期刊
PATHOLOGY RESEARCH AND PRACTICE
卷 199, 期 6, 页码 437-444出版社
URBAN & FISCHER VERLAG
DOI: 10.1078/0344-0338-00443
关键词
dedifferentiated chondrosarcoma; microdissection; DNA methylation; Rb-LOH; p53-LOH; p53 mutation
类别
In this case of a dedifferentiated chondrosarcoma, we searched for genetic or epigenetic alterations in both components of the tumor, the low grade chondroblastic component, and the high grade osteosacomatous component. To date, only little is known about aberrant patterns of DNA methylation in chondrosarcomas. Microdissection was used as a valuable method for clearly separating the tissues. We examined CpG island methylation of 8 tumor suppressor genes and candidate tumor suppressor genes, which are involved in different pathways: cell cycle (p21(WAF1), p16(INK4), p14(ARF)), apoptosis (DAPK, FHIT), DNA repair (hMLH1), and cell adherence (E-Cadherin). We found p16(INK4) and E-cadherin promotor methylation in the low grade chondroid compartment of the dedifferentiated chondrosarcoma. P16(INK4), FHIT, and E-cadherin were methylated in the highly malignant osteosarcomatous compartment of the tumor. Earlier investigations of this chondrosarcoma showed p53 mutation and p53-LOH in the anaplastic component. As shown in this case, it was accompanied by Rb-LOH. Early methylation of p16(INK4) and E-cadherin in the chondroid compartment could point to the monoclonal origin of demonstrated dedifferentiated chondrosarcoma. Further alterations, as shown in p53, Rb and FHIT, are responsible for the switch to a high grade anaplastic sarcoma.
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