Brain cancer immunoediting: novel examples provided by immunotherapy of malignant gliomas

Pellegatta, Serena; Cuppini, Lucia; Finocchiaro, Gaetano

doi:10.1586/era.11.102

Cited by 25 publications

(14 citation statements)

References 153 publications

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“…In the case of gliomas, several tumor vaccine strategies have been explored clinically. Although initial results are encouraging, the small studies precluded definitive proof of improvement in survival (17,18). The brain has been previously thought to be an immunologically privileged site, where no immunosurveillence occurs.…”

Section: Discussionmentioning

confidence: 99%

NY-ESO-1 Expression in Meningioma Suggests a Rationale for New Immunotherapeutic Approaches

Baía

Caballero

et al. 2013

Cancer Immunology Research

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Meningiomas are the most common primary intracranial tumors. Surgical resection remains the treatment of choice for these tumors. However, a significant number of tumors are not surgically accessible, recur, or become malignant, necessitating the repetition of surgery and sometimes radiation. Chemotherapy is rarely used and is generally not recognized as an effective treatment. Cancer/testis (CT) genes represent a unique class of genes, which are expressed by germ cells, normally silenced in somatic cells, but activated in various cancers. CT proteins can elicit spontaneous immune responses in patients with cancer and this feature makes them attractive targets for immunotherapy-based approaches. We analyzed mRNA expression of 37 testis-restricted CT genes in a discovery set of 18 meningiomas by reverse transcription PCR. The overall frequency of expression of CT genes ranged from 5.6% to 27.8%. The most frequently expressed was NY-ESO-1, in 5 patients (27.8%). We subsequently analyzed NY-ESO-1 protein expression in a larger set of meningiomas by immunohistochemistry and found expression in 108 of 110 cases. In some cases, NY-ESO-1 expression was diffused and homogenous, but in most instances it was heterogeneous. Importantly, NY-ESO-1 expression was positively correlated with higher grade and patients presenting with higher levels of NY-ESO-1 staining had significantly worse disease-free and overall survival. We have also shown that NY-ESO-1 expression may lead to humoral immune response in patients with meningioma. Considering the limited treatment options for patients with meningioma, the potential of NY-ESO-1-based immunotherapy should be explored. Cancer Immunol Res; 1(5); 296-302. Ó2013 AACR.

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Section: Discussionmentioning

confidence: 99%

NY-ESO-1 Expression in Meningioma Suggests a Rationale for New Immunotherapeutic Approaches

Baía

Caballero

et al. 2013

Cancer Immunology Research

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“…Indeed, in patients with colorectal carcinoma, it has been proposed that Tregs suppress pro-tumourigenic T helper type 17 (Th17) cell-driven responses against the gut microbiota [16], and a similar down-regulation of pro-tumourigenic inflammatory responses by Tregs has been proposed in head and neck squamous cell carcinoma [16,65]. Conversely, there is also clear evidence that Tregs in colorectal cancer suppress tumour-specific T cell responses, and increase the chance of recurrence after surgical resection [68]. Thus, the type and location of the tumour, and the inflammatory milieu within the tumour mass, may determine precisely how Tregs impact on tumour progression.…”

Section: Regulatory T Cells and Cancer Prognosismentioning

confidence: 96%

Suppression, subversion and escape: the role of regulatory T cells in cancer progression

Oļeiņika

Nibbs

Graham

et al. 2012

Clinical and Experimental Immunology

181

149

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SummaryRegulatory T cells (Tregs) are crucial in mediating immune homeostasis and promoting the establishment and maintenance of peripheral tolerance. However, in the context of cancer their role is more complex, and they are thought to contribute to the progress of many tumours. As cancer cells express both self-and tumour-associated antigens, Tregs are key to dampening effector cell responses, and therefore represent one of the main obstacles to effective anti-tumour responses. Suppression mechanisms employed by Tregs are thought to contribute significantly to the failure of current therapies that rely on induction or potentiation of anti-tumour responses. This review will focus on the current evidence supporting the central role of Tregs in establishing tumour-specific tolerance and promoting cancer escape. We outline the mechanisms underlying their suppressive function and discuss the potential routes of Tregs accumulation within the tumour, including enhanced recruitment, in-situ or local proliferation, and de-novo differentiation. In addition, we review some of the cancer treatment strategies that act, at least in part, to eliminate or interfere with the function of Tregs. The role of Tregs is being recognized increasingly in cancer, and controlling the function of these suppressive cells in the tumour microenvironment without compromising peripheral tolerance represents a significant challenge for cancer therapies.

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“…According to Ehrlich, the magic bullet is a compound that targets a single certain oncoprotein in a highly specifi c fashion and does not damage healthy cells 31 . Today, current research is focused on targeted molecular treatment alternatives.…”

Section: Discussionmentioning

confidence: 99%

In Vitroeffects of Selenium on Human Glioblastoma Multiforme Cell Lines: A Preliminary Study

Harmancı

Erbayraktar

Sayın

et al. 2017

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SUMMARY -Glioblastoma multiforme (GBM) is caused by the central nervous system-derived glial cells, and represents the most common (50%-60%) form of primary brain tumors. Th e aim of this study was to investigate the in vitro eff ects of selenium on human GBM cells. In the present study, GMS-10 and DBTRG-05MG human GBM cell lines were used as a model to examine selenium entering the cell, cell proliferation, cytotoxicity, DNA fragmentation and Ki-67 protein expression in selenomethionine treated and non-treated groups. Seleno-L-methionine (SeMet) as the organic source of selenium exerted eff ects on cell proliferation and cytotoxicity, as assessed with WST-1 and lactate dehydrogenase (LDH) tests, respectively. Apoptosis was assessed by DNA fragmentation with an enzyme-linked immunosorbent assay. Ki-67 protein expression was determined by Western blotting, while selenium measurements were performed in the supernatants and lysates by using Graphite Furnace Atomic Absorption Spectrometry. Th is is the fi rst study to examine the eff ects of SeMet on cell proliferation and death in GMS-10 and DBTRG-05MG cells. Both GBM cell lines responded to SeMet in a dose-and time-dependent manner. WST-1 test showed that low-dose SeMet treatment (50 and 100 μM) increased cell proliferation. Analysis of intracellular SeMet levels by using AAS showed results consistent with viability and cytotoxicity tests. SeMet treatment for 72 h caused increased DNA fragmentation in both cell lines. In conclusion, our results suggest that SeMet induces cell death at high doses, while increasing cell proliferation at low doses. In the view of the data obtained in this investigation, further studies focusing on the possibility of using SeMet against different types of GBM and in combination with prospect synergic compounds are considered to be worthwhile.

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Brain cancer immunoediting: novel examples provided by immunotherapy of malignant gliomas

Cited by 25 publications

References 153 publications

NY-ESO-1 Expression in Meningioma Suggests a Rationale for New Immunotherapeutic Approaches

NY-ESO-1 Expression in Meningioma Suggests a Rationale for New Immunotherapeutic Approaches

Suppression, subversion and escape: the role of regulatory T cells in cancer progression

In Vitroeffects of Selenium on Human Glioblastoma Multiforme Cell Lines: A Preliminary Study

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