Ascites formation is a common complication of cancer with a significant symptomatic burden for patients. Malignant ascites (MA) is defined by the presence of tumor cells within the ascitic fluid. It does not only cause substantial morbidity, but is also associated with impaired survival. Considering the frequent occurrence of MA, it still represents a clinical challenge for physicians with limited therapy options, mainly comprising of the treatment of the primary tumor and effusion drainage. Particularly the lack of pathophysiological insight limits the development of effective, causative therapies. Causes of MA development such as lymphatic vessel obstruction and the effects of tumor secreted vascular endothelial growth factor (VEGF) have been known for decades. Novel research suggests that the intraperitoneal immune system may also induce and maintain MA accumulation. In this review, we assess current knowledge on the pathophysiology of MA and summarize available evidence of treatment approaches. Also, factors contributing to ascites formation without proof of tumor cells in the peritoneal cavity, defined as paramalignant ascites, with potential treatment strategies are discussed. We further focus on novel findings in the pathophysiology of MA that might lead to treatment improvement in the near future and discussed relevant knowledge gaps in this field.

Due to potentially immune-escaping virus variants and waning immunity, a third SARS-CoV-2 vaccination dose is increasingly recommended. However, data in patients with cancer are limited. We measured anti-SARS-CoV-2 spike protein antibody levels after the third vaccination dose in 439 patients with cancer and 41 health care workers (HCW) at an academic centre in Austria and a rural community hospital in Italy. Adverse events were retrieved from questionnaires. Overall, 439 patients and 41 HCW were included. SARS-CoV-2 infections were observed in 62/439 (14.1%) patients before vaccination and in 5/439 (1.1%) patients after ≥1 dose. Longitudinal analysis revealed a decrease of antibody levels between 3 and 6 months after second vaccination in patients with solid tumours (p < 0.001) and haematological malignancies without anti-B cell therapies (p < 0.001). After the third dose, anti-S levels increased compared to the first/second dose. Patients receiving B cell-targeted agents had lower antibody levels than patients with haematological malignancies undergoing other treatments (p < 0.001) or patients with solid tumours (p < 0.001). Moreover, anti-S levels correlated with CD19+ (B cell) and CD56+ (NK cell) counts in peripheral blood. The most frequent adverse events after the third dose were local pain (75/160, 46.9%), fatigue (25/160, 15.6%) and fever/chills (16/160, 10.0%). Patients with cancer had lower anti-S levels than HCW (p = 0.015). This study in patients with cancer shows improved antibody levels after the third vaccination dose at an acceptable side-effect profile. Lower antibody levels than in controls underline the need for further follow-up studies and dedicated trials.

Cancer increases the risk of venous thromboembolism (VTE). To identify patients with cancer at high VTE risk who might benefit from primary thromboprophylaxis, several risk assessment models (RAMs) have been developed. The evolution of anticancer treatment, including the implementation of targeted and immunotherapeutic agents, might affect VTE risk and risk prediction. Therefore, we aimed to evaluate the performance of 6 externally validated RAMs (Khorana score, PROTECHT, CONKO, COMPASS-CAT, CATScore, and EHR-CAT) in a prospective observational cohort study of patients with cancer initiating contemporary systemic anticancer therapies. Eight hundred six patients (49.5% female) with a median age of 61 years (interquartile range, 53-69) were included. The most common cancer types were lung (21.8%), breast (10.8%), and pancreatic (10.3%). Anticancer therapies initiated at study inclusion included chemotherapy (48.3%), a combination of chemotherapy and immune checkpoint inhibitor (ICI; 16.6%), ICI monotherapy (15.4%), and targeted agents (19.7%). During an observation period of 6 months, 91 patients experienced a VTE (cumulative incidence, 11.2%; 95% confidence interval [CI], 9.0-13.3). The discriminatory performance of the RAMs varied, with the best c-statistic seen with the CAT Score, whereas the COMPASS-CAT score showed the lowest area under the curve value (c-statistics: Khorana score, 0.53 [95% CI, 0.50-0.56]; PROTECHT, 0.58 [95% CI, 0.56-0.61]; CONKO, 0.54 [95% CI, 0.51-0.57]; COMPASS-CAT, 0.50 [95% CI, 0.47-0.53]; CAT Score, 0.65 [95% CI, 0.62-0.67]; EHR-CAT, 0.55 [95% CI, 0.52-0.57]). Overall, we observed a poor to modest discriminatory performance of the RAMs in our contemporary cohort of patients with cancer, with the CAT Score performing best among all evaluated scores.

The treatment of metastasized gastroesophageal adenocarcinoma largely depends on molecular profiling based on immunohistochemical procedures. Therefore, the examination of HER2, PD-L1, and dMMR/MSI is recommended by the majority of clinical practice guidelines, as positive expression leads to different treatment approaches. Data from large phase-III trials and consequent approvals in various countries enable physicians to offer their patients several therapy options including immunotherapy, targeted therapy, or both combined with chemotherapy. The introduction of novel therapeutic targets such as CLDN18.2 leads to a more complex decision-making process as a significant number of patients show positive results for the co-expression of other biomarkers besides CLDN18.2. The aim of this review is to summarize the current biomarker landscape of patients with metastatic gastroesophageal tumors, its direct clinical impact on daily decision-making, and to evaluate current findings on biomarker co-expression. Furthermore, possible treatment strategies with multiple biomarker expression are discussed.

Identification of factors associated with survival after ascites diagnosis in metastatic pancreatic cancer (mPC) patients may guide treatment decisions and help to maintain quality of life in this highly symptomatic patient collective. All patients treated for mPC at the Medical University of Vienna between 2010 and 2019 developing ascites throughout their course of disease were identified by retrospective chart review. General risk factors, metastatic sites, systemic inflammation and liver function parameters, as well as type of treatment after ascites diagnosis were investigated for associations with survival. One hundred and seventeen mPC patients with ascites were included in this study. Median time from mPC to ascites diagnosis was 8.9 months (range 0-99 months) and median overall survival (OS) after ascites diagnosis was 27.4 days (range 21.3-42.6 days). Identified prognostic factors at ascites diagnosis independently associated with an impaired OS were presence of liver metastases [hazard ratio (HR): 2.07, 95% confidence interval (CI) 1.13-3.79, P = 0.018), peritoneal carcinomatosis (HR: 1.74, 95% CI 1.11-2.71, P = 0.015), and portal vein obstruction (HR: 2.52, 95% CI 1.29-4.90, P = 0.007). Compared with best supportive care, continuation of systemic therapy after ascites diagnosis was independently associated with survival (HR: 0.35, 95% CI 0.20-0.61, P < 0.001) with a median OS of 62 days (95% CI 51-129 days, P < 0.001) versus 16 days (95% CI 11-24 days), respectively. Liver and peritoneal metastases as well as portal vein obstruction were found to be prognostic factors after ascites diagnosis in mPC patients. Continuation of systemic therapy after ascites diagnosis was associated with a longer OS, which needs to be evaluated in larger clinical trials including quality-of-life assessment.

Here, we present the case of a patient with a metastatic neuroendocrine tumor with cytologically negative ascites treated for spontaneous bacterial peritonitis (SBP). Ascitic cultures remained negative for bacterial growth but were positive for Candida albicans 8 days after SBP diagnosis. ss-D-glucan was only positive in ascites, while being negative in blood. Blood cultures remained negative throughout the whole admission. Fungal peritonitis presumably originated from an impending bowl perforation or an increasing vascular permeability caused by an increase in VEGF secondary to diffuse infiltration by the underlying malignant disease.