Lung Cancer: A Classic Example of Tumor Escape and Progression While Providing Opportunities for Immunological Intervention

Jadus, Martin R.; Natividad, Josephine; Mai, Anthony; Ouyang, Yi; Lambrecht, Nils; Szabó, Sándor; Ge, Lisheng; Hoa, Neil; Dacosta-Iyer, Maria

doi:10.1155/2012/160724

Cited by 42 publications

(42 citation statements)

References 210 publications

(190 reference statements)

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“…The interaction between PD-1 on T lymphocytes with PD-L1 expressed on the surface of tumor cells inhibits the activation of effector T cells and induces FasL and the immunosuppressive cytokine interleukin (IL)-10. PD-L1 is expressed in many tumor cells of distinct origin and at a high frequency on BC cells [60] and circulating tumor cells [61]. Inhibition of PD-L1 significantly blocks T-cell apoptosis in tumor models [61,62].…”

Section: Expression Of Co-inhibitory Moleculesmentioning

confidence: 99%

The Role of Immune Escape and Immune Cell Infiltration in Breast Cancer

2018

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While detailed analysis of aberrant cancer cell signaling pathways and changes in cancer cell DNA has dominated the field of breast cancer biology for years, there now exists increasing evidence that the tumor microenvironment (TME) including tumor-infiltrating immune cells support the growth and development of breast cancer and further facilitate invasion and metastasis formation as well as sensitivity to drug therapy. Furthermore, breast cancer cells have developed different strategies to escape surveillance from the adaptive and innate immune system. These include loss of expression of immunostimulatory molecules, gain of expression of immunoinhibitory molecules such as PD-L1 and HLA-G, and altered expression of components involved in apoptosis. Furthermore, the composition of the TME plays a key role in breast cancer development and treatment response. In this review we will focus on i) the different immune evasion mechanisms used by breast cancer cells, ii) the role of immune cell infiltration in this disease, and (iii) implication for breast cancer-based immunotherapies.

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Section: Expression Of Co-inhibitory Moleculesmentioning

confidence: 99%

The Role of Immune Escape and Immune Cell Infiltration in Breast Cancer

2018

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“…Mutations of the TGF-β-receptor, Smad signal transduction pathway genes, and TGF-β-inducible gene-h3 were associated with reduced p53 expression, ovarian cancer risk, and paclitaxel resistance respectively [335][336][337]. On the contrary, some polymorphisms of TGF gene make individuals less prone to development of lung cancer (reviewed in [338]). The source of TGF-β could be both tumor cells and M2-type TAMs [220].…”

Section: Inflammation and Cancer Escapementioning

confidence: 99%

“…Lung cancers overexpress TGF-β, and are characterized by several mutations of TGF-β receptors, which prevents cancer cells from negative autocrine regulation of growth by this cytokine. As a result, high TGF-β concentration produces a suppressory environment inside the tumor (reviewed in [338]). In advanced tumors, TGF-β is engaged in Th17 cell differentiation, inhibition of DCs maturation, stimulation of VEGF production, generating the CD4 + CD25 + Foxp3 + Tregs, and decreasing activity of NKT, T CD8 + , and NK cytotoxic cells.…”

Section: Inflammation and Cancer Escapementioning

confidence: 99%

“…Squamous, adenocarcinoma, and small-cell lung cancers are able to produce prostaglandin E 2 , and express a variety of prostaglandin receptors. PGE 2 functions as a stimulator of lung cancer growth by augmenting angiogenesis and proliferation, and simultaneously inhibits T and NK effector cells (reviewed in [338]). Peroxisome proliferator-activated receptor-γ (PPARγ) is an inhibitor of COX-dependent inflammatory reaction, and in mouse studies produced a decrease of PGE 2 levels, reduction of MVD, enhanced tumor apoptosis and improved mice survival [362].…”

Section: Inflammation and Cancer Escapementioning

confidence: 99%

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Cancer Immunoediting: Elimination, Equilibrium, and Immune Escape in Solid Tumors

Wilczyński

Nowak

2013

Interaction of Immune and Cancer Cells

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Emphasizing the dynamic processes between cancer and host immune system, the initially discovered concept of cancer immunosurveillance has been replaced by the current concept of cancer immunoediting consisting of three phases: elimination, equilibrium, and escape. Solid tumors composed of both cancer and host stromal cells are an example of how the three phases of cancer immunoediting functionally evolve, and how a tumor shaped by the host immune system gets a finally resistant phenotype. Elimination, equilibrium, and escape are described in this chapter in detail, including the role of immune surveillance, cancer dormancy, disruption of the antigen-presenting machinery, tumor-infiltrating immune cells, and resistance to apoptosis, as well as the function of tumor stroma, microvesicles, exosomes and inflammation.

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“…Worldwide, lung cancer is the primary cause of cancerrelated death, accounting for approximately 12.5% of newly diagnosed cancers (World Cancer Research Foundation International) and 1.3 million deaths worldwide each year (Jadus et al, 2012). Unfortunately, there are no effective therapies for lung cancer, and there has been little change in the overall 5-year survival rate since the 1970s (Marshall 2011).…”

Section: Introductionmentioning

confidence: 99%

Fused Polypeptide with DEF Induces Apoptosis of Lung Adenocarcinoma Cells

Liang

Zhang²,

Zhou³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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To analyze the effects of a new unknown peptide DEF on the growth of tumor cells, a fused polypeptide TAT-DV1-DEF was designed and synthesized. The lung adenocarcinoma cell line GLC-82 treated with TAT-DV1-DEF was analyzed with a cell counting kit 8, and the location of polypeptides in cells was observed under laser confocal microscopy. The efficiency of polypeptide transfection and changes in nuclear morphology were analyzed by flow cytometry and fluorescence microscopy, respectively. Finally, the mechanism of tumor cell growth inhibition was evaluated by Western blotting. We found that TAT-DV1-DEF could significantly inhibit the growth of the lung adenocarcinoma cell line GLC-82, but not the normal human embryonic kidney cell line HEK-293. Polypeptides were found to be mostly localized in the cytoplasm and some mitochondria. The efficiency of polypeptide transfection in the two cell types was approximately 99%. Apoptotic nuclei were observed under fluorescence microscopy upon treatment with polypeptides and DAPI staining. Western blot analyses indicated that the polypeptide inhibition of tumor cell growth was apoptosis dependent. In the present study, we demonstrated that fused polypeptides could induce apoptosis of the lung adenocarcinoma cell line GLC-82, indicating that the new unknown peptide DEF has antitumor effects.

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Lung Cancer: A Classic Example of Tumor Escape and Progression While Providing Opportunities for Immunological Intervention

Cited by 42 publications

References 210 publications

The Role of Immune Escape and Immune Cell Infiltration in Breast Cancer

The Role of Immune Escape and Immune Cell Infiltration in Breast Cancer

Cancer Immunoediting: Elimination, Equilibrium, and Immune Escape in Solid Tumors

Fused Polypeptide with DEF Induces Apoptosis of Lung Adenocarcinoma Cells

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