Development of drug-loaded particles for intraperitoneal therapy
Wim P. Ceelen, Edward A. Levine in Intraperitoneal Cancer Therapy, 2015
Cancers originating from organs within the peritoneal cavity (pancreatic, ovarian, colorectal, gastric, liver) account for 250,000 new cases in the United States. Peritoneal metastases due to locoregional spread are common (e.g., 70% for ovarian, 50% for pancreatic, 32% for colon, ~20% for gastric) [1,2]. In the peritoneal cavity, tumors are disseminated by exfoliation of cells, which spread directly to pelvic and abdominal peritoneal surfaces. Movement of cells tends to follow the circulation of peritoneal fluid from the right pericolic gutter cephalad to the right hemidiaphragm. Tumors also spread to intestinal mesenteries, with omentum and mesentery as the common sites for peritoneal metastasis. Adhesions of tumors between loops of intestines produce intestinal obstruction, whereas obstruction of the abdominal or diaphragmatic lymphatic drainage by tumor cells leads to decreased outflow of peritoneal fluid resulting in ascites [3,4]. Patients with malignant ascites suffer from abdominal distention, loss of appetite, shortness of breath, abdominal pain, low blood pressure, weakness, and fatigue and have short survival (e.g., 1.5–6 months).
Introduction to Vascular Complications in Oncology Patients
Paloma Tejero, Hernán Pinto in Aesthetic Treatments for the Oncology Patient, 2020
Secondary Budd-Chiari syndrome is a rare condition caused by occlusion of the suprahepatic veins due to tumoral thrombosis or compression, characterized by the insidious or acute occurrence of painful hepatomegaly, jaundice, ascites, splenomegaly, venous collateral circulation, and edema of the extremities. The most common oncological etiology is hepatocellular carcinoma, followed by renal carcinoma, adrenal gland carcinoma, nephroblastoma, or Wilms tumor and leiomyosarcoma. The diagnosis is confirmed by the clinic on analysis of ascites characterized by high protein content, except in acute forms and imaging studies (abdominal ultrasound, computed tomography [CT] scans, and magnetic resonance imaging [MRI]). Morbidity and mortality are usually associated with the evolution of liver failure and basic neoplastic pathology [1].
Test Paper 7
Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike in Get Through, 2017
A previously healthy 36-year-old woman presents with acute hepatic failure of unknown cause. Her international normalized ratio (INR) is 2.6 and fails to normalise despite treatment. An ultrasound scan shows ascites. The liver team asks you to consider a liver biopsy. Which of the following is the most appropriate reply? Unable to perform because of INR and ascitesAdvise the patient of the increased risk of bleeding and go ahead with liver biopsyDrain the ascites and the perform the biopsyPerform transjugular liver biopsyPerform transarterial liver biopsy
Immune profiling and identification of prognostic immune-related risk factors in human ovarian cancer
Published in OncoImmunology, 2019
Emelie Rådestad, Charlotte Klynning, Arwen Stikvoort, Ole Mogensen, Silvia Nava, Isabelle Magalhaes, Michael Uhlin
There was a hierarchy in the proportion of T-cells expressing many of the analyzed markers, such as CD25, HLA-DR and OX40 (as well as all co-inhibitory receptors)(Figures 2–3). The highest frequencies were often observed among TILs, followed by TALs and then PBLs. For some markers, such as CD28 and CD127, the opposite pattern was observed and the lowest frequencies were instead found among intratumoral T-cells and highest among peripheral blood T-cells. Again, ascites-derived T-cells had a frequency between tumor and blood. Ascites fluid can be considered to be part of a diluted tumor microenvironment as tumor cells, soluble factors and immune cells move around freely in the large abdominal space. Seemingly, proximity to tumor cells and exposure to the tumor microenvironment drives and skews these changes in phenotype and composition.
Ultrastructural analysis of the Krebs-2 ascites cancer cells treated with extracellular double-stranded DNA preparation
Published in Ultrastructural Pathology, 2019
Svetlana S Kirikovich, Oleg S. Taranov, Vladimir V. Omigov, Ekaterina A. Potter, Evgenia V. Dolgova, Anastasia S. Proskurina, Yaroslav R. Efremov, Sergey S. Bogachev
The status of the cell surface is quite important for cellular functions. Intact cancer cells were shown to be of spherical shape; their surface membrane forms multiple, thin, and in most cases regularly located microvilli (Figure 2a,b). This issue is quite poorly attended in the existing literature. There are only a few reports on the topography of the ascitic tumor cells surface, which mediates the cellular interaction with the environment and with each other. In contrast to solid tumors that grow as more or less dense nodes, ascites tumors form a dense suspension of tumor cells proliferating in ascitic fluid and such a suspension is a natural condition for their viability.36,38,39 Ascites tumor cells are known to be of spherical shape, while their surfaces look extremely uneven, with multiple microvilli, protrusions, and folds, which significantly increase absorption surface.
Ovarian Cancer: Differentially Expressed microRNAs in Tumor Tissue and Cell-Free Ascitic Fluid as Potential Novel Biomarkers
Published in Cancer Investigation, 2019
Luděk Záveský, Eva Jandáková, Vít Weinberger, Luboš Minář, Veronika Hanzíková, Daniela Dušková, Lenka Záveská Drábková, Aleš Hořínek
Ovarian cancer is a complex, heterogeneous disease capable of escaping both the body's mechanisms of elimination and the diverse anti-cancer treatments. Ascites (effusion), the accumulation of fluid in the peritoneal (and/or pleural) cavity, has often been associated with ovarian cancer and is a possible medium playing an important role in the spread, invasion and metastasis of ovarian cancer in the peritoneum and omentum and eventually the organs in the peritoneal cavity. The presence of ascites is thus an indicator of poor outcomes, even in early stages. Relapses of the disease, even in patients originally responding to chemotherapy, may be attributed to ascites, because residual cancer cells not removed by surgery may aggregate in this peritoneal fluid and form microscopic tumor spheroids that are more resistant to chemotherapy. The spheroids can then adhere to the surface of organs in the peritoneum and may form new tumors, assisted by chemokines and growth factors in the peritoneal fluid (27). Researchers have previously assumed that the spread of ovarian cancer proceeded directly by the shedding of malignant cells into the intraperitoneal cavity, supported by the novel concept that many ovarian cancers arise in the fallopian tube. Invasion of the lymphovascular space, the occurrence of circulating ovarian cancer cells and experimental evidence, however, suggest that ovarian cancer may also spread hematogenously (28).
Related Knowledge Centers
- Cirrhosis
- Shortness of Breath
- Spontaneous Bacterial Peritonitis
- Abdomen
- Peritoneal Cavity
- Tuberculosis
- Cancer
- Pancreatitis
- Shortness of Breath
- Heart Failure
- Budd–Chiari Syndrome