HPV is an essential driver in recurrence of cervical cancer.

Introduction: High-risk human papillomavirus (HPV) has been detected in distant metastases from cervical cancer (CC) patients, suggesting a role of HPV.

Material And Methods: Here, we included 26 patients with recurrence of CC (2019-2023). With next generation sequencing (NGS) and immunohistochemical staining, primary and recurrent tissues were analyzed for HPV DNA and HPV RNA, p16 expression, and somatic TP53 and RB1 mutations.

Circulating cell-free HPV DNA is a strong marker for disease severity in cervical cancer.

For cervical cancer (CC), circulating cell-free HPV DNA (ccfHPV) may establish disease severity. Furthermore, HPV integration has been correlated to viral load and survival. In this study, pre-treatment plasma from 139 CC cases (50 primary surgery patients, 22 primary surgery + adjuvant oncological therapy patients, and 67 primary oncological therapy patients) was collected (2018-2020).

The Diagnostic Value of Circulating Cell-Free HPV DNA in Plasma from Cervical Cancer Patients.

Circulating cell-free HPV DNA (ccfHPV DNA) may serve as a marker for cervical cancer. In this study, we used digital droplet PCR (ddPCR) to detect and quantify ccfHPV DNA in plasma from patients with HPV16- or HPV18-associated cervical cancer. Blood samples from 60 patients diagnosed with cervical cancer (FIGO IA1-IVA) at Aarhus or Odense University Hospital (June 2018 to March 2020) were collected prior to treatment, and patients were subdivided into an early stage ( = 30) and a late-stage subgroup ( = 30) according to disease stage.

Anti-fibrotic mechanisms of angiotensin AT -receptor stimulation.

The angiotensin AT -receptor is a main receptor of the protective arm of the renin-angiotensin system. Understanding of this unconventional G-protein coupled receptor has significantly advanced during the past decade, largely because of the availability of a selective non-peptide AT -receptor agonist, which allowed the conduct of a multitude of studies in animal disease models. This article reviews such preclinical studies that in their entirety provide strong evidence for an anti-fibrotic effect mediated by activation of the AT -receptor.

Identification of protein phosphatase involvement in the AT receptor-induced activation of endothelial nitric oxide synthase.

The Angiotensin II type 2 receptor (ATR) promotes vasodilation by nitric oxide (NO) release from endothelial cells. However, the mechanisms underlying the ATR-induced stimulation of endothelial NO synthase (eNOS) is still not completely understood. Therefore, we investigated whether in addition to the known ATR-mediated phosphorylation of eNOS at Ser, activation of phosphatases and dephosphorylation of eNOS at Tyr and Thr are also involved.