Characterizing LAM With 11C-Choline PET/CT

Status Not yet recruiting

Clinical Trial 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.

Clinical Trial 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. ;

Study Design

Related Conditions & MeSH terms

Lymphangioleiomyomatosis

Clinical Trial Details

NCT number	NCT05087134
Study type	Interventional
Source	Peking Union Medical College Hospital
Contact	Guozhu Hou, MD
Phone	15611145656
Email	15611145656@163.com
Status	Not yet recruiting
Phase	Early Phase 1
Start date	November 2021
Completion date	September 2023

View Details

See also
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