Immune consequences of anti-angiogenic therapy in renal cell carcinoma

Brodaczewska, Klaudia; Szczylik, Cezary; Kiéda, Claudine

doi:10.5114/wo.2018.73878

Cited by 7 publications

(7 citation statements)

References 134 publications

(121 reference statements)

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“…Blockade of angiogenesis signaling significantly inhibits brain CSCs due to reduced blood vasculature in tumors. In line with clinical data, metastatic renal cancer patients who receive antiangiogenic therapy have an overall survival strongly correlated with the reduction in Treg numbers (Brodaczewska et al, 2018). Additionally, the angiogenetic situation is aggravated by TAM preferential secretion of VEGF and IL-8, doubling the effect on promoting CSC proliferation (Werno et al, 2010).…”

Section: Regulatory T Cellsmentioning

confidence: 77%

Cancer Stem Cells: Emerging Key Players in Immune Evasion of Cancers

Lei

2021

Front. Cell Dev. Biol.

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Cancer stem cells (CSCs) are subpopulations of undifferentiated cancer cells within the tumor bulk that are responsible for tumor initiation, recurrence and therapeutic resistance. The enhanced ability of CSCs to give rise to new tumors suggests potential roles of these cells in the evasion of immune surveillance. A growing body of evidence has described the interplay between CSCs and immune cells within the tumor microenvironment (TME). Recent data have shown the pivotal role of some major immune cells in driving the expansion of CSCs, which concurrently elicit evasion of the detection and destruction of various immune cells through a number of distinct mechanisms. Here, we will discuss the role of immune cells in driving the stemness of cancer cells and provide evidence of how CSCs evade immune surveillance by exerting their effects on tumor-associated macrophages (TAMs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), T-regulatory (Treg) cells, natural killer (NK) cells, and tumor-infiltrating lymphocytes (TILs). The knowledge gained from the interaction between CSCs and various immune cells will provide insight into the mechanisms by which tumors evade immune surveillance. In conclusion, CSC-targeted immunotherapy emerges as a novel immunotherapy strategy against cancer by disrupting the interaction between immune cells and CSCs in the TME.

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Section: Regulatory T Cellsmentioning

confidence: 77%

Cancer Stem Cells: Emerging Key Players in Immune Evasion of Cancers

Lei

2021

Front. Cell Dev. Biol.

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“…Unfortunately, there are little data in the literature on the specific effect of lenvatinib on immune cells, especially MDSCs. Changes in CD8+/CD4+ T‐cells, Tregs, and MDSCs have been mixed with other MKIs such as sorafenib, sunitinib, pazopanib etc., likely due to variability in which tyrosine kinase receptors are targeted, affinity, differential effects on separate compartments, along with disparate behavior in different tumor models . Sunitinib appears to most consistently decrease circulating, tumor‐associated, and splenic MDSCs in multiple tumor models .…”

Section: Discussionmentioning

confidence: 99%

Anti‐PD‐1/PD‐L1 therapy augments lenvatinib's efficacy by favorably altering the immune microenvironment of murine anaplastic thyroid cancer

Gunda

Gigliotti

Ashry

et al. 2019

Intl Journal of Cancer

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Patients with anaplastic thyroid cancer (ATC) have an extremely poor prognosis despite multimodal therapy with surgery and chemoradiation. Lenvatinib, a multi-targeted tyrosine kinase inhibitor, as well as checkpoint inhibitors targeting the programmed cell death pathway, have proven effective in some patients with advanced thyroid cancer. Combination of these therapies is a potential means to boost effectiveness and minimize treatment resistance in ATC. We utilized our novel immunocompetent murine model of orthotopic ATC to demonstrate that lenvatinib led to significant tumor shrinkage and increased survival, while combination therapy led to dramatic improvements in both. Lenvatinib monotherapy increased tumorinfiltrating macrophages, CD8 + T-cells, regulatory T-cells, and most notably, polymorphonuclear myeloid derived suppressor cells (PMN-MDSCs). While both combination therapies led to further increases in CD8 + T-cells, only the lenvatinib and anti-PD-1 combination decreased PMN-MDSCs. PMN-MDSC expansion was also seen in the blood of mice and one patient receiving lenvatinib therapy for ATC. RNA-Seq of the ATC cell line used in our mouse model demonstrated that lenvatinib has multifaceted effects on angiogenesis, response to hypoxia, the epithelial-to-mesenchymal transition, and on multiple pathways implicated in inflammation and host immunity. Combination of lenvatinib with anti-Gr-1 antibody ameliorated lenvatinib's expansion of MDSCs and significantly improved lenvatinib's anti-tumor effect. These data suggest that MDSCs play a negative role in ATC's response to lenvatinib and support future study of their role as a potential biomarker and treatment target.

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“…Unfortunately, regardless of significant advances in therapy, RCC is nowadays among the 10 most prevalent malignancies, and the incidence is growing. Additionally, RCC has a poor prognosis, considering that up to 30% of patients present metastasis at the time of diagnosis and about 20% will further develop metastasis, even if they are undergoing therapy [ 109 ].…”

Section: Ckd and Malignancy—dangerous Scenarios In The Framework Omentioning

confidence: 99%

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Mihai

Codrici

Popescu

et al. 2018

Journal of Immunology Research

459

317

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Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.

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Immune consequences of anti-angiogenic therapy in renal cell carcinoma

Cited by 7 publications

References 134 publications

Cancer Stem Cells: Emerging Key Players in Immune Evasion of Cancers

Cancer Stem Cells: Emerging Key Players in Immune Evasion of Cancers

Anti‐PD‐1/PD‐L1 therapy augments lenvatinib's efficacy by favorably altering the immune microenvironment of murine anaplastic thyroid cancer

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

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