Statistical dissection of cytogenetic patterns in lung cancer reveals multiple modes of karyotypic evolution independent of histological classification.

Lung carcinomas are cytogenetically highly complex. In spite of this, patterns of recurrent chromosome aberrations have emerged. Apart from the frequent loss of 3p, losses of 4q, 5q, 8p, 9p, 10q, 13q, and 17p are common and gains often include 1q, 3q, 5p, and 8q.

Dissecting karyotypic patterns in renal cell carcinoma: an analysis of the accumulated cytogenetic data.

Renal cell carcinoma (RCC) is one of the most frequent malignancies in Western societies. The most common subtypes are conventional (clear-cell) and papillary carcinomas, which account for about 75 and 10% of cases, respectively. Cytogenetically, conventional RCC is the best-studied subtype and is characterized by chromosomal losses: loss of the short arm of chromosome 3 being the most common.

A model for karyotypic evolution in testicular germ cell tumors.

Testicular germ cell tumor karyotypes are characterized by near-triploidy, with chromosome numbers ranging from 50 to 70, and by the frequent appearance of i(12p). The high chromosome number has been attributed to the formation of tetraploid carcinoma in situ cells followed by chromosomal losses that ultimately lead to tumor forms that are more advanced. In the present investigation, we show by analysis of the accumulated cytogenetic data on testicular germ cell tumors and computer simulations that two distinct processes are operating in the karyotypic evolution of these tumors.

Wilms tumors develop through two distinct karyotypic pathways.

Wilms tumor is an embryonic neoplasm characterized by a large variation in histologic patterns. Cytogenetic investigations have identified nonrandom chromosomal changes characteristic for this tumor type, of which numerical changes, mostly trisomies for chromosomes 7, 8, and 12, are particularly frequent. Despite the abundance of cytogenetic information, with more than 350 published karyotypes, very little is known about the mode of karyotypic evolution.

Statistical analyses of karyotypic complexity in head and neck squamous cell carcinoma.

More than 250 head and neck squamous cell carcinomas (HNSCCs) with clonal chromosomal abnormalities have been reported. Even though the pattern of aberrations is nonrandom, no specific primary or secondary karyotypic abnormalities have been identified. One explanation for the still-rudimentary understanding of the cytogenetic evolution in HNSCC could be the pronounced karyotypic complexity seen in these tumors.

Dissecting karyotypic patterns in malignant melanomas: temporal clustering of losses and gains in melanoma karyotypic evolution.

Malignant melanomas can be divided into two major subtypes, involving either the skin or eye melanomas. Both tumor forms exhibit highly complex karyotypes with nonrandom recurrent chromosomal imbalances. Loss of chromosome 3, the short arm of chromosome 1, and gain of 8q have been suggested to be associated with eye melanomas, whereas gain of 6p and loss of 6q have been more often seen in skin melanomas.

Ovarian carcinoma develops through multiple modes of chromosomal evolution.

Ovarian carcinoma has the highest mortality of all of the gynecologic cancers. The chromosomal changes in this tumor type are highly complex, and the karyotypes typically show severe aneuploidy. Despite the abundance of cytogenetic information, with approximately 400 published karyotypes, very little is known about the mode of karyotypic evolution and the possible presence of cytogenetic pathways related to tumor development.

Dissecting karyotypic patterns in colorectal tumors: two distinct but overlapping pathways in the adenoma-carcinoma transition.

More than 500 colorectal tumors with clonal chromosomal abnormalities have been reported. Although the pattern of aberrations is nonrandom, no specific primary or secondary karyotypic abnormality has been identified. Also, the chronological order in which the aberrations appear during disease progression is not well known.

Multivariate analysis of chromosomal imbalances in breast cancer delineates cytogenetic pathways and reveals complex relationships among imbalances.

More than 550 breast adenocarcinomas with clonal chromosomal abnormalities have been reported. Although the aberration pattern is clearly nonrandom, no specific primary or secondary karyotypic abnormality has been identified, and furthermore the chronological order in which the aberrations appear during disease progression is not well known. The high degree of karyotypic complexity in epithelial tumors such as breast cancer is one reason why our understanding of the sequential order of cytogenetic evolution is unclear.