Elevated serum C-reactive protein, carcinoembryonic antigen and N2 disease are poor prognostic indicators in non-small cell lung cancer

Ni, Xuefeng; Wu, Ping; Wu, Changping; Ji, Mei; Wu, Jun; Gu, Xiaofang; Jiang, Zhenxing

doi:10.1111/ajco.12091

Cited by 20 publications

(23 citation statements)

References 47 publications

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“…Among them, TNF-α is likely to play a central role in tumorigenesis, as it has been reported that mice deficient with TNF-α is protected from the cancer development [44,45]. Furthermore, CRP is considered to play a major role in cancer development [28,29]. Our study demonstrated that Ang II could directly induce inflammatory cytokines TNF-α and CRP productions in HCC cell lines.…”

Section: Discussionsupporting

confidence: 55%

Angiotensin II Enhances Proliferation and Inflammation through AT1/PKC/NF-κB Signaling Pathway in Hepatocellular Carcinoma Cells

Ji¹,

Wang²,

Li³

et al. 2016

Cell Physiol Biochem

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Background/Aims: The pathogenesis of hepatocellular carcinoma (HCC) is mainly characterized by persistent cycles of liver injury, inflammation, and compensatory hepatocyte proliferation. Angiotensin II (Ang II) behaves as an endogenous pro-inflammatory molecule playing a significant role in HCC, however, the molecular link between Ang II, proliferation and inflammation remains unclear. Methods: Human HCC cell lines (HepG-2, SMMC-7721, MHCC97-H) were incubated with Ang II at the indicated concentrations for 24, 48, 72 h. MTT, BrdU ELISA, plate colony formation assay, immunohistochemistry, ELISA, small-interfering RNA(siRNA) transfection, quantitative real-time PCR and western blot were applied to assess their functional, morphological and molecular mechanisms in HCC cell lines. Results: High expression of Ang II type 1 receptor (AT1) and low expression of AT2 in HCC cells and tissues were found. Next, Ang II could significantly enhance cell growth and proliferation. Albeit Ang II slightly increased the percentage of HCC cells in the G0/G1 phase using flow cytometry analysis, no statistically significant alterations were shown. Further studies suggested that Ang II could directly induce proliferation associated proteins C-myc and proliferating cell nuclear antigen (PCNA) expressions, and inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP) productions in HCC cells. Interestingly, blocking AT1 and AT1 siRNA evidently inhibited Ang II-induced cell proliferation and inflammatory responses in HCC cells. More importantly, these effects may be mediated by AT1/PKC/NF-κB signaling pathway in HCC cell lines. Conclusions: The results propose that Ang II/AT1/PKC/NF-κB signaling pathway is necessary for proliferation and inflammation of HCC cells, which increases our understanding of the pathogenesis and provides clues for developing new strategies against Ang II-related progress of HCC.

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Section: Discussionsupporting

confidence: 55%

Angiotensin II Enhances Proliferation and Inflammation through AT1/PKC/NF-κB Signaling Pathway in Hepatocellular Carcinoma Cells

Ji¹,

Wang²,

Li³

et al. 2016

Cell Physiol Biochem

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“…This might be a result of different inclusion criteria and the addition of PLR and other factors in the multivariate survival analyses. Some other recent studies have also demonstrated that elevated CRP is independently associated with poor survival …”

Section: Discussionmentioning

confidence: 86%

Combination of platelet to lymphocyte ratio and neutrophil to lymphocyte ratio is a useful prognostic factor in advanced non‐small cell lung cancer patients

Yao

Bai

et al. 2015

Thoracic Cancer

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BackgroundThe neutrophil to lymphocyte ratio (NLR) was recently shown to be a remarkable prognostic factor in tumors. Moreover, some studies have indicated that the combination of NLR and platelet to lymphocyte ratio (PLR) could be a better prognostic factor. As the combined prognostic value of NLR and PLR in non-small cell lung cancer (NSCLC) is not clear, we conducted this study to explore this further.MethodsA total of 366 primary NSCLC patients with stage III or IV were finally included. The neutrophil, platelet, and lymphocyte counts were recorded before treatment was initiated. NLR and PLR were calculated and NLR > 2.68 or PLR > 119.50 was defined as elevated. Univariate and multivariate survival analyses were conducted to test their prognostic value.ResultsThe median of NLR and PLR were 3.14 and 152.63, respectively, in all patients. It was indicated that PLR is linearly associated with NLR. PLR is associated with survival, but is not an independent prognostic factor. Removing NLR, PLR is an independent prognostic factor (overall survival [OS]: hazard ratio [HR] = 1.918, P = 0.003; progression-free survival [PFS]: HR = 1.822, P = 0.007 in condition of NLR ≤ 2.68). It was also indicated that elevated NLR is an independent prognostic factor (OS: HR = 1.778, P = 0.009; PFS: HR = 1.535, P = 0.022) in all patients.ConclusionsPLR is a useful complement of NLR, thus, advanced NSCLC patients could be divided into three prognostic groups prior to treatment: poor: NLR > 2.68; moderate: NLR ≤ 2.68 and PLR > 119.50; and good: NLR ≤ 2.68 and PLR ≤ 119.50.

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“…The tumor group of our study population comprised patients with lung cancer as the largest subgroup of patients. Interestingly, several studies have recently indicated the value of CEA in the diagnosis and prognosis of lung cancer with PEs, among other biomarkers . Indeed, high serum CRP and CEA levels were identified as independent prognostic indicators for the survival of patients with stage III–IV non‐small cell lung cancer (NSCLC) .…”

Section: Discussionmentioning

confidence: 99%

Pleural fluid carcinoembryonic antigen as a biomarker for the discrimination of tumor‐related pleural effusion

Huang

Tang

et al. 2016

Clinical Respiratory J

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We read with interest the article by Li et al. (accepted article in Clin Respir J) on pleural fluid carcinoembry-onic antigen (CEA) as a biomarker for the discrimination of tumor-related pleural effusion (1). We would like to ask three points. First, the authors described that a diagnosis of probable tumor pleural effusion was made in patients with a known primary malignancy showing negative pleural fluid cytology results, after ruling out benign causes of pleural fluid. We agree with the method, but what is the number of the lung cancer patients with negative malignant cells in pleural fluid in this study. Second, recommended CEA level in pleural fluid would be changed if the ratio of patients with adenocarcinoma and those with non-adenocarcinoma are changed. We do wonder whether the authors determine the CEA cutoff level in pleural fluid taking the ratio into the consideration. How the authors evaluate the relationship between the ratio of types of lung cancer (adenocarcinoma and non-adeno-carcinoma) and the cutoff CEA level. Third, the authors showed that they used Roche's CEA kit in this study. This may be CEA kit for serum/plasma CEA measurement. We would like to ask how much cutoff serum/plasma CEA level was. Was the cutoff level of CEA different from that the authors recommend cutoff CEA level in pleural fluid? We do appreciate hearing from the authors why cutoff CEA level in pleural fluid are different from cutoff CEA level in serum/plasma.

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Elevated serum C-reactive protein, carcinoembryonic antigen and N2 disease are poor prognostic indicators in non-small cell lung cancer

Abstract: High levels of serum CRP and CEA, and N2 disease are independent prognostic indicators for the survival of patients with stage III-IV NSCLC.

Cited by 20 publications

References 47 publications

Angiotensin II Enhances Proliferation and Inflammation through AT1/PKC/NF-κB Signaling Pathway in Hepatocellular Carcinoma Cells

Angiotensin II Enhances Proliferation and Inflammation through AT1/PKC/NF-κB Signaling Pathway in Hepatocellular Carcinoma Cells

Combination of platelet to lymphocyte ratio and neutrophil to lymphocyte ratio is a useful prognostic factor in advanced non‐small cell lung cancer patients

Pleural fluid carcinoembryonic antigen as a biomarker for the discrimination of tumor‐related pleural effusion

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