“…Since miR146a inhibited the NF-ĸB proinflammatory pathway, lower miR146s led to increased IL-8 expression on EV surfaces [ 58 ]. To assess the effect of IL-8 on immune checkpoint inhibitor [ 59 , 60 , 61 ] resistance, the researchers measured plasma IL-8 levels before and after nivolumab treatment in patients with head and neck SCC, and they found that high circulating IL-8 levels were associated with low responsiveness to immunotherapy. In their follow-up study, Flemming et al [ 40 ] found that increased Dsg2 expression on cSCC-derived EVs was associated with lower EV density.…”
Cutaneous squamous cell carcinoma (cSCC) as one of the most prevalent cancers worldwide is associated with significant morbidity and mortality. Full-body skin exam and biopsy is the gold standard for cSCC diagnosis, but it is not always feasible given constraints on time and costs. Furthermore, biopsy fails to reflect the dynamic changes in tumor genomes, which challenges long-term medical treatment in patients with advanced diseases. Extracellular vesicle (EV) is an emerging biological entity in oncology with versatile clinical applications from screening to treatment. In this systematic review, pre-clinical and clinical studies on cSCC-derived EVs were summarized. Seven studies on the genomics, transcriptomics, and proteomics of cSCC-derived EVs were identified. The contents in cSCC-derived EVs may reflect the mutational landscape of the original cancer cells or be selectively enriched in EVs. Desmoglein 2 protein (Dsg2) is an important molecule in the biogenesis of cSCC-derived EVs. Ct-SLCO1B3 mRNA, and CYP24A1 circular RNA (circRNA) are enriched in cSCC-derived EVs, suggesting potentials in cSCC screening and diagnosis. p38 inhibited cSCC-associated long intergenic non-coding RNA (linc-PICSAR) and Dsg2 involved in EV-mediated tumor invasion and drug resistance served as prognostic and therapeutic predictors. We also proposed future directions to devise EV-based cSCC treatment based on these molecules and preliminary studies in other cancers.
“…Since miR146a inhibited the NF-ĸB proinflammatory pathway, lower miR146s led to increased IL-8 expression on EV surfaces [ 58 ]. To assess the effect of IL-8 on immune checkpoint inhibitor [ 59 , 60 , 61 ] resistance, the researchers measured plasma IL-8 levels before and after nivolumab treatment in patients with head and neck SCC, and they found that high circulating IL-8 levels were associated with low responsiveness to immunotherapy. In their follow-up study, Flemming et al [ 40 ] found that increased Dsg2 expression on cSCC-derived EVs was associated with lower EV density.…”
Cutaneous squamous cell carcinoma (cSCC) as one of the most prevalent cancers worldwide is associated with significant morbidity and mortality. Full-body skin exam and biopsy is the gold standard for cSCC diagnosis, but it is not always feasible given constraints on time and costs. Furthermore, biopsy fails to reflect the dynamic changes in tumor genomes, which challenges long-term medical treatment in patients with advanced diseases. Extracellular vesicle (EV) is an emerging biological entity in oncology with versatile clinical applications from screening to treatment. In this systematic review, pre-clinical and clinical studies on cSCC-derived EVs were summarized. Seven studies on the genomics, transcriptomics, and proteomics of cSCC-derived EVs were identified. The contents in cSCC-derived EVs may reflect the mutational landscape of the original cancer cells or be selectively enriched in EVs. Desmoglein 2 protein (Dsg2) is an important molecule in the biogenesis of cSCC-derived EVs. Ct-SLCO1B3 mRNA, and CYP24A1 circular RNA (circRNA) are enriched in cSCC-derived EVs, suggesting potentials in cSCC screening and diagnosis. p38 inhibited cSCC-associated long intergenic non-coding RNA (linc-PICSAR) and Dsg2 involved in EV-mediated tumor invasion and drug resistance served as prognostic and therapeutic predictors. We also proposed future directions to devise EV-based cSCC treatment based on these molecules and preliminary studies in other cancers.
“…The presence of comorbidities was determined using ICD-9-CM or ICD-10-CM codes based on one inpatient visit or two or more outpatient visits. In addition to these factors, we also considered Epstein-Barr virus and human papillomavirus infection, as well as the indications for H1-antihistamine use (e.g., asthma, dermatitis, rhinitis, and urticaria) [22,23].…”
This study aimed to examine the association between the use of H1-antihistamines (AHs) and head and neck cancer (HNC) risk in patients with type 2 diabetes mellitus (T2DM). Data from the National Health Insurance Research Database of Taiwan were analyzed for the period from 2008 to 2018. A propensity-score-matched cohort of 54,384 patients each in the AH user and nonuser groups was created and analyzed using Kaplan-Meier method and Cox proportional hazards regression. The results showed that the risk of HNC was significantly lower in AH users (adjusted hazard ratio: 0.55, 95% CI: 0.48 to 0.64) and the incidence rate was also lower (5.16 vs. 8.10 per 100,000 person-years). The lower HNC incidence rate in AH users (95% CI: 0.63; 0.55 to 0.73) suggests that AH use may reduce the risk of HNC in T2DM patients.
“…In addition to novel drug discovery, repurposing existing drugs for new indications has become a cost‐effective strategy that can potentially improve the survival outcomes of cancer patients. 2 , 3 , 4 , 5 , 6 , 7 …”
Section: Introductionmentioning
confidence: 99%
“…It is therefore imperative to develop strategies to augment and improve the response to ICI treatment. In addition to novel drug discovery, repurposing existing drugs for new indications has become a cost‐effective strategy that can potentially improve the survival outcomes of cancer patients 2–7 …”
Section: Introductionmentioning
confidence: 99%
“…In addition to novel drug discovery, repurposing existing drugs for new indications has become a cost-effective strategy that can potentially improve the survival outcomes of cancer patients. [2][3][4][5][6][7] Accumulating evidence from previous studies showed a trend of better survival outcomes in ICI patients who were concomitantly treated with certain medications, such as renin-angiotensin-aldosterone system inhibitors (RAASi). 3,[7][8][9][10][11] Experimental studies have shown that the renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating the immune response against tumor cells.…”
Background
Certain angiotensin receptor blockers (ARBs) have peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) activation property, which has been associated with improved programmed cell death ligand 1 blockade and cytotoxic T lymphocyte‐mediated antitumor activity.
Methods
We conducted a retrospective cohort study to investigate the impact of PPAR‐γ‐activating ARBs on patient survival in patients treated with immune checkpoint inhibitors (ICIs) across all types of cancers.
Results
A total of 167 patients receiving both angiotensin receptor blockers (ARBs) and immune checkpoint inhibitors (ICIs) were included. Compared with non‐PPAR‐γ‐ARB users (
n
= 102), PPAR‐γ‐ARB users (
n
= 65) had a longer median overall survival (not reached [IQR, 16.0—not reached] vs. 18.6 [IQR, 6.1–38.6] months) and progression‐free survival (17.3 [IQR, 5.1—not reached] vs. 8.2 [IQR, 2.4–18.6] months). In Cox regression analysis, the use of PPAR‐γ‐activating ARBs had an approximately 50% reduction in all‐cause mortality and disease progression. Patients who received PPAR‐γ‐activating ARBs also had higher clinical benefit rates than non‐PPAR‐γ‐ARB users (82% vs. 61%,
p
= 0.005).
Conclusion
The use of ARBs with PPAR‐γ‐activating property is linked with better survival among patients receiving ICIs.
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