BMC Cancer 2007, 7:226 http://www.biomedcentral.com/1471-2407/7/226 resolution of this technique is limited to several mega- bases [9]. Also, the involvement of presumptive target genes can only be inferred from the positional compari- son of the genomic ratio profiles to the underlying chro- mosomal matrix. However, recent molecular-cytogenetic screening techniques (array-or matrix-CGH [10-12]) have the potential for direct identification of oncogenetic target genes. Based on the comparably easy access to dividing tumor cells, and the early reognition of specific cytogenetic aber- rations in some entities [13-15], metaphase analysis has been especially successfull in acute leukemias (review e.g. in [16]) and other hematologic malignancies. This has been reflected in the content of the Mitelman Database of Chromosome Aberrations in Cancer [17], in which hema- tologic neoplasias account for 73% of the database con- tent (approx. 40,000 cases), while epithelial tumors constitute only 12% (approx. 6,600 cases). In contrast, especially through it's application to the genomic screen- ing of frozen and archival tissue, the potential of CGH for the analysis of solid tumors had been recognized early on [7,18]. Some previous reviews of CGH data have either reported on specific types of aberrations [19,20] or were focused on solid tumors [21] or hematologic malignancies [22]. Struski et al. [23] provided a census of 11,984 solid tumors and hematologic malignancies analyzed by CGH. Since in the majority of publications data is presented as summary information (e.g. percentage of frequently involved chromosomal regions), these data reviews were able to develop a granular overview of the major regions frequently imbalanced in different tumor entities. Recently, Myllykangas et al. [24] provided an overview of genomic gain/amplification patterns, thereby omitting genomic losses. The study covered a large panel of human neoplasias, based on more than 4500 single cases. The authors were able to show a general relation genomic amplification patterns to general histo-pathological fea- tures, but could not prove overall relation of hot-spot sites to some known genetic features. The current study attempts a descriptive overview of genomic imbalances in epithelial neoplasias, based on published CGH data. Starting point for the data explora- tion is the Progenetix molecular-cytogenetic database [25- 27], which was initiated in December 2000 to collect all published cancer related CGH data and make it available for reference and research purposes. In contrast to other CGH data assembly attempts, but comparable to the Mitelman Database of Chromosome Aberrations in Can- cer, complete experimental results are collected on a case- by-case basis. Publications describing (molecular-) cytogenetic analyses of tumor samples and established cell lines are mined for case specific annotation of the experimental results. Focus is the exhaustive collection of chromosomal CGH data, with occasional inclusion of results from Metaphase banding, SKY and M-FISH data, as well as the recent addition of array or matrix CGH [10,28] results. The detailed discussion of identified or suspected target genes in the different chromosomal regions is not part of this study. However, some examples of genes with onco- gene and tumor suppressor function, respectively, will be mentioned. Methods As of 2006-12-04, 15429 cases from 609 publications had been included into the Progenetix database. Of those, 13818 had been analyzed by chromosomal CGH, either alone or in combination with Metaphase analyses tech- niques (355 cases). Minimum requirement for addition to the database was the availability of case specific data for the complete (molecular-) cytogenetic analysis result and clinical diagnosis. In most cases, locus information was available or could be inferred. Additional data (grading, staging/TNM, age, gender, follow-up parameters) was recorded if accessible. As main disease descriptors, diag- nosis and locus information was recoded to ICD-O-3 standard [29], based on the available information. For the purpose of this article, cases ascribed to epithelial origin (ICD-O 8010/x-8780/x) were selected for further analysis. This base dataset comprised 6899 cases, col- lected from 254 publications. The oldest included data was from 1994 [30], the latest from 2006 [31]. The largest number of cases was found in a report about skin neopla- sias (169 cases; [32]), followed by an extensive compari- son of BRCA1 and BRCA2 mutated breast carcinomas (132 cases; [33]). Only 8 articles were single case reports. To limit the bias in disease entities frequently analyzed in pre-malignant stages, only the 5918 clearly malignant epi- thelial neoplasias were selected (ICD-O-3 xxxx/2 and xxxx/3). For comparative purposes, common clinico- pathological disease categories were generated through a combination of diagnostic and locus codes (Table 1). Only the 22 entities with more than 50 cases were ana- lyzed separately, while 377 cases were not assigned to one of these entities. During database entry, CGH results were converted to standard "rev ish" ISCN 1995 format. This procedure con- tained software based syntax errors checking. The cor- rected "rev ish" data was processed by dedicated software [27] implemented in the Perl scripting language [34] using complex Regular Expression based parsing algo- rithms. Data matrices were generated, containing the Page 2 of 15 (page number not for citation purposes)