While metastasis is the primary factor predicting poor outcomes in solid tumors, survival is lowest in patients initially diagnosed with a localized malignancy that then progresses to metastatic disease. For example, nearly 25% of early-stage breast cancers (BCs) metastasize during treatment or following an initial positive response to therapeutic intervention. Thus, the acquisition of therapy resistance is also closely linked to aggressive disease progression. In this session, recent and ongoing work from our lab, aimed at understanding the cellular crosstalk mechanisms within primary, premetastatic and metastatic niches that contribute to solid tumor progression, will be discussed. Specific consideration will be given to data on fibroblast-tumor cell, extracellular matrix (ECM)-tumor cell and tumor-T cell signaling mechanisms that support metastatic dissemination and therapy resistance across breast and pancreatic cancers. Additional consideration will be given to how these molecular pathways may be leveraged to improve patient outcomes. Funding to support this work has been provided by Baylor University, California State University, NIH SC1GM121182 (to J.A.K.), NIH T34GM136450 (to M.E.Z. in support of J.C.), Sidney SternFoundation (to J.A.K.), Aylozyan FamilyFoundation (to J.A.K.) and Sutter Family (to J.A.K.).
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Jonathan A. Kelber (2024) studied this question.
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