Non-steroidal anti-inflammatory agents to induce regression and prevent the progression of cervical intraepithelial neoplasia

Grabosch, Shannon; Shariff, Osman M; Wulff, Judith L; Helm, C. William

doi:10.1002/14651858.cd004121.pub3

Cited by 19 publications

(7 citation statements)

References 49 publications

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“…However, the efficacy of anti‐inflammation therapies in inhibition of postoperative tumor progression remains unclear. For example, Elecoxib, a COX2‐specific inhibitor, did not significantly affect apoptosis in prostate, and breast cancer as well as cervical intraepithelial neoplasia 142,148,149 . Similarly, intraoperative use of a single dose of parecoxib, another NSAIDs drug, was not associated with decreased cancer recurrence after bladder cancer surgery 150 …”

Section: Potential Therapeutic Strategiesmentioning

confidence: 99%

Surgical trauma‐induced immunosuppression in cancer: Recent advances and the potential therapies

Tang

Tie

et al. 2020

Clinical & Translational Med

105

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Surgical resection remains the mainstay treatment for solid cancers, especially for localized disease. However, the postoperative immunosuppression provides a window for cancer cell proliferation and awakening dormant cancer cells, leading to rapid recurrences or metastases. This immunosuppressive status after surgery is associated with the severity of surgical trauma since immunosuppression induced by minimally invasive surgery is less than that of an extensive open surgery. The systemic response to tissue damages caused by surgical operations and the subsequent wound healing induced a cascade alteration in cellular immunity. After surgery, patients have a high level of circulating damage‐associated molecular patterns (DAMPs), triggering a local and systemic inflammation. The inflammatory metrics in the immediate postoperative period was associated with the prognosis of cancer patients. Neutrophils provide the first response to surgical trauma, and the production of neutrophil extracellular traps (NETs) promotes cancer progression. Activated macrophage during wound healing presents a tumor‐associated phenotype that cancers can exploit for their survival advantage. In addition, the amplification and activation of myeloid‐derived suppressor cells (MDSCs), regulatory T cells (Tregs) or the elevated programmed death ligand‐1 and vascular endothelial growth factor expression under surgical trauma, exacerbate the immunosuppression and favor of the formation of the premetastatic niche. Therapeutic strategies to reduce the cellular immunity impairment after surgery include anti‐DAMPs, anti‐postoperative inflammation or inflammatory/pyroptosis signal, combined immunotherapy with surgery, antiangiogenesis and targeted therapies for neutrophils, macrophages, MDSCs, and Tregs. Further, the application of enhanced recovery after surgery also has a feasible outcome for postoperative immunity restoration. Overall, current therapies to improve the cellular immunity under the special condition after surgery are relatively lacking. Further understanding the underlying mechanisms of surgical trauma‐related immunity dysfunction, phenotyping the immunosuppressive cells, and developing the related therapeutic intervention should be explored.

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Section: Potential Therapeutic Strategiesmentioning

confidence: 99%

Surgical trauma‐induced immunosuppression in cancer: Recent advances and the potential therapies

Tang

Tie

et al. 2020

Clinical & Translational Med

105

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“…Human papilloma virus (HPV) infection of the cervical epithelium is well regarded as the main cause of cervical cancer [83], and a link between HPV E6 and E7 oncoproteins and COX-2 transcription has been established [84,85]. However, current data supporting a benefit for NSAIDs in the treatment of cervical intraepithelial neoplasia—the premalignant cervical lesion—are uncertain [86]. COX-1 up-regulation in cervical carcinoma was reported more than 10 years ago, and COX-1-dependent autocrine/paracrine regulation of COX-2, PGE 2 receptors, and angiogenic factors was demonstrated in vitro [87].…”

Section: Cox-1 Involvement In Neoplastic Diseasesmentioning

confidence: 99%

Cyclooxygenase-1 (COX-1) and COX-1 Inhibitors in Cancer: A Review of Oncology and Medicinal Chemistry Literature

2018

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Prostaglandins and thromboxane are lipid signaling molecules deriving from arachidonic acid by the action of the cyclooxygenase isoenzymes COX-1 and COX-2. The role of cyclooxygenases (particularly COX-2) and prostaglandins (particularly PGE2) in cancer-related inflammation has been extensively investigated. In contrast, COX-1 has received less attention, although its expression increases in several human cancers and a pathogenetic role emerges from experimental models. COX-1 and COX-2 isoforms seem to operate in a coordinate manner in cancer pathophysiology, especially in the tumorigenesis process. However, in some cases, exemplified by the serous ovarian carcinoma, COX-1 plays a pivotal role, suggesting that other histopathological and molecular subtypes of cancer disease could share this feature. Importantly, the analysis of functional implications of COX-1-signaling, as well as of pharmacological action of COX-1-selective inhibitors, should not be restricted to the COX pathway and to the effects of prostaglandins already known for their ability of affecting the tumor phenotype. A knowledge-based choice of the most appropriate tumor cell models, and a major effort in investigating the COX-1 issue in the more general context of arachidonic acid metabolic network by using the systems biology approaches, should be strongly encouraged.

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“…3 Several studies have suggested that some drugs can prevent CIN, but the clinical efficacy of such drugs remains controversial. 70,71 In recent years, studies have found that alprostadil can prevent CIN in patients undergoing CAG/PCI. 30…”

Section: Discussionmentioning

confidence: 99%

Effect of Alprostadil on the Prevention of Contrast-Induced Nephropathy: A Meta-Analysis of 36 Randomized Controlled Trials

et al. 2019

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Contrast-induced nephropathy (CIN) is the third leading cause of acquired acute renal injury in hospitalized patients. Alprostadil plays a role in the maintenance and redistribution of intrarenal blood flow and the excretion of electrolytes and water. However, the effectiveness of alprostadil in preventing CIN remains controversial. Thirty-six articles with a total of 5495 patients were included in this study. Both groups (experimental group and control group) received standard hydration therapy. In the experimental group, patients received different doses of alprostadil. Serum creatinine (SCr), blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), cystatin C, creatinine clearance rate (CCr), and β2-microglobulin (β2-MG) were measured at 24, 48, and 72 hours after contrast media injection. The incidence of CIN in the experimental group was significantly lower than that in the control group (6.56% vs 16.74%). The level of SCr, cystatin C, BUN, and β2-MG in the experimental group was lower than those in the control group; CCr and eGFR in the experimental group were higher than those in the control group. This study demonstrated that alprostadil may reduce the incidence of CIN in patients undergoing coronary angiogram and/or percutaneous coronary intervention.

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Non-steroidal anti-inflammatory agents to induce regression and prevent the progression of cervical intraepithelial neoplasia

Abstract: There are currently no convincing data to support a benefit for NSAIDs in the treatment of CIN (very low quality evidence according to GRADE criteria). Results from a large on-going randomised study of celecoxib are awaited.

Cited by 19 publications

References 49 publications

Surgical trauma‐induced immunosuppression in cancer: Recent advances and the potential therapies

Surgical trauma‐induced immunosuppression in cancer: Recent advances and the potential therapies

Cyclooxygenase-1 (COX-1) and COX-1 Inhibitors in Cancer: A Review of Oncology and Medicinal Chemistry Literature

Effect of Alprostadil on the Prevention of Contrast-Induced Nephropathy: A Meta-Analysis of 36 Randomized Controlled Trials

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