The inflammatory cytokine interleukin-23 is elevated in lung cancer, particularly small cell type

Cam, Caner; Karagöz, Bülent; Müftüoğlu, Tuba; Bigi, Oguz; Emirzeoglu, Levent; Celi̇k, Serkan; Ozgun, Alpaslan; Tuncel, Tolga; Top, Cihan

doi:10.5114/wo.2016.61562

Cited by 13 publications

(10 citation statements)

References 26 publications

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“…The correlation between high levels of sIL‐23R with poor prognosis of NSCLC patients indicated the potential of sIL‐23R as a new serum tumor marker. Increasing levels of IL‐23 and IL‐17 were also associated with poor prognosis of NSCLC patients, which were similar to the results of other studies . Moreover, we found that too low or too high sIL‐23R/IL‐23 ratios suggested a poor prognosis of NSCLC patients.…”

Section: Discussionsupporting

confidence: 90%

Prognostic value of serum soluble interleukin‐23 receptor and related T‐helper 17 cell cytokines in non‐small cell lung carcinoma

et al. 2020

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractThe signaling of interleukin (IL)-23 and its receptor (IL-23R) play a crucial role in the development of cancers. However, the clinical significance of human serum soluble IL-23R (sIL-23R) and its relationship with IL-23 are still not explored in non-small cell lung cancer (NSCLC). In our study, sIL-23R was first identified in the serum of NSCLC patients, but not in healthy controls, by proteomics. The IL-23R mRNA and protein were upregulated in NSCLC cell lines and tissues tested by quantitative PCR, western blot analysis and immunohistochemistry. The levels of sIL-23R, IL-23, and IL-17 in 195 NSCLC patients' serum were determined by ELISA, and high levels of sIL-23R were significantly associated with advanced N stage (P = .039), clinical stage (P = .007), and poor 5-year survival rate. In vitro, sIL-23R was shown binding to IL-23 and the balance could affect patients' N and T stage, overall survival, and downstream cytokine IL-17 in a potential antagonistic relationship. Although sIL-23R, IL-23, and IL-17 were all associated with poor prognosis, only the sIL-23R/IL-23 ratio (hazard ratio, 1.945; 95% confidence interval, 1.147-3.299; P = .014) was found to be an independent factor for prognosis. Therefore, we identified fragments of soluble cytokine receptor of IL-23R with affinity ability to its natural ligand IL-23 in NSCLC patients' serum. The balance between the 2 antagonists can work as a potential prognostic serum marker. K E Y W O R D Scombination, IL-23, NSCLC, prognosis, sIL-23R [Correction added on 15 April 2020, after first online publication: Affiliation 4 was revised by adding "the Second Affiliated

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Section: Discussionsupporting

confidence: 90%

Prognostic value of serum soluble interleukin‐23 receptor and related T‐helper 17 cell cytokines in non‐small cell lung carcinoma

et al. 2020

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“…Although elevated IL-22 expression has been detected in the primary lung tumor, serum, and malignant pleural effusion in patients (27,28), its expression did not correlate with prognostic outcome in smokers with NSCLC (27). Further, IL-23, another cytokine that is secreted by myeloid cells and can polarize naive CD4 + T cells to Th17 cells (29,30), was found to be elevated in the serum of lung cancer patients compared with healthy controls (31). Similarly, however, there is no known correlation between IL-23 expression and NSCLC prognosis to date.…”

Section: Pro-tumor Effect Of Il17amentioning

confidence: 99%

Lung Cancer Heterogeneity in Modulation of Th17/IL17A Responses

et al. 2019

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The interplay between tumors and their immune microenvironment is critical for cancer development and progression. The discovery of tumor heterogeneity has provided a window into a complex interplay between tumors, their secreted products, and host immune responses at the cellular and molecular levels. Tumor heterogeneity can also act as a driving force in promoting treatment resistance and correlates with distinct tumor-mediated acquired immune responses. A prevailing question is how genetic aberrations in solid tumors can shape the immune landscape, resulting in pro-tumor or anti-tumor activities. Here we review evidence for clinical and pathophysiological mechanisms that underlie different types of non-small cell lung cancer (NSCLC) and provide new insights for future immunomodulatory-based therapies. Some of the more common driver mutations in NSCLC heterogeneity includes the opposing immune responses in oncogenic mutations in K-ras vs. non-K-ras models and their pro-inflammatory cytokines such as interleukin (IL)17A. We will discuss possible molecular and metabolic mechanisms that may govern the opposing immune responses observed in distinct genetic models of NSCLCs. A deeper understanding of how tumor heterogeneity modulates immune response can improve current therapeutic strategies and provide precise treatment to individual lung cancer patients.

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“…Interleukin (IL)-17 and IL-23 play roles in inflammation and autoimmunity and are increased in patients with ANCA-associated vasculitis [ 49 ]. Recent studies have shown that the serum IL-23 level, but not that of IL-17, is also elevated in small cell lung cancer [ 50 , 51 ]. As lung cancer is not a common event in GPA patients, it seems that there might be another possible triggering factor.…”

Section: Discussionmentioning

confidence: 99%

New lung mass in a patient with granulomatosis with polyangiitis

et al. 2020

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Granulomatosis with polyangiitis (GPA) is a potentially lethal ANCA-associated small-vessel vasculitis characterized by a typical triad of upper respiratory tract, lung, and kidney involvement. Lung involvement in GPA occurs in 25–80% of cases. The most common radiographic and computed tomography (CT) abnormalities of pulmonary GPA are lung nodules and masses, very often multiple and with cavitation. As there are various clinical presentations, the diagnosis of GPA can be challenging, and the illness is difficult to distinguish from other diseases such as infection or malignancy. Following the improved survival rates in patients with GPA, there is accumulating evidence to suggest an increased occurrence of different types of cancer. Exposure to cyclophosphamide seems to be one of its main causes. We present the case of a patient with chronic GPA who was hospitalized owing to a new infiltrate in the lung, suggesting relapse of the disease, and finally diagnosed with small cell lung cancer. Data regarding lung cancer in GPA patients are limited. While there are some case reports and short case series in the literature, there are no detailed data regarding an association between CYC exposure and lung cancer development in vasculitis. It is necessary to consider the causes of pulmonary masses other than a GPA relapse. Bronchoscopy with biopsy and histopathological examination are crucial in proper differential diagnosis. GPA patients require long-term follow-up to monitor for the development of complications during treatment.

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The inflammatory cytokine interleukin-23 is elevated in lung cancer, particularly small cell type

Cited by 13 publications

References 26 publications

Prognostic value of serum soluble interleukin‐23 receptor and related T‐helper 17 cell cytokines in non‐small cell lung carcinoma

Prognostic value of serum soluble interleukin‐23 receptor and related T‐helper 17 cell cytokines in non‐small cell lung carcinoma

Lung Cancer Heterogeneity in Modulation of Th17/IL17A Responses

New lung mass in a patient with granulomatosis with polyangiitis

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