<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ansari KI</submitter><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>Department of Defense</funding><funding>NIGMS NIH HHS</funding><pagination>4723-4735</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8986153</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>81(18)</volume><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&lt;sup>+&lt;/sup> subtype, is its most common origin. HER2&lt;sup>+&lt;/sup> breast LC (HER2&lt;sup>+&lt;/sup> LC) remains incurable, with few treatment options, and the molecular mechanisms underlying proliferation of HER2&lt;sup>+&lt;/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&lt;sup>+&lt;/sup> LC development as well as those that restrict its growth to leptomeninges. P</pubmed_abstract><journal>Cancer research</journal><pubmed_title>Autocrine GMCSF Signaling Contributes to Growth of HER2&lt;sup>+&lt;/sup> Breast Leptomeningeal Carcinomatosis.</pubmed_title><pmcid>PMC8986153</pmcid><funding_grant_id>K12 CA001727</funding_grant_id><funding_grant_id>W81XWH-19-1-0310</funding_grant_id><funding_grant_id>P30 CA033572</funding_grant_id><funding_grant_id>P20GM104360</funding_grant_id><funding_grant_id>P20 GM104360</funding_grant_id><pubmed_authors>Tyagi A</pubmed_authors><pubmed_authors>Bhan A</pubmed_authors><pubmed_authors>Takaku M</pubmed_authors><pubmed_authors>Ansari KI</pubmed_authors><pubmed_authors>Saotome M</pubmed_authors><pubmed_authors>De Kumar B</pubmed_authors><pubmed_authors>Jandial R</pubmed_authors><pubmed_authors>Chen C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Autocrine GMCSF Signaling Contributes to Growth of HER2&lt;sup>+&lt;/sup> Breast Leptomeningeal Carcinomatosis.</name><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&lt;sup>+&lt;/sup> subtype, is its most common origin. HER2&lt;sup>+&lt;/sup> breast LC (HER2&lt;sup>+&lt;/sup> LC) remains incurable, with few treatment options, and the molecular mechanisms underlying proliferation of HER2&lt;sup>+&lt;/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&lt;sup>+&lt;/sup> LC development as well as those that restrict its growth to leptomeninges. P</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Sep</publication><modification>2025-04-04T07:34:53.629Z</modification><creation>2025-04-04T07:34:53.629Z</creation></dates><accession>S-EPMC8986153</accession><cross_references><pubmed>34247146</pubmed><doi>10.1158/0008-5472.CAN-21-0259</doi><doi>10.1158/0008-5472.can-21-0259</doi></cross_references></HashMap>