No description available.

No description available.

No description available.

Background: Pharmacy-specific podcasts are widely available and appear to be widely consumed. However, little is known about consumption of such podcasts. Objective: To describe the scope of listenership to OncoPharm, an oncology pharmacy podcast, and determine if any episode category is more popular than another. Methods: OncoPharm episodes released from Jan. 1, 2018 to May 10, 2019 were analyzed. The number of downloads or listens (DLs) was extracted from the podcast's hosting platform for evaluation. The number of DLs were tabulated from episode release date through May 31, 2019. The nation of DL was also extracted. Descriptive statistics were used to analyze DL numbers. One-way ANOVA was used to determine if any episode category (Foundational Topic, New Approval, Updates, Landmark Study, or Other) was more popular than another. Student's t-test was used to compare the mean DLs for the first 20 OncoPharm episodes to the last 20 episodes of the evaluation period. Results: Seventy-one podcast episodes were included in the evaluation period. These episodes were downloaded or listened to 17,816 times in 71 nations and territories. The average DLs per episode were 250.9 (SD 87.7). There was no difference in mean DLs by podcast episode category (p = 0.078). The last 20 episodes had more average DLs than the first 20 episodes (p = 0.04). Conclusion: OncoPharm has found a broad and growing audience interested in a variety of oncology pharmacy topics. This expanding and international audience suggests OncoPharm is filling an unmet educational need.

Clinical evidence has demonstrated that the anxiolytic effects produced by the selective 5-hydroxytryptamine1A (5-HT1A) receptor agonist, gepirone, increase progressively over one to three weeks of treatment.

No description available.

Background: Red cell transfusions can lead to alloimmunization; however, pediatric alloimmunization frequency has not been well studied, and it may vary among diagnostic subgroups. Subgroups such as pediatric hematology/oncology patients require numerous transfusions during chemotherapy, but the immunosuppressive effect of chemotherapy on alloimmunization is unknown. One study demonstrated reduction in IgM and IgG in pediatric leukemia patients (Martín Ibáñez 2003); hence, one could hypothesize that chemotherapy suppresses alloimmunization. Objectives: This study aimed to: 1) describe alloimmunization frequency and antibody specificities in transfused pediatric patients; and 2) determine if chemotherapy affects the frequency of alloimmunization. Methods: A retrospective cohort study of pediatric patients (transfused between April 2002 and November 2011 at Hamilton Health Sciences) was performed. Data were extracted from 3 sources: a blood utilization database; the Laboratory Information System; and chart reviews. The chemotherapy treatment group included pediatric hematology/oncology patients stratified by HSCT status and diagnosis; control cohort included other pediatric patients not diagnosed with cancer. Control patients with hemoglobinopathies were analyzed separately due to increased alloimmunization. Alloimmunization was defined as clinically significant IgG alloantibody formation. Results: There were 1273 patients in the study: 949 in control group; 324 in study group. Alloimmunization was 1.6% overall: 0.6% (95% CI: 0, 1.47) in study group; 1.3% (95% CI: 0.58, 2.06) in control group. The association between chemotherapy and alloimmunization was not significant (p value = 0.38 Fisher’s exact test; OR 0.46, 95% CI: 0.10, 2.09). Due to low outcome rate, logistic regression to explore the association was not feasible. Conclusions: This is the first study exploring the frequency of alloimmunization in pediatric patients by diagnosis and the association between chemotherapy and alloimmunization. The frequency of alloimmunization was low and no association between chemotherapy and alloimmunization was observed. Low event rate would have contributed to low power. / Thesis / Master of Science (MSc)

Chemotherapy-associated thrombosis is a common complication in cancer patients. Cancer patients have a 5- to 7-fold increased risk for a thrombotic event compared to healthy individuals. While the overall risk for a thrombotic event in lung cancer patients is approximately 1.4%, the rates of thrombosis vary depending on the stage of the disease and the chemotherapeutic agents used. Activation of coagulation after initiation of chemotherapy has been reported in clinical studies. However, the mechanisms by which lung cancer chemotherapy agents modulate coagulation in lung cancer patients are not completely understood. The focus of this thesis is to investigate the mechanisms by which chemotherapy agents cisplatin, carboplatin, gemcitabine, and paclitaxel (in platinum-based combinations) induce procoagulant effects utilizing in vitro and in vivo approaches. First, we investigated the mechanisms by which lung cancer chemotherapy modulates cell-surface tissue factor (TF) activity on endothelial cells (HUVEC), monocytes, and non-small cell lung carcinoma (NSCLC) A549 cells. We observed that treatment of all three cell lines with platinum-based lung cancer chemotherapy increased cell surface TF activity. We found that the increased TF activity on chemotherapy-treated monocytes was due to increased phosphatidylserine (PS) exposure, whereas the increased TF activity on HUVEC and A549 cells was due to protein disulfide isomerase (PDI)-mediated decryption of TF. These studies demonstrate that lung cancer chemotherapy agents can exert procoagulant effects by increasing PS exposure and by inducing TF decryption on healthy and tumour cells. Next, we determined the effects of lung cancer chemotherapy on the generation of microparticles (MP) and the impact of MPs on thrombin generation. Our in vitro and in vivo studies demonstrate that lung cancer chemotherapy agents increase the generation of TF- and PS-positive MPs from tumour cells and that the MPs contribute to thrombin generation in a FVII-dependent manner. We also investigated the role of cell-free DNA (CFDNA) in mediating procoagulant effects induced by lung cancer chemotherapy agents. We found that lung cancer chemotherapy agents induce CFDNA release from healthy host neutrophils and that this leads to additional generation of thrombin by the intrinsic pathway of coagulation. Lastly, CFDNA levels have been shown to increase in cancer models through formation of neutrophil extracellular traps (NETs). Formation of NETs by NETosis, a process by which neutrophils release extracellular web-like structures composed of DNA, histones, and granular proteins, is dependent on histone citrullination by protein arginine deaminase-4 (PAD-4). In addition, PAD4 inhibition prevents NET formation. Therefore, we wanted to demonstrate that the neutrophil-derived CFDNA release induced by lung cancer chemotherapy is PAD4-dependent. Chemotherapy treatment of PAD4 knockout mice failed to increase CFDNA levels. Furthermore, chemotherapy-treatment did not increase thrombin generation in PAD4 knockout mice. This suggests that chemotherapy-induced CFDNA release occurs through NETosis. In conclusion, lung cancer chemotherapy leads to increased thrombin generation which occurs through increased TF decryption, MP generation, and CFDNA release. Therefore, lung cancer chemotherapy results in simultaneous activation of the extrinsic and intrinsic pathways of coagulation. These studies provide novel insight into the mechanisms of lung cancer chemotherapy-associated thrombosis. / Thesis / Doctor of Philosophy (PhD)

Introduction: Acute chemotherapy toxicity is common and can have negative effects for the patient and health economy and hospitalisation can be necessitated. Aims: To identify the incidence of toxicity and admission, and predictors of toxicity occurrence, severity, hospitalisation and length of stay. Method: Data was obtained from a proactive telephone assessment of acute toxicity 24 hours after administration of a first cycle of chemotherapy to patients in a large UK NHS teaching hospital. Results: 1539 patients were studied and the overall incidence of toxicity was 35.6% (530 patients). Disease site and number of chemotherapy agents given were shown to predict toxicity, with breast and upper gastrointestinal cancers having a higher likelihood of toxicity. Disease was predictive of toxicity grade, with urology, gynaecology and lung cancer patients experiencing higher grades of toxicity than other tumour sites. The rate of hospital admission due to toxicity was 13.1% (203 patients) and median length of stay 3 days (1-28). The risk of admission had some risk factors in common with toxicity. Disease and the number of drugs in the regimen affected the risk of admission, with gynaecology, head and neck and lung cancer patients and patients who received 3 drugs having a higher likelihood of admission. Predictors in the subgroups of breast, colorectal and lung cancer patients did not differ greatly from the whole population and the number of drugs was shown to be a predictor of nausea, vomiting and fatigue when explored as secondary outcomes. Conclusion: The research partly addressed the main aim and highlighted areas where further research is required. Keywords

No description available.