ArticleThe American journal of pathology2016
Evidence Supporting a Lymphatic Endothelium Origin for Angiomyolipoma, a TSC2(-) Tumor Related to Lymphangioleiomyomatosis.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
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- Prdx5 in the Regulation of Tuberous Sclerosis Complex Mutation-Induced Signaling Mechanisms.Cells · 2023Article
- ETV2 regulates PARP-1 binding protein to induce ER stress-mediated death in tuberin-deficient cells.Life science alliance · 2022Article
- A Mixed Blood-Lymphatic Endothelial Cell Phenotype in Lymphangioleiomyomatosis and Idiopathic Pulmonary Fibrosis but Not in Kaposi's Sarcoma or Tuberous Sclerosis Complex.American journal of respiratory cell and molecular biology · 2022Article
- Evidence for shared genetic risk factors between lymphangioleiomyomatosis and pulmonary function.ERJ open research · 2022Article
- Renal cystic disease in tuberous sclerosis complex.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Activated p53 in the anti-apoptotic milieu of tuberous sclerosis gene mutation induced diseases leads to cell death if thioredoxin reductase is inhibited.Apoptosis : an international journal on programmed cell death · 2021Article
- Insight into norcantharidin, a small-molecule synthetic compound with potential multi-target anticancer activities.Chinese medicine · 2020Review
- Renal Manifestations of Tuberous Sclerosis Complex.Journal of kidney cancer and VHL · 2020Review
- Article
- The Lymphangioleiomyomatosis Lung Cell and Its Human Cell Models.American journal of respiratory cell and molecular biology · 2018Review
- Article
- Evidence of renal angiomyolipoma neoplastic stem cells arising from renal epithelial cells.Nature communications · 2017Article
- New developments in the genetics and pathogenesis of tumours in tuberous sclerosis complex.The Journal of pathology · 2017Review
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7 authors at 2 institutions in 1 country.
Funding
Abstract
Angiomyolipoma (AML) is a tumor closely related to lymphangioleiomyomatosis (LAM). Both entities are characterized by the proliferation of smooth muscle actin and melanocytic glycoprotein 100 (recognized by antibody HMB-45)-positive spindle-shaped and epithelioid cells. AML and LAM are etiologically linked to mutations in the tsc2 and tsc1 genes in the case of LAM. These genes encode the proteins tuberous sclerosis complex (TSC)-1 and TSC2, which are directly involved in suppressing the mechanistic target of rapamycin cell growth signaling pathway. Although significant progress has been made in characterizing and pharmacologically slowing the progression of AML and LAM with rapamycin, our understanding of their pathogenesis lacks an identified cell of origin. We used an AML-derived cell line to determine whether TSC2 restitution brings about the cell type from which AML arises. We found that AML cells express lymphatic endothelial cell markers consistent with lymphatic endothelial cell precursors in vivo and in vitro. Moreover, on TSC2 correction, AML cells mature into adult lymphatic endothelial cells and have functional attributes characteristic of this cell lineage, suggesting a lymphatic endothelial cell of origin for AML. These effects are dependent on TSC2-mediated mechanistic target of rapamycin inactivation. Finally, we demonstrate the in vitro effectiveness of norcantharidin, a lymphangiogenesis inhibitor, as a potential co-adjuvant therapy in the treatment of AML.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.