{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ansari KI"],"funding":["NCI NIH HHS","National Institutes of Health","Department of Defense","NIGMS NIH HHS"],"pagination":["4723-4735"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8986153"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["81(18)"],"pubmed_abstract":["Leptomeningeal carcinomatosis (LC) occurs when tumor cells spread to the cerebrospinal fluid-containing leptomeninges surrounding the brain and spinal cord. LC is an ominous complication of cancer with a dire prognosis. Although any malignancy can spread to the leptomeninges, breast cancer, particularly the HER2<sup>+</sup> subtype, is its most common origin. HER2<sup>+</sup> breast LC (HER2<sup>+</sup> LC) remains incurable, with few treatment options, and the molecular mechanisms underlying proliferation of HER2<sup>+</sup> breast cancer cells in the acellular, protein, and cytokine-poor leptomeningeal environment remain elusive. Therefore, we sought to characterize signaling pathways that drive HER2<sup>+</sup> LC development as well as those that restrict its growth to leptomeninges. P"],"journal":["Cancer research"],"pubmed_title":["Autocrine GMCSF Signaling Contributes to Growth of HER2<sup>+</sup> Breast Leptomeningeal Carcinomatosis."],"pmcid":["PMC8986153"],"funding_grant_id":["K12 CA001727","W81XWH-19-1-0310","P30 CA033572","P20GM104360","P20 GM104360"],"pubmed_authors":["Tyagi A","Bhan A","Takaku M","Ansari KI","Saotome M","De Kumar B","Jandial R","Chen C"],"additional_accession":[]},"is_claimable":false,"name":"Autocrine GMCSF Signaling Contributes to Growth of HER2<sup>+</sup> Breast Leptomeningeal Carcinomatosis.","description":"Leptomeningeal carcinomatosis (LC) occurs when tumor cells spread to the cerebrospinal fluid-containing leptomeninges surrounding the brain and spinal cord. LC is an ominous complication of cancer with a dire prognosis. Although any malignancy can spread to the leptomeninges, breast cancer, particularly the HER2<sup>+</sup> subtype, is its most common origin. HER2<sup>+</sup> breast LC (HER2<sup>+</sup> LC) remains incurable, with few treatment options, and the molecular mechanisms underlying proliferation of HER2<sup>+</sup> breast cancer cells in the acellular, protein, and cytokine-poor leptomeningeal environment remain elusive. Therefore, we sought to characterize signaling pathways that drive HER2<sup>+</sup> LC development as well as those that restrict its growth to leptomeninges. P","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2025-04-04T07:34:53.629Z","creation":"2025-04-04T07:34:53.629Z"},"accession":"S-EPMC8986153","cross_references":{"pubmed":["34247146"],"doi":["10.1158/0008-5472.CAN-21-0259","10.1158/0008-5472.can-21-0259"]}}