p53, p16 and ki67 as immunohistochemical prognostic markers in uterine smooth muscle tumors of uncertain malignant potential (STUMP).

The risk stratification in gynecologic smooth muscle tumors of uncertain malignant potential (STUMP) is a crucial issue, but at present there are no validated prognostic markers. We aimed to assess p53, p16 and ki67 as immunohistochemical prognostic markers in STUMP through a systematic review and meta-analysis. Electronic databases were searched from their inception to July 2020. All studies assessing p53, p16 and/or ki67 immunohistochemistry in gynecologic STUMP series were included. Immunohistochemical patterns were categorized as "abnormal" vs "wild-type" for p53, "diffuse" vs "focal/negative" for p16, ≥ 10% vs 10% for ki67. The prognostic value for recurrence was assessed through Cox regression analysis; a p-value 0.05 was considered significant. Markers that resulted significant were assessed for prognostic accuracy with calculation of area under the curve (AUC) and post-test probability of recurrence. Seven studies with 171 patients were included. Significant association with disease-free survival was found for p53 (p 0.0001) and p16 (p 0.0001), but not for ki67 (p = 0.911). p53 showed sensitivity= 83%, specificity= 86%, AUC= 0.89, and post-test recurrence probabilities of 54% and 7% in the case of abnormal and wild-type expression, respectively. p16 showed sensitivity= 84%, specificity= 88%, AUC= 0.91 and post-test recurrence probabilities of 56% and 7% in the case of diffuse and focal/negative expression, respectively. In conclusion, p53 and p16 might be useful in the risk assessment of STUMP, despite not being suitable as stand-alone prognostic markers.

Clinical Evidence for Q10 Coenzyme Supplementation in Heart Failure: From Energetics to Functional Improvement.

Oxidative stress and mitochondrial dysfunction are hallmarks of heart failure (HF). Coenzyme Q10 (CoQ10) is a vitamin-like organic compound widely expressed in humans as ubiquinol (reduced form) and ubiquinone (oxidized form). CoQ10 plays a key role in electron transport in oxidative phosphorylation of mitochondria. CoQ10 acts as a potent antioxidant, membrane stabilizer and cofactor in the production of adenosine triphosphate by oxidative phosphorylation, inhibiting the oxidation of proteins and DNA. Patients with HF showed CoQ10 deficiency; therefore, a number of clinical trials investigating the effects of CoQ10 supplementation in HF have been conducted. CoQ10 supplementation may confer potential prognostic advantages in HF patients with no adverse hemodynamic profile or safety issues. The latest evidence on the clinical effects of CoQ10 supplementation in HF was reviewed.