Open Access

Ovarian carcinoma (OC) is the most lethal gynecological malignancy. Response to platinum-based chemotherapy is poor in some patients and, thus, current research is focusing on new therapy options. The various histological types of OC are characterized by distinctive molecular genetic alterations that are relevant for ovarian tumorigenesis. The understanding of these molecular pathways is essential for the development of novel therapeutic strategies. Purpose We want to give an overview on the molecular genetic changes of the histopathological types of OC and their role as putative therapeutic targets. In Depth Review of Existing Data In 2012, the vascular endothelial growth factor (VEGF) inhibitor, bevacizumab, was approved for OC treatment. Bevacizumab has shown promising results as single agent and in combination with conventional chemotherapy, but its target is not distinctive when analyzed before treatment. At present, mammalian target of rapamycin (mTOR) inhibitors, poly-ADP-ribose polymerase (PARP) inhibitors and components of the EGFR pathway are in the focus of clinical research. Interestingly, some phytochemical substances show good synergistic effects when used in combination with chemotherapy. Conclusion Ongoing studies of targeted agents in conjunction with chemotherapy will show whether there are alternative options to bevacizumab available for OC patients. Novel targets which can be assessed before therapy to predict efficacy are needed. The assessment of therapeutic targets is continuously improved by molecular pathological analyses on tumor tissue. A careful selection of patients for personalized treatment will help to reduce putative side effects and toxicity.

Background/Objectives: Ambient air pollution is a significant public health concern, known to affect cardiovascular health adversely. Research has identified both long-term and short-term cardiovascular risks associated with various air pollutants, including those linked to acute coronary syndromes. However, the observed effects are rather small, with most data sourced from highly polluted regions. Methods: This study utilized a prospective registry database, documenting 12,581 myocardial infarction (MI) events in Styria, Austria from January 2007 to December 2015. Pollutants analyzed included particulate matter (PM2.5, PM10) and gases, such as NO2, CO, SO2, O3 and NOx. We employed generalized linear models to examine the interaction of each of these pollutants on the daily incidence of MI. Additionally, we conducted separate analyses for patients with specific comorbidities: diabetes mellitus (DM), arterial hypertension (HTN), heart failure with reduced ejection fraction (HFrEF), chronic obstructive pulmonary disease (COPD) and current smokers. Results: No significant associations were identified between any of the pollutants and MI incidence, both in the overall cohort and in patient subgroups with DM, HTN, HFrEF or COPD. However, among active smokers, we observed a decreased relative risk of MI associated with elevated levels of NO2, CO, SO2 and NOx on the day of MI (p < 0.01 for all pollutants). Conversely, an increased MI risk was associated with rising ozone levels (p = 0.0027). This counterintuitive finding aligns with previously published data and may suggest a new dimension to the “smoker’s paradox”. Conclusions: In regions with low pollution levels, air pollutants pose only minor or insignificant short-term risks for myocardial infarction. Active smokers exhibit an altered response to ambient air pollution.