Implementation of a Smoking Cessation e-Learning Education Program for Oncology Clinic Healthcare Providers: Evaluation With Implications for Evidence-Based Practice.

BACKGROUND: Continued smoking after a cancer diagnosis increases the risk for treatment complications, primary cancer recurrence, and secondary malignancy development, while also reducing treatment efficacy, survival, and overall health. The lack of formal evidence-based smoking cessation education programs for oncology healthcare providers is a barrier to smoking cessation practices. PURPOSE: To evaluate the use of an evidence-based, smoking cessation e-learning education program for oncology healthcare providers. METHODS: A single group, pre- and post-test, nonexperimental design was used in this evidence-based quality improvement project. To assess the provider's knowledge in smoking cessation, a baseline assessment, a post-test, and an online survey were completed by the providers. A telephone survey was conducted to assess the patients' perception of cessation services received. RESULTS: The healthcare providers' (N = 58) test scores on smoking cessation knowledge increased significantly (p < .0001) after completing the e-learning education program. A majority of the providers reported that the education program increased their confidence (86%) in successfully helping the patient to quit smoking and agreed to make smoking cessation a priority (89%) in their practice. A majority of the patients (85%) were satisfied or extremely satisfied with the smoking cessation services received. Many patients (71%) self-reported having tried to quit smoking. CONCLUSION: An evidence-based e-learning education program is effective in increasing oncology healthcare providers' knowledge and confidence in tobacco dependence treatment practices. The program also has a positive impact on oncology patients' perception of cessation services received. LINKING EVIDENCE TO ACTION: A self-paced e-learning program is a feasible and effective way to educate healthcare providers in smoking cessation treatment. Incorporating evidence-based tobacco dependence treatment into their daily oncology practice is warranted.

BTKC481S-Mediated Resistance to Ibrutinib in Chronic Lymphocytic Leukemia.

Purpose Therapeutic targeting of Bruton tyrosine kinase (BTK) with ibrutinib in chronic lymphocytic leukemia has led to a paradigm shift in therapy, and relapse has been uncommon with current follow-up. Acquired mutations in BTK and PLCG2 can cause relapse, but data regarding the prevalence and natural history of these mutations are limited. Patients and Methods Patients accrued to four sequential studies of ibrutinib were included in these analyses. Deep sequencing for BTK and PLCG2 was performed retrospectively on patients who experienced relapse and prospectively on a screening population. Results With a median follow-up time of 3.4 years, the estimated cumulative incidence of progression at 4 years is 19% (95% CI, 14% to 24%). Baseline karyotypic complexity, presence of del(17)(p13.1), and age less than 65 years were risk factors for progression. Among patients who experienced relapse, acquired mutations of BTK or PLCG2 were found in 85% (95% CI, 71% to 94%), and these mutations were detected an estimated median of 9.3 months (95% CI, 7.6 to 11.7 months) before relapse. Of a group of 112 patients examined prospectively, eight patients have experienced relapse, and all of these patients had acquired resistance mutations before relapse. A resistance mutation was detected in an additional eight patients who have not yet met criteria for clinical relapse. Conclusion Relapse of chronic lymphocytic leukemia after ibrutinib is an issue of increasing clinical significance. We show that mutations in BTK and PLCG2 appear early and have the potential to be used as a biomarker for future relapse, suggesting an opportunity for intervention.

Phase I dose escalation trial of the novel proteasome inhibitor carfilzomib in patients with relapsed chronic lymphocytic leukemia and small lymphocytic lymphoma.

The proteasome complex degrades proteins involved in a variety of cellular processes and is a powerful therapeutic target in several malignancies. Carfilzomib is a potent proteasome inhibitor which induces rapid chronic lymphocytic leukemia (CLL) cell apoptosis in vitro. We conducted a phase I dose-escalation trial to determine the safety and tolerability of carfilzomib in relapsed/refractory CLL or small lymphocytic lymphoma (SLL). Nineteen patients were treated with carfilzomib initially at 20 mg/m(2), then escalated in four cohorts (27, 36, 45 and 56 mg/m(2)) on days 1, 2, 8, 9, 15 and 16 of 28-day cycles. Therapy was generally well tolerated, and no dose limiting toxicities were observed. The most common hematologic toxicities were thrombocytopenia and neutropenia. All patients evaluable for response had stable disease, including patients with del17p13 and fludarabine-resistant disease. This trial shows acceptable tolerability and limited preliminary efficacy of carfilzomib in CLL and SLL.