CHAPTER 4 94 associated with resistance to platinum-based chemotherapy in high-risk EC 36. The number of CCCs in that study was limited underlining the need for studies investigating the association between L1CAM expression and therapy responsiveness within this particular subgroup. We have performed a comprehensive molecular, immunohistochemical and clinical analyses in a series of both pure and mixed uterine CCCs. However, there are some limitations. Due to the rare nature of these tumors, the number of patients within this series was limited. Also, because of the retrospective nature of the study and the use of FFPE tumor tissue, quality of the extracted DNA was variable, and DNA sequencing was unsuccessful in some cases. Of the 21 mixed uterine CCCs, it was possible to extract the DNA of both histological components separately in 10 cases. In the other cases, both histological components merged into one another and could not be isolated separately. Concluding, we observed different molecular background between pure and mixed uterine CCCs. TP53 mutations were found more frequently in patients with pure CCCs, and MSI was found more frequently in mixed uterine CCCs. An improved clinical outcome was found in patients with mixed uterine CCCs, compared to patients with pure uterine CCCs. Inferior outcome in pure CCCs may be explained by frequent TP53 mutations, whereas superior outcome in mixed CCCs may be explained by frequent occurrence of MSI. These results underline the relevance of both morphological and molecular evaluation, and may assist in tailoring treatment.
RkJQdWJsaXNoZXIy MTk4NDMw