Erratum: A distinct pre-existing inflammatory tumour microenvironment is associated with chemotherapy resistance in high-grade serous epithelial ovarian cancer

Koti, Madhuri; A, Siu; Clément, I; Bidarimath, Mallikarjun; Turashvili, Gulisa; Edwards, Andrew K.; Rahimi, Kurosh; Mes-Masson, Anne-Marie; Squire, Jeremy A.

doi:10.1038/bjc.2015.459

Cited by 31 publications

(5 citation statements)

References 42 publications

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“…32,33 Our data analyses from the TCGA datasets showed that though neither PD-1nor PD-L1 was correlated with the OS and PFS of patients with OC, 34,35,36,37,38,39,40,41,42,43,44,45,46 STAT1 expression was associated with the OS and PFS of patients with OC. 47,48,49 The presence of positive correlation between STAT1 and PD-L1 in ovarian tumors and the overexpression of STAT1 in patients with OC may favor the immune checkpoint inhibitors and thus, provide the novel strategy of therapy against human OC.…”

Section: Discussionmentioning

confidence: 99%

Expression of STAT1 is positively correlated with PD-L1 in human ovarian cancer

Liu

Zhang

et al. 2020

Cancer Biology & Therapy

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Signal transducer and activator of transcription 1 (STAT1) is related to the immune microenvironment of tumorigenesis. The programmed cell death 1 (PD-1) and its ligand (PD-L1) have been reported to be important in immunotherapy by mediating tumor immune evasion. Blocking the PD-1/PD-L1 pathway can restore the endogenous anti-tumor immune response. This study aimed to examine the expression of STAT1, PD-1, and PD-L1 and the correlation between selected markers in human epithelial ovarian cancer (EOC). The results showed that malignant tumors contained more STAT1, PD-1, and PD-L1 positive cells. The expression of STAT1 and PD-L1 was associated with age, whereas PD-1 and PD-L1 associated with histopathological type, in patients with ovarian tumors. Moreover, the expression of STAT1 was found to be associated with disease stages and the grade of serous carcinoma. STAT1 expression was higher in OC cells than normal ovarian surface epithelial cells and was positively correlated with PD-L1 expression. The knockdown of STAT1 decreased PD-L1 expression, whereas overexpression of STAT1 increased PD-L1 expression. Furthermore, the expression of STAT1, PD-1, and PD-L1 was lower in paclitaxel-resistant cells than sensitive cells. Finally, STAT1 affected the overall survival and progression-free survival of patients with EOC. These findings suggest that STAT1, PD-1, and PD-L1 are the tissue markers of EOC and imply the possibility that the high level of STAT1, PD-1, and PD-L1 may favor the checkpoint immunotherapy in patients with EOC, but may have a limit in paclitaxel-resistant patients because of the low expression of STAT1, PD-1, and PD-L1 in paclitaxel-resistant cells.

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Section: Discussionmentioning

confidence: 99%

Expression of STAT1 is positively correlated with PD-L1 in human ovarian cancer

Liu

Zhang

et al. 2020

Cancer Biology & Therapy

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“…It is proposed that the dysregulation of cytokines (increased IL-6, TNF- α and IL−1β), adipokines (increased leptin and decreased Apn and resistin), chemokines, as well as extracellular matrix proteins (collagen IV) from adipocytes (12, 64, 202, 203) (Figure 2), affect the expression of transcription factors involved in lipid metabolism. Examples include, HSL, FABP-4 and CEBP-α (14, 72).…”

Section: Breast Cancer Treatmentmentioning

confidence: 99%

“…Macrophage chemoattractant protein-1 and CCLC-5 may also be active in the host microenvironment promoting survival, invasion metastasis, and unfavorable drug responses. Here, it is proposed that the recruitment of immune cells to the tumor microenvironment, promotes inflammation, stimulating the secretion of matrix metalloproteinase-9 (role in matrix degradation) and evading the host's immune responses (202). Additionally, MCP-1 benefits vascular endothelial cell survival and activate the JAK2/STAT5 and p38 MAPK pathways, inducing angiogenesis (205).…”

Section: Breast Cancer Treatmentmentioning

confidence: 99%

Chemoresistance: Intricate Interplay Between Breast Tumor Cells and Adipocytes in the Tumor Microenvironment

et al. 2018

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Excess adipose tissue is a hallmark of an overweight and/or obese state as well as a primary risk factor for breast cancer development and progression. In an overweight/obese state adipose tissue becomes dysfunctional due to rapid hypertrophy, hyperplasia, and immune cell infiltration which is associated with sustained low-grade inflammation originating from dysfunctional adipokine synthesis. Evidence also supports the role of excess adipose tissue (overweight/obesity) as a casual factor for the development of chemotherapeutic drug resistance. Obesity-mediated effects/modifications may contribute to chemotherapeutic drug resistance by altering drug pharmacokinetics, inducing chronic inflammation, as well as altering tumor-associated adipocyte adipokine secretion. Adipocytes in the breast tumor microenvironment enhance breast tumor cell survival and decrease the efficacy of chemotherapeutic agents, resulting in chemotherapeutic resistance. A well-know chemotherapeutic agent, doxorubicin, has shown to negatively impact adipose tissue homeostasis, affecting adipose tissue/adipocyte functionality and storage. Here, it is implied that doxorubicin disrupts adipose tissue homeostasis affecting the functionality of adipose tissue/adipocytes. Although evidence on the effects of doxorubicin on adipose tissue/adipocytes under obesogenic conditions are lacking, this narrative review explores the potential role of obesity in breast cancer progression and treatment resistance with inflammation as an underlying mechanism.

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“…Several studies have shown the importance of different cytokines secreted by the tumor microenvironment in the regulation of CSCs [ 30 ]. In the case of ovarian cancer, it is known that an inflammatory state is considered a risk factor and can be associated with ovarian cancer development, drug resistance, and metastasis [ 31 , 32 ]. Several cytokines have been described in circulation, ascites, and cyst fluid of patients with ovarian cancer [ 33 – 38 ] and also in the stroma and epithelium of tumors [ 39 ].…”

Section: Ovarian Cscs and Inflammatory Networkmentioning

confidence: 99%

The Crosstalk between Ovarian Cancer Stem Cell Niche and the Tumor Microenvironment

Varas-Godoy

Rice

Illanes

2017

Stem Cells International

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Ovarian cancer is one of the most important causes of cancer-related death among women in the world. Despite advances in ovarian cancer treatment, 70–80% of women who initially respond to therapy eventually relapse and die. There is evidence that a small population of cells within the tumors called cancer stem cells (CSCs) could be responsible for treatment failure due to their enhanced chemoresistance and tumorigenicity. These cells reside in a niche that maintains the principal properties of CSCs. These properties are associated with the capacity of CSCs to interact with different cells of the tumor microenvironment including mesenchymal stem cells, endothelial cells, immune cells, and fibroblasts, promoting cancer progression. This interaction can be mediated by cytokines, growth factors, lipids, and/or extracellular vesicles released in the CSC niche. In this review, we will discuss how the interaction between ovarian CSCs and the tumor microenvironment can contribute to the maintenance of the CSC niche and consequently to tumor progression in ovarian cancer.

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Erratum: A distinct pre-existing inflammatory tumour microenvironment is associated with chemotherapy resistance in high-grade serous epithelial ovarian cancer

Cited by 31 publications

References 42 publications

Expression of STAT1 is positively correlated with PD-L1 in human ovarian cancer

Expression of STAT1 is positively correlated with PD-L1 in human ovarian cancer

Chemoresistance: Intricate Interplay Between Breast Tumor Cells and Adipocytes in the Tumor Microenvironment

The Crosstalk between Ovarian Cancer Stem Cell Niche and the Tumor Microenvironment

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