Anaplastic Astrocytoma (AA)

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Anaplastic Astrocytoma (AA)
AAMRI.jpg
Axial FLAIR MRI of left insular AA
Tumor Class astrocytoma
Cell of origin Glial Cell
WHO Grade III
Survival 36-60 Months
Treatment Surgery,Radiation and Chemotherapy
Histologic Features
Radiographic Features

Contents

Definition

AA is an astrocytic neoplasm, typically affecting adults in middle age, biologically characterized by a marked proliferative potential. AA corresponds to WHO Grade III astrocytoma. They have an intrinsic tendency for malignant progression to GBM.

Epidemiology

Mean age of diagnosis is approximately 41 years. There is a male predominance (1.8:1).

Localization

AA has a preference for the cerebral hemispheres.

Clinical presentation

Patients may present with seizure or signs and symptoms attributable to mass effect or brain invasion.


Imaging

On MRI, AA is usually hypointense on T1-weighted imaging and hyperintense on FLAIR and T2-weighted imaging. These lesions usually demonstrate partial enhancement, with associated brain edema and evidence of mass effect. Notably, some 30% of non enhancing astrocytomas will have histologic features consistent with AA.

There is increased cellularity and cellular pleomorphism (variability in size and shape of the cells). You can see at least one mitotic figure. [1]

Macroscopy

AA is often difficult to distinguish grossly from Low Grade Glioma (LGG). The tumor-brain interface may be more readily discerned that the tumor-brain interface in LGG. As in LGG, there is usually enlargement or distortion, rather than overt destruction, of surrounding anatomical structures. Macrocysts are uncommon.

Histopathology

AA is composed of diffusely infiltrating neoplastic astrocytes with increased cellularity, nuclear atypia and marked mitotic activity. Microvascular proliferation and necrosis are absent. GFAP, vimentin, and S-100 are diffusely expressed.

Proliferation

Growth fraction, as determined by the Ki-67/MIB-1 index, is usually 5-10%.

Molecular genetics

TP53 mutations are common in these lesions. Deletion of p16(Ink4A) is found in about 30% of AA, as are alterations in RB (25%) and p19 (15%). CDK4 amplification occurs in about 10% of these lesions. LOH on chromosomes 10q, 19q, and 22q are also common. EGFR amplification is rare.

Prognosis

Mean survival time following surgical intervention is 3 years. Progression to GBM occurs with a mean interval time of 2 years. Young age, high Karnofsky score, and gross total tumor resection are considered predictive of increased survival.

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