2024
DOI: 10.1016/j.redox.2023.102991
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Cold atmospheric plasma sensitizes head and neck cancer to chemotherapy and immune checkpoint blockade therapy

Yanhong Wang,
Xinyu Mang,
Danni Li
et al.
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Cited by 9 publications
(7 citation statements)
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“…22 Previously, SGLT2I was proposed as an potential anti-tumour agents since sodium-glucose cotransporter 2 was over-expressed in multiple tumour models, including head and neck cancer. 23, 24 In this study, we found that SGLT2I was associated with lower risk of NPC compared to DPP4I.…”
Section: Discussionmentioning
confidence: 51%
“…22 Previously, SGLT2I was proposed as an potential anti-tumour agents since sodium-glucose cotransporter 2 was over-expressed in multiple tumour models, including head and neck cancer. 23, 24 In this study, we found that SGLT2I was associated with lower risk of NPC compared to DPP4I.…”
Section: Discussionmentioning
confidence: 51%
“…Inhibiting HO1 activity or Nrf2/HO1 gene silencing results in significantly greater apoptosis by CP [123]. Therefore, Nrf2/HO1 inhibition and CP adjunct therapy could synergise as a cancer therapy, similar to HO1 inhibition improving conventional chemo/radiotherapy and reducing tumour growth [173], or synergistic activity of CP with chemo/radiotherapy in vitro and in vivo [124,130,[174][175][176][177][178][179][180]. Unfortunately, the absence of clinically safe HO1 inhibitors currently precludes testing, but may be grounds for future clinical research.…”
Section: Keap1-nrf2-antioxidant Response Pathwaysmentioning
confidence: 99%
“…Regardless, both of these studies showed that CP induced JNK and p38 activity to slow tumour growth, but CP therapy alone was not effective enough to halt tumour progression. Fortunately, mouse xenografted tumour models have shown that combination therapy of CP/PAL and chemotherapeutic drugs can synergistically reduce tumour growth rate and even lead to tumour size reduction [124,130,177,179,180]. However, more animal models that test adjunct CP treatment with chemotherapy against progressive tumours are warranted to determine parameters for CP-augmenting chemotherapies before progressing to clinical trials.…”
Section: Mapk Inducing Cancer Cell Deathmentioning
confidence: 99%
“…Inhibiting HO1 activity or Nrf2/HO1 gene silencing results in significantly greater apoptosis by CP [138]. Therefore, Nrf2/HO1 inhibition and CP adjunct therapy could synergise as a cancer therapy, similar to HO1 inhibition improving conventional chemo/radiotherapy and reducing tumour growth [187], or synergistic activity of CP with chemo/radiotherapy in vitro and in vivo [139,145,[188][189][190][191][192][193][194]. Unfortunately, the absence of clinically safe HO1 inhibitors currently precludes testing, but may be grounds for future clinical research.…”
Section: Keap1-nrf2-antioxidant Response Pathwaysmentioning
confidence: 99%
“…Regardless, both of these studies showed that CP induced JNK and p38 activity to slow tumour growth, but CP therapy alone was not effective enough to halt tumour progression. Fortunately, mouse xenografted tumour models have shown that combination therapy of CP/PAL and chemotherapeutic drugs can synergistically reduce tumour growth rate and even lead to tumour size reduction [139,145,191,193,194]. However, more animal models that test adjunct CP treatment with chemotherapy against progressive tumours are warranted to determine parameters for CP-augmenting chemotherapies before progressing to clinical trials.…”
Section: Mapk Inducing Cancer Cell Deathmentioning
confidence: 99%