Journal
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
Volume 1508, Issue 1, Pages 35-53Publisher
WILEY
DOI: 10.1111/nyas.14700
Keywords
breast cancer stem cells; GD2; GD3 synthase; triple-negative breast cancer; immunotherapy; dinutuximab; mTOR signaling; ADCC
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Funding
- U.S. Department of Defense (DOD) [BC181493]
- Breast Cancer Research Foundation (BCRF)
- CPRIT Research Training Program Grant [RP170067]
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TNBC is a heterogeneous disease characterized by lack of hormone receptor expression, with high recurrence and distant metastasis rates. Targeting breast cancer stem-like cells is an effective strategy for preventing metastatic spread and enhancing sensitivity to chemotherapy.
Triple-negative breast cancer (TNBC) is a heterogeneous disease characterized by lack of hormone receptor expression and is known for high rates of recurrence, distant metastases, and poor clinical outcomes. TNBC cells lack targetable receptors; hence, there is an urgent need for targetable markers for the disease. Breast cancer stem-like cells (BCSCs) are a fraction of cells in primary tumors that are associated with tumorigenesis, metastasis, and resistance to chemotherapy. Targeting BCSCs is thus an effective strategy for preventing cancer metastatic spread and sensitizing tumors to chemotherapy. The CD44(hi)CD24(lo) phenotype is a well-established phenotype for identification of BCSCs, but CD44 and CD24 are not targetable markers owing to their expression in normal tissues. The ganglioside GD2 has been shown to be upregulated in primary TNBC tumors compared with normal breast tissue and has been shown to identify BCSCs. In this review, we discuss GD2 as a BCSC- and tumor-specific marker in TNBC; epithelial-to-mesenchymal transition and the signaling pathways that are upstream and downstream of GD2 and the role of these pathways in tumorigenesis and metastasis in TNBC; direct and indirect approaches for targeting GD2; and ongoing clinical trials and treatments directed against GD2 as well as future directions for these strategies.
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