Abstract
The historical descriptions of glial tumors are often poorly understood and interpreted. The gross and histological depictions of glial tumors are often credited to Virchow, and while the first true histological description is truly his, gross descriptions can be traced back to the beginning of the 1800s, with their classification and histogenesis attributed to Percival Bailey and Harvey Cushing. Without any question, the most prominent and under-credited researcher in the field of glioma pathobiology was the German neuropathologist Hans Joachim Scherer. Despite the limited armamentarium available to him, his systematic approach led to conclusions, some of which have now been molecularly explained today while some are still being widely researched. Scherer defined pseudopalisadic necrosis as a pathognomonic feature of glioblastoma multiforme (GBM), as well as secondary features due to tumor growth, known collectively as secondary Scherer figures, for example, neuronal and vascular satellitosis, tract and subpial aggregation. All these features are key points in the modern histological diagnosis of glial tumors. Other contributions by Scherer include the definition of glomeruloid vascular proliferation and his conclusion that they are caused by vascular factors released by the tumor, decades before vascular endothelial growth factor and its receptors were discovered and their role in glioma evolution was established. Furthermore, he concluded that GBMs can arise de novo (primary) or from a preceding lower-grade glioma (secondary). All his contributions find their place in all modern aspects of glioma research, with some giving a simple explanation of the phenomena observed in glial tumors.
Highlights
BackgroundThe history of glial tumors and the major contributors to the establishment of their concepts are often misunderstood and interpreted
The gross and histological depiction of glial tumors are often credited to the German pathologist Rudolph Virchow, and while the first true histological description is truly his, gross descriptions can be traced back to the beginning of the 1800s in the English, French, and German scientific literature [1,2,3,4]
Almost always they are credited to the American neuropathologist Percival Bailey and prolific neurosurgeon Harvey Cushing, and while their classification is the basis of the modern World Health Organization classification of tumors of the central nervous system (CNS), it was aimed at purely comparing the tumor conglomerates with the healthy cells of the CNS and underwent several revisions by the authors themselves [3,5,6]
Summary
The history of glial tumors and the major contributors to the establishment of their concepts are often misunderstood and interpreted. Tumor growth was an important area studied by Scherer, as again on autopsy material he described the phenomena of subpial and tractal aggregation, and perineuronal and perivascular satellitosis (tumors cells distant from the main tumors mass surrounding and aggregating along with the healthy structures of the brain parenchyma) [12] These phenomena explain the diffuse growth of glial tumors and explain why they present clinically at a late stage, the reason being the long-time period needed for the neurons and other structures to be destroyed by the neoplastic cells, unlike in metastatic disease. Observed on biopsy material, these phenomena of invasive but non-destructive growth are collectively known as secondary Scherer figures, not as pathognomonic as the primary features for GBM but indicative of glial tumors and not metastatic (Figure 2) [12] All these observations by Scherer are key points in the diagnostic process and clinical management of patients with glial tumors, yet they are often attributed to other authors. Tumor cell remnants, such as exosomes in GBM, are found in the systemic circulation, and their quantity is comparable to exosomes found in other cancer types, further supporting the theory that GBM has access to metastatic pathways; its unique pattern of growth inhibits the evolution of metastatic disease [18,19]
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