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Brief Title: Characterizing LAM With 11C-Choline PET/CT
Official Title: Characterizing Lymphangioleiomyomatosis (LAM) With 11C-Choline PET/CT
Study ID: NCT05087134
Brief Summary: It was reported that TSC2-deficient cells enhance phosphatidylcholine synthesis via the Kennedy pathway. 11C-Choline can reflect the metabolic process of choline in vivo by intravenous injection. The purpose of this study is the ability of 11C-Choline PET/CT to evaluate the baseline condition of LAM patients and the efficacy of rapamycin after treatment.
Detailed Description: Tuberous Sclerosis Complex (TSC) is an autosomal dominant disorder caused by inactivating mutations of the TSC1 or TSC2 gene, characterized by neurocognitive impairment and benign tumors of the brain, skin, heart, and kidneys. Lymphangioleiomyomatosis (LAM) is a diffuse proliferation of α-smooth muscle actin-positive cells associated with cystic destruction of the lung. LAM occurs almost exclusively in women, as a TSC manifestation or a sporadic disorder (TSC1/TSC2 somatic mutations). Biomarkers of whole-body tumor burden/activity and response to rapalogs or other therapies remain needed in TSC/LAM. It was reported that TSC2-deficient cells enhance phosphatidylcholine synthesis via the Kennedy pathway. 11C-Choline can reflect the metabolic process of choline in vivo by intravenous injection. The purpose of this study is the ability of 11C-Choline PET/CT to evaluate the baseline condition of LAM patients and the efficacy of rapamycin after treatment.
Minimum Age: 18 Years
Eligible Ages: ADULT, OLDER_ADULT
Sex: ALL
Healthy Volunteers: No
Peking union medical college hospital, Beijing, Dongcheng, China
Name: Fang Li, MD
Affiliation: Peking Union Medical College Hospital
Role: PRINCIPAL_INVESTIGATOR