Epidermal Growth Factor Receptor Gene in Non-Small-Cell Lung Cancer: The Importance of Promoter Polymorphism Investigation

Jurišić, Vladimir; Obradovic, Jasmina; Pavlović, Sonja; Djordjević, Nataša

doi:10.1155/2018/6192187

Cited by 46 publications

(39 citation statements)

References 106 publications

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“…Heterogeneous subsets of tumor with different molecular targets may lead to different resistance levels to cancer therapy and the progression of final clinical outcomes [5 , 6] . This is mainly due to the presence of heterogeneity of EGFR polymorphisms (variation) and clinical response, and EGFR variations has a better therapy outcome [7 , 8] .…”

Section: Introductionmentioning

confidence: 99%

A signature of 17 immune-related gene pairs predicts prognosis and immune status in HNSCC patients

Jiang

et al. 2021

Translational Oncology

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Highlights We utilized multidimensional bioinformatics methods to validate the robustness of prognostic value for our 17 IRGPs signature and explored the relationship between the IRGPs model and immune status. The low-risk group demonstrated a distinctly favorable prognosis, including OS, DSS, and PFS. Through comparing PD-L1, MSI, and TIDE between high and low risk groups, low-risk group was much more sensitive to immunotherapy. Compared to the high-risk group, the low-risk group demonstrated a distinctly favourable prognosis, and the low-risk group was much more sensitive to immunotherapy. The IRGPs model is an independent biomarker for estimating the prognosis, and could be used to predict immunotherapeutic response in HNSCC patients .

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Section: Introductionmentioning

confidence: 99%

A signature of 17 immune-related gene pairs predicts prognosis and immune status in HNSCC patients

Jiang

et al. 2021

Translational Oncology

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“…Lung carcinogenesis is a multistep process that typically takes many years to develop since several mechanisms may prevent it, such as immune and antioxidative systems, as well as DNA repair mechanisms. The recent development of new technologies has increased our knowledge of molecular carcinogenetic mechanisms, including gene amplification and protein expression, irregular cell activation, and allelic and epigenetic abnormalities [5,6]. In addition, the acquisition of multiple genetic mutations may determine a progressive development of the malignant phenotype characterized by apoptosis resistance, unregulated proliferation, angiogenesis, and metastasis [5,6].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update

et al. 2019

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Lung carcinogenesis is a multistep process involving genetic mutations and epigenetic changes, with the acquisition of a malignant phenotype characterized by apoptosis resistance, unregulated proliferation and differentiation, invasion, and metastatic abilities. However, neoplastic development and progression seem to be aided by non-neoplastic cells; the molecules they produced can either promote the immune response or, alternatively, support tumor pathogenesis. Consequently, the relative contribution of tumor-associated inflammatory pathways to cancer development has become crucial information. Interleukin-33 (IL-33) is an IL-1-like alarmin, and it is a ligand for the suppressor of tumorigenicity 2 (ST2) receptor. IL-33 functions as a dual role cytokine with the ability to induce T-helper-type 2 (Th2) immune cells and translocate into the nucleus, suppressing gene transcription. Although its function in immunity- and immune-related disorders is well known, its role in tumorigenesis is still debated. The IL-33/ST2 axis is emerging as a powerful modulator of the tumor microenvironment (TME) by recruiting immune cells, able to modify the TME, supporting malignant proliferation or improving antitumor immunity. In the present review, we discuss IL-33′s potential role in lung carcinogenesis and its possible application as a therapeutic target.

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“…The majority of lung cancers originate from epithelial cells and can be divided into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), morphologically. NSCLC is predominant type of lung cancer and accounts for about 85% of lung cancers (2). Although smoking is the primary cause of most lung cancer cases, approximately 10–15% are caused by genetics and other factors including nutritional factors (3).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Lung Tumor Development in ApoE Knockout Mice via Enhancement of TREM-1 Dependent NK Cell Cytotoxicity

et al. 2019

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Apolipoprotein E (ApoE) is known to regulate lipid homeostasis and associated with atherosclerogenesis. Eventhough atherosclerogenesis is associated with tumor development, the role of ApoE in lung tumorigenesis and metastasis is not clear. Thus, the tumor growth and metastasis were compared in WT and ApoE knockout (KO) mice. Urethane-induced lung tumor incidence and B16F10 lung metastasis in ApoE knockout (KO) mice were significantly reduced in comparison to that in WT mice. Knockdown of ApoE expression in lung cancer cells and B16F10 cells also decreased cancer cell growth and metastasis. The inhibitory effect of ApoE KO on tumor development and metastasis was associated with increase of infiltration of NK cells. NK cells derived from ApoE KO mice showed much greater cytotoxicity than those from WT mice. These cytotoxic effect of NK cells derived from ApoE KO mice was associated with higher expression of Granzyme B, Fas Ligand, IFN-γ, TNF-α, NKG2D, NKp46, and DNAM-1 expression. Triggering receptor expressed on myeloid cell (TREM)-1 is a proinflammatory mediator expressed on NK cells, and is known to be associated with NK cell cytotoxicity. Thus, we investigated the role of TREM-1 on ApoE KO mice originated NK cell mediated cytotoxicity for cancer cells. Blockade of TREM-1 expression with a TREM-1 antagonist prevented NK cell-mediated cytotoxicity. TREM-1 antibody recovered cytotoxic effect of NK cells derived from KO mice of T-bet, which upregulating gene for TREM-1. These data indicate that ApoE KO suppressed lung tumor development and metastasis via increase of TREM-1-dependent anti-tumor activity of NK cells.

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Epidermal Growth Factor Receptor Gene in Non-Small-Cell Lung Cancer: The Importance of Promoter Polymorphism Investigation

Cited by 46 publications

References 106 publications

A signature of 17 immune-related gene pairs predicts prognosis and immune status in HNSCC patients

A signature of 17 immune-related gene pairs predicts prognosis and immune status in HNSCC patients

Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update

Inhibition of Lung Tumor Development in ApoE Knockout Mice via Enhancement of TREM-1 Dependent NK Cell Cytotoxicity

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