AI Article Synopsis
- Kaposiform hemangioendotheliomas (KHEs) are aggressive vascular tumors that can have severe outcomes and may not respond well to traditional therapies like surgery.
- Sirolimus, a drug that inhibits a specific cellular pathway, has shown promise in treating KHEs by preventing platelet activation and inflammation, inhibiting blood vessel formation, and reducing fibrosis.
- The text also explores reasons why some patients may resist sirolimus treatment and discusses recent discoveries of genetic mutations in KHE lesions that could lead to new treatment strategies.
Article Abstract
Kaposiform hemangioendotheliomas (KHEs) are vascular tumors that are considered borderline or locally aggressive and may lead to lethal outcomes. Traditional therapies, such as surgery and embolization, may be insufficient or technically impossible for patients with KHE. Sirolimus (or rapamycin), a specific inhibitor of mechanistic target of rapamycin, has recently been demonstrated to be very useful in the treatment of KHEs. Here, we highlight recent substantial progress regarding the effects of sirolimus on KHEs and discuss the potential mechanisms of action of sirolimus in treating this disease. The prevention of platelet activation and inflammation, along with antiangiogenic effects, the inhibition of lymphangiogenesis, the attenuation of fibrosis, or a combination of all these effects, may be responsible for the therapeutic effects of sirolimus. In addition, the mechanism of sirolimus resistance in some KHE patients is discussed. Finally, we review the somatic mutations that have recently been identified in KEH lesions, and discuss the potential of novel therapeutic targets based on these further understandings of the cellular and molecular pathogenesis of KHE.
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| http://dx.doi.org/10.1002/ijc.35207 | DOI Listing |
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