The effects of interleukin 2 and rAd-p53 as a treatment for glioblastoma

Qiao, Haibo; Li, Jia; Lv, Lian‐Jie; Nie, Ben‐Jin; Lu, Peng; Xue, Feng; Zhang, Zhiming

doi:10.3892/mmr.2018.8408

Cited by 8 publications

(9 citation statements)

References 35 publications

(38 reference statements)

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“…Inhibiting the MDM2-p73 interaction activated the p73-driven expression of the proapoptotic gene Bim and subsequent apoptosis [ 185 ]. Therefore, developing therapeutic strategies that would selectively activate p53 but not p73, would help induce cell death in tumour cells, sparing the T cells from elimination and contributing to the overall anticancer immune response [ 186 ].…”

Section: Tumour-promoting Inflammation and Evading Immune Destructionmentioning

confidence: 99%

Dual Role of p73 in Cancer Microenvironment and DNA Damage Response

Rozenberg

Zvereva

Dalina

et al. 2021

Cells

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Understanding the mechanisms that regulate cancer progression is pivotal for the development of new therapies. Although p53 is mutated in half of human cancers, its family member p73 is not. At the same time, isoforms of p73 are often overexpressed in cancers and p73 can overtake many p53 functions to kill abnormal cells. According to the latest studies, while p73 represses epithelial–mesenchymal transition and metastasis, it can also promote tumour growth by modulating crosstalk between cancer and immune cells in the tumor microenvironment, M2 macrophage polarisation, Th2 T-cell differentiation, and angiogenesis. Thus, p73 likely plays a dual role as a tumor suppressor by regulating apoptosis in response to genotoxic stress or as an oncoprotein by promoting the immunosuppressive environment and immune cell differentiation.

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Section: Tumour-promoting Inflammation and Evading Immune Destructionmentioning

confidence: 99%

Dual Role of p73 in Cancer Microenvironment and DNA Damage Response

Rozenberg

Zvereva

Dalina

et al. 2021

Cells

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“… 36 Considering its dual role, we cannot reliably use the IL-10 secretion level as a marker to assess the efficacy of glioma treatment. In contrast, IL-2, known to induce anticancer effects such as T-cell proliferation and trigger innate and adaptive immunity, 39 , 40 can be used to assess the efficacy of the vaccine. IL-2 levels increased in the vaccine-, thymosin-, and combined-treatment groups, indicating the effectiveness of all three treatments.…”

Section: Discussionmentioning

confidence: 99%

<p>A Hybrid Glioma Tumor Cell Lysate Immunotherapy Vaccine Demonstrates Good Clinical Efficacy in the Rat Model</p>

Li¹,

Zeng²,

He³

et al. 2020

OTT

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Background: Conventional immunotherapy for glioma is not only expensive but also demonstrates less-than-desired clinical efficacy. In this study, we evaluated the immunotherapeutic efficacy of a tumor cell lysate-based hybrid glioma vaccine developed using a molecular-based approach. Methods: First, the ability of the autologous (9L-cell lysate) and allogeneic (C6-cell lysate) vaccines against glioma, individually and in combination, to activate Fischer344 rat dendritic cells (DCs) was determined. Next, the activated DCs were co-cultured with T lymphocytes and screened for the optimal DC-toT cell ratio. The in vitro efficacy of the DC/T-cell vaccine formulations subjected to different immunogen treatments and co-cultured with glioma cells was evaluated based on glioma cell viability and monocyte chemoattractant protein (MCP)-2 and interferon (IFN)-γ secretion. Subsequently, the efficacy of the 9L + C6 hybrid vaccine was evaluated in 32 glioma rat models, randomly allocated to the following five treatment groups: blank control, tumor, vaccine treatment, thymosin treatment, and vaccine + thymosin treatment (combined treatment). Changes in survival duration, intracranial tumor volume, peripheral blood immune-cell (CD4+ T, CD8+ T, and natural killer [NK] cell) count, and serum cytokine (interleukin [IL]-2, IL-10) levels were assessed in these groups. Results: The hybrid vaccine demonstrated the highest glioma cell apoptosis and the lowest cell viability and promoted MCP-2 and IFN-γ secretion in vitro. The vaccine treatment and combined treatment groups demonstrated longer survival duration, lower intracranial tumor volume, and higher immune cell glioma tissue infiltration and IL-2 secretion than the untreated tumor group, indicating the vaccine's good in vivo efficacy. Thymosin treatment had minimal effect in enhancing anti-glioma immunity. Conclusion: We demonstrated the feasibility of combining autologous and allogeneic tumor cell lysates to stimulate specific host cell immune response against glioma cells. The good clinical efficacy of our developed glioma hybrid vaccine in rat models suggests its potential clinical application.

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“…Moreover, IL-2 can also be used during the ex vivo expansion of NK cells [164], or after the adoptive NK cell transfer, in an effort to improve the survival and function of these cells in vivo [158,201,[273][274][275]. For the GBM therapy, studies such as those conducted by Colombo et al (2005) [276] and Qiao et al (2018) [277] evaluated the combination of IL-2 with other therapeutic strategies, but mainly focusing on the effect promoted on T cells. Clinical studies involving the combination with other therapeutic strategies-such as expression of IL-13, resistance to glucocorticoids, and stem cell transplantation-have also been conducted for the treatment of brain tumors (NCT01082926, NCT00014573).…”

Section: Cytokine Therapymentioning

confidence: 99%

The War Is on: The Immune System against Glioblastoma—How Can NK Cells Drive This Battle?

et al. 2022

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Natural killer (NK) cells are innate lymphocytes that play an important role in immunosurveillance, acting alongside other immune cells in the response against various types of malignant tumors and the prevention of metastasis. Since their discovery in the 1970s, they have been thoroughly studied for their capacity to kill neoplastic cells without the need for previous sensitization, executing rapid and robust cytotoxic activity, but also helper functions. In agreement with this, NK cells are being exploited in many ways to treat cancer. The broad arsenal of NK-based therapies includes adoptive transfer of in vitro expanded and activated cells, genetically engineered cells to contain chimeric antigen receptors (CAR-NKs), in vivo stimulation of NK cells (by cytokine therapy, checkpoint blockade therapies, etc.), and tumor-specific antibody-guided NK cells, among others. In this article, we review pivotal aspects of NK cells’ biology and their contribution to immune responses against tumors, as well as providing a wide perspective on the many antineoplastic strategies using NK cells. Finally, we also discuss those approaches that have the potential to control glioblastoma—a disease that, currently, causes inevitable death, usually in a short time after diagnosis.

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The effects of interleukin 2 and rAd-p53 as a treatment for glioblastoma

Cited by 8 publications

References 35 publications

Dual Role of p73 in Cancer Microenvironment and DNA Damage Response

Dual Role of p73 in Cancer Microenvironment and DNA Damage Response

<p>A Hybrid Glioma Tumor Cell Lysate Immunotherapy Vaccine Demonstrates Good Clinical Efficacy in the Rat Model</p>

The War Is on: The Immune System against Glioblastoma—How Can NK Cells Drive This Battle?

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