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Chemokines in triple-negative breast cancer heterogeneity: New challenges for clinical implications
Umar Mehraj1, Umar Mushtaq2, Manzoor A Mir1
1Department of Bioresources, School of Life Sciences, University of Kashmir, Srinagar, Jammu & Kashmir, India.
Abstract:
Tumor heterogeneity is a hallmark of cancer and one of the primary causes of resistance to therapies. Triple-negative breast cancer (TNBC), which accounts for 15-20% of all breast cancers and is the most aggressive subtype, is very diverse, connected to metastatic potential and response to therapy. It is a very diverse disease at the molecular, pathologic, and clinical levels. TNBC is substantially more likely to recur and has a worse overall survival rate following diagnosis than other breast cancer subtypes. Chemokines, low molecular weight proteins that stimulate chemotaxis, have been shown to control the cues responsible for TNBC heterogeneity. In this review, we have focused on tumor heterogeneity and the role of chemokines in modulating tumor heterogeneity, since this is the most critical issue in treating TNBC. Additionally, we examined numerous cues mediated by chemokine networks that contribute to the heterogeneity of TNBC. Recent developments in our knowledge of the chemokine networks that regulate TNBC heterogeneity may pave the way for developing effective therapeutic modalities for effective treatment of TNBC.
Insights
Tumor heterogeneity in triple-negative breast cancer (TNBC) drives therapy resistance. Chemokines are key regulators of this diversity, offering new therapeutic targets for aggressive TNBC treatment.
Area of Science:
- Oncology
- Cancer Biology
- Immunology
Background:
- Tumor heterogeneity is a primary driver of cancer therapy resistance.
- Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by significant molecular, pathologic, and clinical diversity.
- TNBC exhibits higher recurrence rates and poorer survival outcomes compared to other breast cancer subtypes.
Purpose of the Study:
- To review the critical role of tumor heterogeneity in TNBC.
- To elucidate the function of chemokines in modulating TNBC heterogeneity.
- To explore chemokine networks as potential therapeutic targets for TNBC.
Main Methods:
- Literature review focusing on tumor heterogeneity in TNBC.
- Analysis of the role of chemokines and their networks in TNBC.
- Examination of molecular and clinical data related to TNBC diversity.
Main Results:
- Chemokines are identified as crucial mediators controlling the cues responsible for TNBC heterogeneity.
- Specific chemokine networks significantly contribute to the diverse nature of TNBC.
- Understanding these chemokine networks is essential for addressing TNBC's aggressive characteristics.
Conclusions:
- Chemokine-mediated signaling pathways are central to TNBC tumor heterogeneity.
- Targeting chemokine networks presents a promising strategy for overcoming therapeutic resistance in TNBC.
- Advances in understanding chemokine roles may lead to novel treatment modalities for TNBC.
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