Interleukin-3 production by basal-like breast cancer cells is associated with poor prognosis

Thompson, EJ; Escarbe, S; Tvorogov, D; Farshid, G; Gregory, PA; Khew-Goodall, Y; Madden, S; Ingman, WV; Lindeman, GJ; Lim, E; Lopez, AF; Bonder, CS

Author(s): Thompson, EJ; Escarbe, S; Tvorogov, D; Farshid, G; Gregory, PA; Khew-Goodall, Y; Madden, S; Ingman, WV; Lindeman, GJ; Lim, E; Lopez, AF; Bonder, CS;
Details: Publication Year 2024-02-01,Volume 42,Issue #2,Page 1-13
Journal Title: Growth Factors
Abstract: Breast cancer represents a collection of pathologies with different molecular subtypes, histopathology, risk factors, clinical behavior, and responses to treatment. "Basal-like" breast cancers predominantly lack the receptors for estrogen and progesterone (ER/PR), lack amplification of human epidermal growth factor receptor 2 (HER2) but account for 10-15% of all breast cancers, are largely insensitive to targeted treatment and represent a disproportionate number of metastatic cases and deaths. Analysis of interleukin (IL)-3 and the IL-3 receptor subunits (IL-3RA + CSF2RB) reveals elevated expression in predominantly the basal-like group. Further analysis suggests that IL-3 itself, but not the IL-3 receptor subunits, associates with poor patient outcome. Histology on patient-derived xenografts supports the notion that breast cancer cells are a significant source of IL-3 that may promote disease progression. Taken together, these observations suggest that IL-3 may be a useful marker in solid tumors, particularly triple negative breast cancer, and warrants further investigation into its contribution to disease pathogenesis.
Keywords: Humans; Female; *Breast Neoplasms/metabolism/pathology; *Interleukin-3/metabolism; Animals; Prognosis; Mice; Cell Line, Tumor; Triple negative breast cancer; immunohistochemistry; interleukin-3
Research Division(s): Cancer Biology And Stem Cells
PubMed ID: 38299881
Publisher's Version: https://doi.org/10.1080/08977194.2023.2297693
Open Access at Publisher's Site: https://doi.org/10.1080/08977194.2023.2297693
Terms of Use/Rights Notice: Refer to copyright notice on published article.
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Creation Date: 2024-02-29 09:16:18

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