Immunotherapy with Monoclonal Antibodies in Lung Cancer of Mice: Oxidative Stress and Other Biological Events

Tang, Jun; Ramis-Cabrer, Daniel; Wang, Xuejie; Barreiro, Esther

doi:10.3390/cancers11091301

Cited by 13 publications

(7 citation statements)

References 55 publications

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“…Treatment-induced reduction in tumor burden is associated with decreased tumor proliferation but increased oxidative stress, apoptosis, autophagy, and T cell infiltration. The data suggest that treatment with therapeutic antibodies may induce oxidative stress that drives cell cycle arrest and tumor cell death [ 167 ].…”

Section: The Impact Of Cancer Immunotherapies On Oxidative Stress mentioning

confidence: 99%

Oxidative Stress in the Tumor Microenvironment and Its Relevance to Cancer Immunotherapy

Aboelella

Brandle

Kim

et al. 2021

Cancers

100

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It has been well-established that cancer cells are under constant oxidative stress, as reflected by elevated basal level of reactive oxygen species (ROS), due to increased metabolism driven by aberrant cell growth. Cancer cells can adapt to maintain redox homeostasis through a variety of mechanisms. The prevalent perception about ROS is that they are one of the key drivers promoting tumor initiation, progression, metastasis, and drug resistance. Based on this notion, numerous antioxidants that aim to mitigate tumor oxidative stress have been tested for cancer prevention or treatment, although the effectiveness of this strategy has yet to be established. In recent years, it has been increasingly appreciated that ROS have a complex, multifaceted role in the tumor microenvironment (TME), and that tumor redox can be targeted to amplify oxidative stress inside the tumor to cause tumor destruction. Accumulating evidence indicates that cancer immunotherapies can alter tumor redox to intensify tumor oxidative stress, resulting in ROS-dependent tumor rejection. Herein we review the recent progresses regarding the impact of ROS on cancer cells and various immune cells in the TME, and discuss the emerging ROS-modulating strategies that can be used in combination with cancer immunotherapies to achieve enhanced antitumor effects.

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Section: The Impact Of Cancer Immunotherapies On Oxidative Stress mentioning

confidence: 99%

Oxidative Stress in the Tumor Microenvironment and Its Relevance to Cancer Immunotherapy

Aboelella

Brandle

Kim

et al. 2021

Cancers

100

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“…Another fragment was frozen immediately in liquid nitrogen and preserved at −80 • C for the measurement of protein levels. [37] using conventional immunohistochemistry as previously described [10,38]. Briefly, paraffin-embedded specimens were cut into three-micrometer sections on a microtome.…”

Section: Collection and Preservation Of Samplesmentioning

confidence: 99%

Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Tang

Curull

Wang

et al. 2020

Cancers

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(1) Background: Lung cancer (LC) is a major leading cause of death worldwide. Poly (ADP-ribose) polymerase (PARP)-1 and PARP-2 are key players in cancer. We aimed to assess PARP-1 and PARP-2 expression and activity and DNA damage in tumors and non-tumor lungs from patients with/without chronic obstructive pulmonary disease (COPD). (2) Methods: Lung tumor and non-tumor specimens were obtained through video-assisted thoracoscopic surgery (VATS) in LC patients with/without underlying COPD (two groups of patients, n = 15/group). PARP-1 and PARP-2 expression (ELISA), PARP activity (PARP colorimetric assay kit) and DNA damage (immunohistochemistry) levels were identified in all samples. (3) Results: Both PARP-1 and PARP-2 expression levels were significantly lower in lung tumors (irrespective of COPD)compared to non-tumor specimens, while DNA damage and PARP activity levels significantly increased in lung tumors compared to non-tumor specimens only in LC-COPD patients. PARP-2 expression was positively correlated with smoking burden in LC-COPD patients. (4) Conclusions: In lung tumors of COPD patients, an overactivation of PARP enzyme was observed. A decline in PARP-1 and PARP-2 protein expression was seen in lung tumors irrespective of COPD. Other phenotypic features (airway obstruction) beyond cancer may account for the increase in PARP activity seen in the tumors of patients with underlying COPD.

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“…At present, the interaction between immune checkpoints and oxidative stress has barely been studied. Tang et al found that treatment with a cocktail of immune checkpoint antibodies increased oxidative stress and T cell in ltration in lung adenocarcinoma [33]. Our data identi ed various immune checkpoints that have a positive correlation with risk scores, among which PD1, PD-L1, and CTLA4 are common targets for ICI therapy in clinical application.…”

Section: Discussionmentioning

confidence: 53%

An Oxidative Stress Response Gene Model for the Prediction of Prognosis and Therapeutic Responses in Hepatocellular Carcinoma

Hong

Cai

2021

Preprint

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BackgroundOxidative stress response genes are critical for the development and progression of hepatocellular carcinoma (HCC). Still, the predictive value for prognosis and treatment response of oxidative stress response genes needs further elucidation. MethodsWe obtained the transcriptomic data and corresponding clinicopathological information of HCC patients from The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) databases. Oxidative stress response genes (OSRGs) were retrieved from the MSigDB database. LASSO Cox regression analysis was utilized to establish an integrated multi-gene signature in the TCGA cohort, and its prediction performance was validated in the ICGC cohort. The risk score of each patient ware determined by the multi-gene signature. The CIBERSORT algorithm was employed to evaluate the immune cell infiltration. Response rate to immune checkpoint inhibition (ICI) therapy was assessed using a TIDE platform. Tumor mutation burden was estimated using VarScan processed somatic mutation data. The drug activity data from the Cancer Genome Project and NCI-60 human cancer cell lines were used to predict sensitivity to chemotherapy. ResultsThe gene signature comprises G6PD, MT3, CBX2, CDKN2B, CCNA2, MAPT, EZH2, and SLC7A11. Patients with high risk scores had shorter overall survival. The risk score was identified as an independent prognostic marker. The immune cell infiltration patterns, response rates to immune checkpoint inhibition (ICI) therapy, and the estimated sensitivity of 89 chemotherapeutic drugs were associated with risk scores. Individual prognostic gene was also associated with the susceptibility of various FDA-approved drugs. ConclusionOur study indicates that an integrated transcriptomic analysis may provide a reliable molecular model that better predicts diagnosis and forecasts the response of ICI therapy and chemotherapy.

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Immunotherapy with Monoclonal Antibodies in Lung Cancer of Mice: Oxidative Stress and Other Biological Events

Cited by 13 publications

References 55 publications

Oxidative Stress in the Tumor Microenvironment and Its Relevance to Cancer Immunotherapy

Oxidative Stress in the Tumor Microenvironment and Its Relevance to Cancer Immunotherapy

Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

An Oxidative Stress Response Gene Model for the Prediction of Prognosis and Therapeutic Responses in Hepatocellular Carcinoma

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