In recent years, there have been great advances in our understanding of the
genetic events and the molecular biology of human brain gliomas. Cytogenet
ic information has suggested that a pattern of non-random abnormalities inv
olving numerical deviations such as the gain, partial deletion, or total lo
ss of chromosomes as well as translocations and structural rearrangements o
f certain chromosome lesions are characteristic features for some tumors. I
n addition, the somatic activation of cellular oncogenes and inactivation o
f tumor suppressor genes represent important genetic alterations leading to
progressive disorder of normal cellular growth control mechanisms. This re
view describes the abnormal chromosomal and molecular abnormalities that oc
cur during formation of brain tumors of astrocytic origin, particularly fib
rillary astrocytic neoplasms. The most frequent genetic alterations include
inactivation of the p53, p16, Rb and PTEN genes, and overexpression of the
CDK4, EGFR and VEGF genes. Other less well defined abnormalities include a
berrations in chromosomes 1, 9, 10, 11, 19 and 22.