[Analysis of 13q14 chromosomal instability in soft tissue tumors by fluorescence in-situ hybridization]
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Published on: April 15, 2022
Wei-xun Zhou1, Xuan Zeng, Tong-hua Liu
1Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Objective:
To investigate the genetic status of 13q and its role in the oncogenesis and progress of soft tissue tumors.
Methods:
Forty-one soft tissue tumors, including 9 benign tumors, 9 tumors of malignant potential and 23 sarcomas, were studied by fluorescence in-situ hybridization (FISH) using dual color probes. The probes were generated from BAC clones RP11-685I15, RP11-352N7 and RP11-505F3, corresponding to Rb, RFP2, KCNRG and KLF5 genes respectively.
Results:
Loss of heterozygosity (LOH) of RP11-685I15 were found in 8/41 cases, LOH of RP11-352N7 was seen in 4/41 cases and LOH of RP11-505F3 was present in 3/41 cases. LOH of all 3 loci were detected in 2 cases. LOH of RP11-61K9, an internal control locus, was detected in 2 cases. One case of malignant peripheral nerve sheath tumor showed amplification at all 3 loci. Amplification of RP11-505F3 was seen in another 2 cases.
Conclusions:
A significant percentage of soft tissue tumors exhibited chromosomal instability, reflected by an increase of LOH at tumor-suppressing gene loci. The incidence of 13q abnormality was different in various types of soft tissue tumors, indicating that alterations of Rb, RFP2, KCNRG and KLF5 tumor suppressing genes may play diverse roles in different types of soft tissue tumor.
