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Research Article
Frequent Loss of Chromosome 4q, Homozygous FSTL5 Deletion at the 4q32.2 in Gastric Adenocarcinoma

Jiun Kang

International Journal of Cancer Research, 2018, 14(1), 13-20.


Background and Objective: Chromosomal alterations are a predominant genetic force that contributes to the development of gastric adenocarcinoma (GC). This study was performed to identify critical genetic landmarks that may be important mediators in the formation or progression of GC. Materials and Methods: The whole genome-wide copy numbers were screened in 25 patients with GC using array comparative genomic hybridization (CGH) consisting of 4,030 bacterial artificial chromosome clones. Categorical analyses were applied to analyze whether chromosomal changes were related to clinico-pathological characteristics. Results: The most notable finding was the high frequency of copy number losses and hemizygous deletions on the long arm of chromosome 4, which was detected in 96.0 and 24.0% of the cases, respectively. More strikingly, three homozygous deletions in the 4q27-q34.2 regions were detected in 12.0% of GCs. Among the homozygous deleted regions, it was identified a potential tumor suppressor gene of FSTL5 at the 4q32.2 region (14.3%), which has not been previously implicated to play a pathogenic role in GC. Furthermore, it was identified possible target genes that have not been previously described in GC, such as the losses of LPHN3 on 4q13.1, MGC35043 on 4q21.21, DKFZP434G072, RG9MTD2 and MTP on 4q23,Tenr and IL2 on 4q32.2, FSTL5 on 4q32.2 and FAT on 4q35.2. Conclusion: This study confirmed and expanded upon a previous finding that 4q genetic alterations accumulate during the multistage pathogenesis of GC. The newly identified candidate genes at the 4q chromosomal sites could provide important clues with regard to the genetic mechanisms of initiation and progression as well as provide novel targets for therapeutic intervention in GC.

ASCI-ID: 36-314

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