ArticleLymphatic research and biology2010
mTOR activation, lymphangiogenesis, and estrogen-mediated cell survival: the "perfect storm" of pro-metastatic factors in LAM pathogenesis.
Article in Lymphatic research and biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- A Systematic Review of Lymphangioleiomyomatosis on Diagnosis and Molecular Mechanism.BioMed research international · 2021Pooled it
- Non-pharmacological therapies for patients with lymphangioleiomyomatosis: a systematic review and meta-analysis.Frontiers in rehabilitation sciences · 2026Review
- Increased malignancy risk in patients with lymphangioleiomyomatosis: findings from a Chinese cohort.Orphanet journal of rare diseases · 2025Article
- Targeting fibroblast-endothelial cell interactions in LAM pathogenesis using 3D spheroid models and spatial transcriptomics.JCI insight · 2025Article
- Inhibitory effects of the combination of rapamycin with gemcitabine plus paclitaxel on the growth of pancreatic cancer tumors.Human cell · 2025Article
- Targeting Fibroblast-Endothelial Interactions in LAM Pathogenesis: 3D Spheroid and Spatial Transcriptomic Insights for Therapeutic Innovation.bioRxiv : the preprint server for biology · 2024Article
- Article
- Lymphangioleiomyomatosis and pregnancy: a mini-review.Archives of gynecology and obstetrics · 2024Review
- Upregulation of acid ceramidase contributes to tumor progression in tuberous sclerosis complex.JCI insight · 2023Article
- Mechanistic Target of Rapamycin (mTOR) Inhibitors.Handbook of experimental pharmacology · 2022Article
- Article
- Inhibition of the mechanistic target of rapamycin induces cell survival via MAPK in tuberous sclerosis complex.Orphanet journal of rare diseases · 2020Article
- Recent advances in human stem cell-based modeling of Tuberous Sclerosis Complex.Molecular autism · 2020Review
- Possible Novel Therapeutic Targets in Lymphangioleiomyomatosis Treatment.Frontiers in medicine · 2020Review
- An unusual case of uterine PEComa presenting with disseminated intravascular coagulation.Gynecologic oncology reports · 2019Article
- The Genetics of Pneumothorax.American journal of respiratory and critical care medicine · 2019Review
- Rapalog resistance is associated with mesenchymal-type changes in Tsc2-null cells.Scientific reports · 2019Article
- The Lymphangioleiomyomatosis Lung Cell and Its Human Cell Models.American journal of respiratory cell and molecular biology · 2018Review
- Immunohistological features related to functional impairment in lymphangioleiomyomatosis.Respiratory research · 2018Article
- Downregulation of PERK activity and eIF2α serine 51 phosphorylation by mTOR complex 1 elicits pro-oxidant and pro-death effects in tuberous sclerosis-deficient cells.Cell death & disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Research interest in lymphangioleiomyomatosis (LAM) has grown dramatically in the past decade, particularly among cancer biologists. There are at least two reasons for this: first, the discovery in the year 2000 that LAM cells carry TSC2 gene mutations, linking LAM with cellular pathways including the PI3K/Akt/mTOR axis, and allowing the Tuberous Sclerosis Complex (TSC)-regulated pathways that are believed to underlie LAM pathogenesis to be studied in cells, yeast, Drosophila, and mice. A second reason for the rising interest in LAM is the discovery that LAM cells can travel to the lung, including repopulating a donor lung after lung transplantation, despite the fact that LAM cells are histologically benign. This "benign metastasis" underpinning suggests that elucidating LAM pathogenesis will unlock a set of fundamental mechanisms that underlie metastatic potential in the context of a cell that has not yet undergone malignant transformation. Here, we will outline the data supporting the metastatic model of LAM, consider the biochemical and cellular mechanisms that may enable LAM cells to metastasize, including both cell autonomous and non-cell autonomous factors, and highlight a mouse model in which estrogen promotes the metastasis and survival of TSC2-deficient cells in a MEK-dependent manner. We propose a multistep model of LAM cell metastasis that highlights multiple opportunities for therapeutic intervention. Taken together, the metastatic behavior of LAM cells and the involvement of tumor-related signaling pathways lead to optimism that cancer-related paradigms for diagnosis, staging, and therapy will lead to therapeutic breakthroughs for women living with LAM.
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Registered trials
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 OpenQuestion graph.