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However, this therapy has variable tolerability and some patients show progressive decline of lung function despite treatment. LAM diagnosis and monitoring can also be challenging due to the heterogeneity of symptoms and insufficiency of non\u2010invasive tests. Here, we propose monoamine\u2010derived biomarkers that provide preclinical evidence for novel therapeutic approaches. The major histamine\u2010derived metabolite methylimidazoleacetic acid (MIAA) is relatively more abundant in LAM plasma, and MIAA values are independent of VEGF\u2010D. Higher levels of histamine are associated with poorer lung function and greater disease burden. Molecular and cellular analyses, and metabolic profiling confirmed active histamine signaling and metabolism. LAM tumorigenesis is reduced using approved drugs targeting monoamine oxidases A\/B (clorgyline and rasagiline) or histamine H1 receptor (loratadine), and loratadine synergizes with rapamycin. Depletion of\n                    <jats:italic>Maoa<\/jats:italic>\n                    or\n                    <jats:italic>Hrh1<\/jats:italic>\n                    expression, and administration of an L\u2010histidine analog, or a low L\u2010histidine diet, also reduce LAM tumorigenesis. These findings extend our knowledge of LAM biology and suggest possible ways of improving disease management.\n                  <\/jats:p>","DOI":"10.15252\/emmm.202113929","type":"journal-article","created":{"date-parts":[[2021,8,11]],"date-time":"2021-08-11T03:40:48Z","timestamp":1628653248000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Histamine signaling and metabolism identify potential biomarkers and therapies for 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