatment Strategies Neurosurg Focus 19 (4):E3, 2005 Emerging concepts in glioma biology: implications for clinical protocols and rational treatment strategies STEPHEN M. WIESNER, M.T., PH.D., ANDREW FREESE, M.D., PH.D., AND JOHN R. OHLFEST, PH.D. Department of Neurosurgery, University of Minnesota, Minneapolis, Minnesota Glioblastoma multiforme (GBM), the most common primary central nervous system neoplasm, is a complex, het- erogeneous disease. The recent identification of stem cells in murine tumor xenografts that were capable of recapitu- lating the tumor phenotype adds a new dimension of complexity to the already challenging treatment of patients with GBMs. Although specific cellular and genetic changes are commonly associated with GBM, the mechanism by which those changes occur may have a significant impact on treatment outcome. Of the many bioinformatics techniques de- veloped in recent years, gene expression profiling has become a commonly used research tool for investigating tumor characteristics, and the development of rationally targeted molecular therapies has also accelerated following the ini- tial success of specifically designed inhibitors in the treatment of malignancies. Despite these advances in research techniques and targeted molecular therapies, however, limited clinical impact has been achieved in the treatment of infiltrative malignancies such as GBMs. Thus, further extension in survival of patients with GBMs may require use of multiple analyses of tumors to develop tailored therapies that reflect the inter- and intratumoral heterogeneity of this disease. In this review, the authors briefly consider the potential use of expression profiling combined with mutation analysis in the development of treatment modalities to address the heterogeneity of this complex tumor phenotype. KEY WORDS • glioblastoma multiforme • microarray • stem cell • targeted therapy OVERVIEW ASPECTS OF GBM Glioblastoma multiforme is the most common primary central nervous system neoplasm, accounting for more than Cellular Characteristics 6,25 half of all such tumors. Despite advances in survival for The GBM is a diffuse and infiltrative tumor. Migrating many patients with malignancies, the prognosis for those GBM cells can be found several centimeters away from the with GBM remains poor, even with modern aggressive in- margins of resection. Accordingly, although tumor recur- tervention, including resection, radiotherapy, and chemo- rence predominantly occurs near the primary resection site, therapy. The overall 2-year survival rate is 25% at best, and 23,44 5-year survival rates remain in the low single digits.25,42 it can arise in distant regions of the brain. The GBM is Thus, it is clear that new treatments are needed to overcome composed of genetically and morphologically diverse cells, the limitations of conventional therapy. Emerging evidence not only among different patients, but also among cells indicates that patient-specific therapies tailored to the within the same tumor. Furthermore, any therapy that relies unique biology of an individual’s GBM may be required to on cell division to kill tumor cells is complicated by the fact achieve significant improvements in clinical outcomes. In that only a fraction of glioma cells are actively mitotic dur- this article we briefly discuss emerging insights into glioma ing a given treatment window.11 cell biology and common genetic mutations. In addition, Mounting evidence indicates that, similarly to leukemia we highlight how understanding the cell biology and gene and breast cancer, GBM tumors are composed of stem cell– expression profiles of each patient’s GBM could be useful like precursor cells and also more differentiated tumor in implementing more effective treatment. cells.44,45,51 The former, which we will call BTSCs, are en- dowed with many features of NSCs, including the capacity Abbreviations used in this paper: BTSC = brain tumor stem cell; for self-renewal, the ability to generate daughter cells with EGFR = epidermal growth factor receptor; GBM = glioblastoma different phenotypes from a single mother cell, the capaci- multiforme; JAK/STAT = Janus tyrosine kinase/signal transducer and activator of transcription; MAPK = mitogen-activated protein ty to differentiate into a diverse population of cells, and ex- 45,51 kinase; NSC = neural stem cell; PDGFR␤ = platelet-derived growth pression of NSC markers. Moreover, BTSCs have been factor receptor–␤; PI3K = phosphatidylinositol 3-kinase; RB = isolated from human GBMs that can form tumors in the retinoblastoma; RTK = receptor tyrosine kinase. brains of mice that bear a morphological resemblance to the Neurosurg. Focus / Volume 19 / October, 2005 1 Unauthenticated | Downloaded 09/27/21 01:09 AM UTC S. M. Wiesner, A. Freese, and J. R. Ohlfest original human tumor.45 These BTSCs demonstrate immu- motes the transcription and translation of proteins that block noreactivity for CD133, a primitive progenitor cell marker, progression through the cell cycle, allowing DNA damage and appear to be the tumor-initiating cells not only in to be repaired.27 Loss of p53 allows cells with DNA damage mouse xenografts but also potentially in spontaneous hu- to progress through the cell cycle unchecked, perpetuating man GBM. Furthermore, when BTSCs were induced to or compounding the DNA damage.1,22,46 Direct mutation, differentiate in vitro, they retained the ability to form neu- deletion, or loss of expression of p53 is commonly observed rospheres when cultured in stem cell–supportive media, an in GBMs, as in many other solid tumors.22 ability that is unique to BTSCs. Thus, BTSCs appear to Furthermore, changes in genes upstream of p53 in this have the capacity to revert from a terminally differentiated pathway are also commonly found in tumors. Amplification state back to a more primitive state, a characteristic distinct or overexpression of MDM2 occurs in 10 to 15% of GBMs, from normal NSCs and consistent with cells found in other resulting in a blunted or absent p53 response, and has in malignancies.51 some studies been associated with poor prognosis in patients The ability of cells isolated from human tumors to self re- with GBM.19,38,39,41 The MDM2 binds to and sequesters p53, new and contribute to various cell types in both in vitro and promoting its rapid degradation within the cell, thus pre- in vivo tumorigenesis models establishes a potential mech- venting transcription of antiproliferative genes.33 The anism for the complex heterogeneity characteristic of GBM MDM2 is in turn regulated by another gene product, human and highlights the need for therapeutic strategies targeting p14ARF (called ARF in this paper); ARF antagonizes not only malignant, more differentiated GBM tumor cells, MDM2, releasing p53 inhibition to induce cell cycle arrest.37 but also GBM stem cells that likely contribute to the in- Although ARF is located in the INK4A genomic locus evitable recurrence of this disease. The potential phenotyp- and shares exons 2 and 3 with p16INK4A, it differs in structure ic differences between GBM stem cells and normal NSCs and function due to a frameshift caused by splicing from an may be subtle, and may in fact be undetectable by currently alternative exon 1.24 This second gene encoded by the used clinical tests. Additionally, the source of BTSCs may INK4A locus, p16INK4A, also functions as a tumor suppressor, not be the tumor itself. In at least one study in which a spon- but with a different mechanism and specificity than ARF. taneous mouse model of GBM was used, it was found that The p16INK4A locus indirectly regulates RB by blocking the tumor-initiating cells might migrate from a separate loca- action of cyclin-dependent kinases, preventing phosphory- tion within the brain, only to repopulate an area with a lation of RB, and maintaining RB-mediated inhibition of favorable microenvironment for tumor growth.53 Although cell cycle progression.22 Thus, each of the genes encoded the combination of invasiveness, the ability to become mi- by the INK4A locus regulate tumor suppressors, and loss of gratory, and complexity of cellular composition in human each has been shown to cause transformation of cells to a GBMs represents a formidable challenge for effective ther- malignant phenotype. Therefore, both are considered tumor apy, the identification of BTSCs provides a rational target suppressors and have been implicated in gliomagenesis. for new therapies, because these cells appear to be the tu- Recent studies in mice indicate that ARF may play a more mor-initiating component of GBM. prominent role in gliomagenesis than p16, although there may be differences in the function of these proteins in mice 22,24 Complex Heterogeneity and Genetic Mutations compared with humans. Separate studies have demonstrated variability of gene Numerous genetic mutations have been identified in expression in different sets of GBMs.16,28,32 In particular, tu- GBM that have been postulated to contribute to gliomagen- mors expressing the EGFR, which is associated with a par- esis. Alterations in tumor suppressors are the genetic le- ticularly poor prognosis, can clearly be identified by micro- sions most commonly found. Retinoblastoma protein, the array expression analysis.32 In other studies, investigators RB-1 gene product, is present ubiquitously and at relative- have been able to identify subtypes of GBM based on their ly constant levels throughout the body.1 In its dephosphor- molecular signature.21,28,32,34 Some of these researchers have ylated state, this protein functions
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