**1. Introduction**

Is not this still the truth? Or, are we today, over 100 years after the first glioma operation, however, nearer to the option that we can treat, even cure, most of gliomas or at least keep the disease under control for very many years? The most frequent primary brain tumor, glioma, is still a nightmare for neurooncologists, neuropathologists, neurosurgeons, and other related professionals, but for patients and their families first of all.

If we look at the results of the papers published in the influential *Medline* database (accessed in December 2018), we will find a paper on glioma published back in 1870 [1]. For the next almost 150 years, in this base alone, we can find more than 87,000 papers on the same topic. On the other hand, in the same base only in the past 5 years, over 22,000 papers have been published having basically a story on gliomas (almost a quarter of all publications on gliomas). Does this mean that in the recent years the glioma field research has been more fruitful than ever before? Does this promise, or at least give hope, that we will find the way to put this serious disease under control?

In the USA, primary brain tumors account for about 2% of all cancers, with an overall annual incidence of 22 per 100,000 population, with nearly 80,000 new cases of which one-third will be malignant [2, 3].

The past three decades have been marked with huge enthusiasm of scientists' and professionals' efforts to bring this serious disease into the context of curable or even cured one. Brain glioma patient treatment has significantly changed over time. Undoubtedly, the architect of this fight, Hurvey Chusing, early in the twentieth century, tried to solve the problem surgically and by tumor removal from the brain. History would very soon show

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

that there are brain tumors for which surgery is not sufficient; for some of them, it is not the first option or treatment at all. However, gliomas have remained in focus of interest not only of neurosurgeons but of oncologists, pathologists, neuroradiologists, forensics, and other related medical and nonmedical disciplines either. Not unimportant is also the interest of pharmaceutical industry and researchers in the field of biomedical technologies in the glioma field.

**3. Where we are now**

similar to GBM [11].

III glioma, without 1p/19q codeletion [13].

Brain glioma is infrequently also denoted as slowly growing neoplasm that is most often discovered in younger adults, and it is presented with minimal symptoms or no such symptoms at all. The World Health Organization (WHO) classification system for glial tumors offered guidelines, which can predict the disease course; treatment modalities are thus recommended [7]. Nevertheless, these guidelines are based mostly on histological diagnosis. European Association for Neuro-Oncology (EANO) also presented its guidelines [8]. Yet, histologically the same tumors may have different courses, response to therapy and eventually to outcome. Molecular markers that carry both diagnostic and prognostic information add valuable tools by redefining tumor subtypes within each WHO category. That is why these molecular biomarkers have become an integral part of tumor assessment in modern neurooncology [9]. In that sense, markers such as biomarkers (IDH mutations, promoter methylation of MGMT, chromosomal deletion of 1p/19q, mutations of EGFR and ATRX genes, and BRAF fusion) can today guide clinicians to make better decisions in some subtypes of gliomas, including anaplastic oligodendroglioma and GBM in the elderly [9, 10]. The integration of genome-wide data delineated three molecular classes of LGG, and we believe today that those without an IDH mutation were molecularly and clinically

Introductory Chapter: Glioma - Merciless Medical Diagnosis

http://dx.doi.org/10.5772/intechopen.82863

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Significant progress has been made generally in glioma treatment with the use of modern radiotherapy ways and new chemotherapeutics. Several studies in the past decade have dealt with very promising temozolomide (TMZ) in glioma treatment. Baumert et al., in recently published randomized study results, have reported that they did not find any significant difference in outcome of the overall patient population treated with either radiotherapy alone or TMZ chemotherapy alone [12]. On the other hand, in the just published EORTC trial, randomized controlled research on phase 2 published in Lancet, van den Bent et al. have found no evidence of improved overall survival with bevacizumab (Avastin) and TMZ combination treatment versus TMZ monotherapy in patients with first recurrence of WHO grades II and

A new swing in glioma treatment was the defining of a molecular genetics signature, which can predict patient's outcome with the loss of 1p and 19q in anaplastic oligodendroglioma. Specifically, such patients responded very well to procarbazine, cyclohexychloroethylnitrosurea CCNU, and vincristine (PCV) chemotherapy or TMZ. When it comes to glioblastoma

Surgically, progress was made possible with the development and use of technological aids, first of all of neuronavigation, cortical mapping, electrocorticography, neuromonitoring, functional and intraoperative MRI, magnetoencephalography (MEG). As great hope was placed on extension of tumor resection, brain mapping in particular offered additional safety to the neurosurgeon to provide as good result as possible with maximal and today popular supratotal resection. The current paradigm shift considers glioma management in a comprehensive perspective that takes into account the intricate connectivity of the cerebral networks. Lesions

multiforme (GBM), hope was set on MGMT gene and its methylation [4].
