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Updated: Jun 20, 2025
A Patient-Derived Xenograft Model for Venous Malformation
Published on: June 15, 2020
A Xenograft Model of Kaposiform Hemangioendothelioma in Nude Mice Recapitulates Kasabach-Merritt Phenomenon
Qian Wang1, Wei-Wei Qiu2, Ming-Yu Li3
1Department of Plastic Surgery, Nanjing Jinling Hospital, The First School of Clinical Medicine, Southern Medical University, Nanjing, Jiangsu, China.
Background:
Kasabach-Merritt phenomenon (KMP) is characterized by profound thrombocytopenia and consumptive coagulopathy associated with vascular tumors, such as Kaposiform hemangioendothelioma (KHE). The pathogenesis of KMP remains unclear and its treatment is challenging. In this study, we tried to establish an animal model of KMP, which may facilitate the research on the etiology and new treatment.
Methods:
A fresh sample of KHE from a one-month-old female infant with KMP was scissored into pieces and transplanted subcutaneously into the back of the nude mice. Blood routine examination was performed before the transplantation and 2, 4, 8, 12, and 16 weeks after the transplantation. Transplanted tumors were harvested 2, 4, 8, 12, and 16 weeks after the transplantation. H-E staining, immunohistochemistry staining of cluster of differentiation 31 (CD31) and alpha-smooth muscle actin (α-SMA), and ultrastructural observation were performed on the plugs.
Results:
Blood test showed a significant decrease in the number of platelets 2 weeks after transplantation. The number of platelets showed an overall trend of recovery from 2 weeks despite a slight decrease at 12 weeks after transplantation. There was no significant difference in the platelet count at 16 weeks after transplantation compared with the original state. H-E staining showed abundant irregular blood sinuses in the transplanted tumors with plenty of blood cells 2 weeks after the transplantation. 4, 8, and 12 weeks after transplantation, the density of blood sinuses decreased progressively. 16 weeks after transplantation, the plugs involuted into fibrous tissue. Immunohistochemistry staining showed the positive expression of CD31 in the endothelial cells and α-SMA in the perivascular cells. Ultrastructural observation also showed the features of KHE and progressive evolution of the tumors.
Conclusions:
We successfully established an experimental model of KMP by the xenograft of KHE in nude mice, which manifested profound thrombocytopenia and typical pathological structure.
Insights
Researchers developed a Kasabach-Merritt phenomenon (KMP) animal model using Kaposiform hemangioendothelioma (KHE) xenografts in mice. This model shows thrombocytopenia and characteristic tumor pathology, aiding KMP research.
Area of Science:
- Vascular biology
- Pediatric oncology
- Animal modeling
Background:
- Kasabach-Merritt phenomenon (KMP) involves severe thrombocytopenia and coagulopathy linked to vascular tumors like Kaposiform hemangioendothelioma (KHE).
- The exact causes and effective treatments for KMP are still not fully understood.
- Establishing a reliable animal model is crucial for advancing KMP research.
Purpose of the Study:
- To create a reproducible animal model of Kasabach-Merritt phenomenon (KMP).
- To utilize a Kaposiform hemangioendothelioma (KHE) xenograft in nude mice for KMP modeling.
- To investigate the etiological factors and potential therapeutic strategies for KMP.
Main Methods:
- Xenotransplantation of human KHE tissue into nude mice.
- Serial blood tests to monitor platelet counts post-transplantation.
- Tumor tissue analysis using H-E staining, CD31, and α-SMA immunohistochemistry, and ultrastructural observation.
Main Results:
- Successful induction of profound thrombocytopenia within 2 weeks of KHE xenograft.
- Observed progressive decrease in blood sinusoids and involution into fibrous tissue by 16 weeks.
- Confirmed characteristic KHE pathology and tumor evolution in the established model.
Conclusions:
- A novel experimental model for Kasabach-Merritt phenomenon (KMP) was successfully established using KHE xenografts in nude mice.
- The model accurately replicates the profound thrombocytopenia and pathological features of KMP.
- This xenograft model provides a valuable platform for future KMP research into its pathogenesis and treatment.
