The global gene expression profiles for 67 human lung tumors representing 56 patients were examined by using 24,000-element cDNA microarrays. Subdivision of the tumors based on gene expression patterns faithfully recapitulated morphological classification of the tumors into squamous, large cell, small cell, and adenocarcinoma. The gene expression patterns made possible the subclassification of adenocarcinoma into subgroups that correlated with the degree of tumor differentiation as well as patient survival. Gene expression analysis thus promises to extend and refine standard pathologic analysis

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Pituitary adenomas most commonly are identified as small, incidental microadenomas. They however may progress to macroadenoma forming intra and later suprasellar tumors which in about 1/3 of cases invade surrounding structures at the time of diagnosis. Mechanism of pituitary tumorigenesis remains still elusive. Because the value of karyotyping is limited by the technical problems related to cytogenetic methods, we studied the spectrum of chromosomal imbalances associated with pituitary adenoma using comparative genomic hybridization (CGH). Copy number aberrations on all 22 autosomes were evaluated by CGH using advanced computer software. In total, fifteen patients were included in the study of 9 non-invasive, 4 invasive and two recurrent adenomas. The mean age of the patients were 48 years ranging from 36 to 68 years. Five tumors showed hormonal activity. The histogram of all 15 cases representing the DNA imbalances as an incidence curve along each chromosome showed losses particularly for chromosomes 1p, 2q, 4, 5, 6, 11q, 12q, 13q and 18q as well as overrepresentation on 9q, 16p, 17p, 19, 20q. Functioning adenomas carried more imbalances than non-functioning, specifically deletions on chromosome 4 and 18q as well as overrepresentations of chromosomes 17 and 19. Invasive adenomas carried more overrepresentations at 1p34 than non-invasive tumors. Recurrent adenomas harbored more alterations than primary tumors, particularly DNA gains. The primary data is accessible at our CGH online tumor database at http://amba.charite.de/cgh. Reviewing the existing literature on the genetics of pituitary adenoma and discussing our results in this context, we hope that our study will contribute to the knowledge of this neoplasm.

Object The authors investigated the spectrum of chromosomal imbalances of pilocytic astrocytoma by using comparative genomic hybridization (CGH). Methods Tumor DNA was extracted from surgically obtained samples of 18 pilocytic astrocytomas that were examined for the presence of neoplastic tissue on frozen sections. Comparative genomic hybridization was performed using standard procedures, and digital image analysis was conducted using out by custom-made software. The chromosomal alterations were determined by a statistical procedure in which Student's t-test (99% confidence interval) was used. Details on CGH analysis and individual ratio profiles are available at http://amba.charite.de/cgh/. Conclusions The results suggests the presence of two distinct genetic subgroups of pilocytic astrocytoma, with imbalances of chromosome 19 being the major change for differentiation. In the first group (10 samples), deletions on chromosome 19 were shown as well as multiple gains mainly on chromosomes 5 and 6q but also on chromosomes 4, 7, 8, 10, and 11. The second group (eight samples) was characterized by overrepresentation on chromosomes 19p and 22q, which were associated with deletions on 4q, 5q, 6q, 9p, 13q, and 18q. To understand the diverse biological and clinical behavior exhibited by this tumor type, it is important that pilocytic astrocytomas be classified into distinct subgroups according to their genetic makeup.