<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(7)</volume><submitter>Ruiz de Garibay G</submitter><pubmed_abstract>Lymphangioleiomyomatosis (LAM) is a rare lung-metastasizing neoplasm caused by the proliferation of smooth muscle-like cells that commonly carry loss-of-function mutations in either the tuberous sclerosis complex 1 or 2 (TSC1 or TSC2) genes. While allosteric inhibition of the mechanistic target of rapamycin (mTOR) has shown substantial clinical benefit, complementary therapies are required to improve response and/or to treat specific patients. However, there is a lack of LAM biomarkers that could potentially be used to monitor the disease and to develop other targeted therapies. We hypothesized that the mediators of cancer metastasis to lung, particularly in breast cancer, also play a relevant role in LAM. Analyses across independent breast cancer datasets revealed associations between low</pubmed_abstract><journal>PloS one</journal><pagination>e0132546</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4500593</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Lymphangioleiomyomatosis Biomarkers Linked to Lung Metastatic Potential and Cell Stemness.</pubmed_title><pmcid>PMC4500593</pmcid><pubmed_authors>Pernas S</pubmed_authors><pubmed_authors>Llatjos R</pubmed_authors><pubmed_authors>Mateo F</pubmed_authors><pubmed_authors>Guma A</pubmed_authors><pubmed_authors>Esteller M</pubmed_authors><pubmed_authors>Varela M</pubmed_authors><pubmed_authors>Valenzuela C</pubmed_authors><pubmed_authors>Casanova A</pubmed_authors><pubmed_authors>Llorente A</pubmed_authors><pubmed_authors>Vidal A</pubmed_authors><pubmed_authors>Gil M</pubmed_authors><pubmed_authors>Aguilar H</pubmed_authors><pubmed_authors>Ruiz de Garibay G</pubmed_authors><pubmed_authors>Gomez-Baldo L</pubmed_authors><pubmed_authors>Molina-Molina M</pubmed_authors><pubmed_authors>Serra-Musach J</pubmed_authors><pubmed_authors>Climent F</pubmed_authors><pubmed_authors>Hernandez-Losa J</pubmed_authors><pubmed_authors>Gonzalez-Suarez E</pubmed_authors><pubmed_authors>Pujana MA</pubmed_authors><pubmed_authors>Roman A</pubmed_authors><pubmed_authors>Ancochea J</pubmed_authors><pubmed_authors>Petit A</pubmed_authors><pubmed_authors>Garcia N</pubmed_authors><pubmed_authors>Extremera AI</pubmed_authors><pubmed_authors>Fernandez A</pubmed_authors><pubmed_authors>Lopez JI</pubmed_authors><pubmed_authors>Sanchez-Mut JV</pubmed_authors><pubmed_authors>Ortega R</pubmed_authors><pubmed_authors>Ussetti P</pubmed_authors><pubmed_authors>Xaubet A</pubmed_authors><pubmed_authors>Pla MJ</pubmed_authors><pubmed_authors>Campos M</pubmed_authors><pubmed_authors>Herranz C</pubmed_authors><pubmed_authors>Boni J</pubmed_authors><pubmed_authors>Falo C</pubmed_authors><pubmed_authors>Cordero A</pubmed_authors><pubmed_authors>Morilla I</pubmed_authors><pubmed_authors>Laporta R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lymphangioleiomyomatosis Biomarkers Linked to Lung Metastatic Potential and Cell Stemness.</name><description>Lymphangioleiomyomatosis (LAM) is a rare lung-metastasizing neoplasm caused by the proliferation of smooth muscle-like cells that commonly carry loss-of-function mutations in either the tuberous sclerosis complex 1 or 2 (TSC1 or TSC2) genes. While allosteric inhibition of the mechanistic target of rapamycin (mTOR) has shown substantial clinical benefit, complementary therapies are required to improve response and/or to treat specific patients. However, there is a lack of LAM biomarkers that could potentially be used to monitor the disease and to develop other targeted therapies. We hypothesized that the mediators of cancer metastasis to lung, particularly in breast cancer, also play a relevant role in LAM. Analyses across independent breast cancer datasets revealed associations between low</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015</publication><modification>2026-04-07T21:11:13.026Z</modification><creation>2019-03-26T22:54:35Z</creation></dates><accession>S-EPMC4500593</accession><cross_references><pubmed>26167915</pubmed><doi>10.1371/journal.pone.0132546</doi></cross_references></HashMap>