Molecular pathology of uterine sarcoma
Recent research has improved our understanding of how changes in certain molecules can cause normal cells to become cancerous. For several years we have known that mutations (damage or defects) to DNA can alter important genes that regulate cell growth. If these genes are damaged, excess growth may result in cancer formation. Analysis of DNA from uterine sarcomas has revealed several changes in the genes that control cell growth.
Each human cell contains 23 pairs of chromosomes. Many endometrial stromal sarcomas have abnormalities involving chromosomes 6, 7, or 17. Often, there is an abnormal “swapping” of chromosomal material (DNA) between chromosomes 7 and 17. Part of chromosome 7 goes to 17 and part of 17 goes to 7. This is known as a translocation. The swapping of DNA between the chromosomes leads to the formation of a new gene, called JAZF1/JJAZ1, which may cause the cells to become malignant.
Scientists expect that these discoveries such as this will eventually lead to new strategies for detection, prevention, and treatment.
Clinical trials
New drugs, as well as new ways to give standard drugs are being tested. One drug under study, trabectedin (Yondelis®) has been approved to treat sarcoma in Europe, but is still under study in the United States. Another drug, temozolomide, which is approved to treat brain tumors, also seems to help patients with sarcoma. Adjuvant radiation and chemotherapy continue to be evaluated for treatment of uterine sarcomas. New compounds are also being evaluated in soft-tissue sarcomas. Some of these compounds act differently from traditional chemotherapy drugs and are called targeted therapies.
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