Abstract
Tuberous sclerosis complex (TSC) is an autosomal dominant multisystemic disorder.1 Pathogenic variants in TSC1 or TSC2 gene lead to hyperactivation of the mammalian target of rapamycin (mTOR) signaling pathway, with a consequent deregulation of cell growth and the development of hamartomas. This tumors are benign, but they can cause life-threatening hemorrhage or organ failure in vital organs, such as the kidney, with angiomyolipoma (AML).1 AML found in 60% to 80% of patients with TSC are tumors composed of smooth muscle-like cells, adipocyte-like cells, and epithelioid cells.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
