| After several decades of rapid advances, biomedical research has generated a rich and complex body of data and knowledge. The answer of a question often lies in this information. With the increase of information, the answer can only be found with the favor of computational means. Explorating the pathogenesis of cancer is also being pushed forward by cooperation of biological experiments and computational means.Several lines of evidence indicate that tumorigenesis in humans is a multistep process and that these steps reflect genetic alterations that drive the progressive transformation of normal human cells into highly malignant derivatives; while six essential genetic alterations should be occurred: self-sufficiency in growth signals, insensitivity to growth-inhibitory (antigrowth) signals, evasion of programmed cell death (apoptosis), limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Moreover, each step is completed through different pathway with various mechanisms, so the progression of cancer is a process of multi-steps, multi-pathways, and multi-mechanisms. The pathogenesis of cancer also lies in large body of data and knowledge.Pathology of cancer indicates that progression of nasopharyngeal carcinoma (NPC) is a process of simple hyperplasia/metaplasia, atypical hyperplasia/metaplasia, in situ cancer, small invasive cancer, and metastatic cancer. But to explore its mechanism is hindered by the absence of human NPC biopsy specimen of each stage and appropriate NPC animal model.Kaitai Yao has suggested the pathogenesis of NPC. With the advance of biotechnology, a large body of knowledge and data of NPC have been generated. The more comprehensive and complex answer of the pathogenesis of NPC may lie in these informations. This study only mined the data of comparative genomic hybridization (CGH), interaction between EBV and human cells, and tumor specific transcription regulation. More information such as microarray, single nucleotide polymorphism (SNP), abnormal signal transduction pathways in NPC cells et al. have been remained for further study.CGH provides a genome-wide survey of chromosomal regions in which tumor cells and normal/control cells have significantly dissimilar amounts of DNA. Copy number aberrations are thought to be important indicators of cancer-related genes in the region gain could indicate a hyperactive oncogene, while a loss could indicate a tumor suppressor gene whose activity level is pathologically low.During the progression of cancer, the abnormality of various chromosomes may co-occur in groups of patients, and in some orders as suggestion by Vogelstein's linear path model. While in late stage cancer, the abnormality of chromosomes may occur extensively, seemingly at random and independently with progression of cancer because of genome instability. For these reasons, Desper et al. used the well-known method of Brodeur et al. to selected abnormality of chromosomes that associated with progression of cancer, and developed two methods- distance-based trees and branching trees -to find these co-occurrence relationships and the orders of occurrences.But in their data analysis, they used only chromosome arms, because when two tumors have copy number aberrations spanning approximately the same bands, they found it impossible to decide whether these reflect the same genetic change or not. It causes large subsequent experiment effort. So, we have used overlap regions to advance their methods to construct chromosome band tree models for pathogenesis of NPC from 164 comparative genomic hybridization (CGH) data on NPC. The result indicated that the abnormalitiesof chromosomes that related with the progression of NPC were losses of 3p26-13 (48.9%), llq22-25 (38.1%), 16ql2-24 (38.1%), 14q24-32 (32.4%), 13q21-32 (22.3%), and 9p23-21(21.6%), and gains of 12pl2 (46%), 12ql3-15 (43.9%), lq22-32 (33.1%), 3ql3.1-26.2 (30.2%), and 8q22.1-24.2 (27.3%). NPC can be classified into three groups. The first group is marked by +3ql3.1-26.2. Whi...
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