Targeting Notch-Driven Cytokine Secretion: Novel Therapies for Triple Negative Breast Cancer.

IF 2.6 4区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

DNA and cell biology Pub Date : 2023-02-01 DOI:10.1089/dna.2022.0578

Wanda Marini, Brooke E Wilson, Michael Reedijk

引用次数: 1

Abstract

Compared with other breast cancer subtypes, triple negative breast cancer (TNBC) is an aggressive malignancy with a high recurrence rate and reduced overall survival. Immune checkpoint inhibition (ICI) has shown modest results in this subgroup, highlighting the need for improved targeted therapeutic options. Notch is a defining feature of TNBC and drives the expression of interleukin-1 beta (IL1β) and C-C motif chemokine ligand 2 (CCL2). These cytokines are involved in the recruitment of tumor-associated macrophages (TAMs) to the tumor, resulting in immune evasion and tumor progression. Targeting Notch, IL1β or CCL2 may reduce TAM recruitment and resistance to ICI, illuminating the potential of combination immunotherapy in TNBC.

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靶向缺口驱动细胞因子分泌:三阴性乳腺癌的新疗法。

与其他乳腺癌亚型相比，三阴性乳腺癌(triple negative breast cancer, TNBC)是一种复发率高、总生存率低的侵袭性恶性肿瘤。免疫检查点抑制(ICI)在该亚组中显示出适度的结果，突出了改进靶向治疗选择的必要性。Notch是TNBC的一个决定性特征，并驱动白细胞介素-1 β (il -1 β)和C-C基序趋化因子配体2 (CCL2)的表达。这些细胞因子参与肿瘤相关巨噬细胞(tam)向肿瘤的募集，导致免疫逃避和肿瘤进展。靶向Notch、il - 1β或CCL2可能会减少TAM的募集和对ICI的耐药性，这说明了联合免疫治疗TNBC的潜力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

DNA and cell biology 生物-生化与分子生物学

CiteScore

6.60

自引率

0.00%

发文量

审稿时长

1.5 months

期刊介绍： DNA and Cell Biology delivers authoritative, peer-reviewed research on all aspects of molecular and cellular biology, with a unique focus on combining mechanistic and clinical studies to drive the field forward. DNA and Cell Biology coverage includes: Gene Structure, Function, and Regulation Gene regulation Molecular mechanisms of cell activation Mechanisms of transcriptional, translational, or epigenetic control of gene expression Molecular Medicine Molecular pathogenesis Genetic approaches to cancer and autoimmune diseases Translational studies in cell and molecular biology Cellular Organelles Autophagy Apoptosis P bodies Peroxisosomes Protein Biosynthesis and Degradation Regulation of protein synthesis Post-translational modifications Control of degradation Cell-Autonomous Inflammation and Host Cell Response to Infection Responses to cytokines and other physiological mediators Evasive pathways of pathogens.