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Review
. 2001 Sep;159(3):779-86.
doi: 10.1016/S0002-9440(10)61750-6.

Glioma classification: a molecular reappraisal

D N Louis  1 , E C Holland, J G Cairncross
Affiliations
Review

Glioma classification: a molecular reappraisal

D N Louis et al. Am J Pathol. 2001 Sep.
No abstract available

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Figures

Figure 1.
Figure 1.
Limitations of the current World Health Organization classification of diffuse gliomas for estimating prognosis and guiding therapy. Left: World Health Organization grades are indicated. Under each tumor type are the range of typical survival (in years) and frequency of response to therapy (in percentages). ?, Percentages for World Health Organization grade II lesions are uncertain; radiographic responses tend to be modest, but may not be indicative of biological response.
Figure 2.
Figure 2.
Anaplastic oligodendroglioma: an example of molecular approaches to glioma classification (adapted from Ino et al 4 ). Four genetic subgroups of World Health Organization grade III anaplastic oligodendrogliomas have differences in response frequency, duration of response, and survival. *, Group 2 patients have 1p loss, but either do not have 19q loss or have other genetic alterations such as TP53 mutation, PTEN mutation, 10q loss, EGFR amplification, or CDKN2A deletion. **, Group 4 patients often had PTEN mutation, 10q loss, EGFR amplification, CDKN2A deletion, and ring enhancement. dx, Diagnosis; PCV, chemotherapy (see text); RT, radiation therapy; novel tx, novel therapy.
Figure 3.
Figure 3.
The need for novel endpoints. Currently, survival provides the major endpoint for guiding subsequent changes in histological classification (see text). In the future, early alternative endpoints will be necessary to provide immediate therapeutic guidance (curved dashed arrows) in the setting of nonresponse to a particular therapy and for eventually refining molecular classifications. In addition, novel long-term outcome measures will be needed to further refine classification and thus indirectly guide subsequent therapy (curved solid arrows). The eventual goal is for molecular subtyping to determine different specific therapies.
Figure 4.
Figure 4.
Generation of glioma subtypes in mice. Schematic diagram illustrates signaling pathways, cells of origin, and histological diagnoses of genetically engineered murine (GEM) gliomas. The similarities with human glioma histology and genetics suggest that histological and molecular signaling classification approaches could be related and complementary.
Figure 5.
Figure 5.
Future classifications. These will be based on input from traditional as well as molecular analyses, and will involve both tissue-based and imaging modalities. The classification will have to incorporate new frameworks based on biological advances. Most significantly, the classification will have to correlate closely with clinically relevant endpoints and, as new outcome measures and effective therapies are developed, will have to modified by such correlations.
See this image and copyright information in PMC

References

    1. Bailey P, Cushing H: A Classification of the Tumors of the Glioma Group on a Histogenetic Basis with a Correlated Study of Prognosis. 1928. JB Lippincott, Philadelphia
    1. Kleihues P, Cavenee WK (Eds): World Health Organization Classification of Tumours of the Nervous System. Lyon, WHO/IARC, 2000
    1. Coons SW, Johnson PC, Scheithauer BW, Yates AJ, Pearl DK: Improving diagnostic accuracy and interobserver concordance in the classification and grading of primary gliomas. Cancer 1997, 79:1381-1393 - PubMed
    1. Ino Y, Betensky RA, Zlatescu MC, Sasaki H, Macdonald DR, Stemmer-Rachamimov AO, Ramsay DA, Cairncross JG, Louis DN: Molecular subtypes of anaplastic oligodendroglioma: implications for patient management at diagnosis. Clin Cancer Res 2001, 7:839-845 - PubMed
    1. Ino Y, Zlatescu MC, Sasaki H, Macdonald DR, Stemmer-Rachamimov AO, Jhung S, Ramsay DA, von Deimling A, Louis DN, Cairncross JG: Long patient survival and therapeutic responses in histologically disparate high grade gliomas with chromosome 1p loss. J Neurosurg 2000, 92:983-990 - PubMed

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