Reducing Smoking Cessation Disparities: Capacity for a Primary Care- and Technology-Based Approach Among Medicaid Recipients

While cigarette use among U.S adults has recently decreased, vulnerable subgroups continue to smoke at high rates, including individuals receiving Medicaid insurance. These individuals have also experienced treatment access disparities, highlighting the need for approaches that leverage their strong desire to quit. We conducted interviews with 100 adult primary care patients receiving Medicaid who were current tobacco users about their use, openness to technology-based interventions, and readiness to change. Most (92%) reported current cigarette use and readiness to change averaged 6.98 out of 10 (SD = 2.82). Nearly all were open to completing an iPad-based tobacco screening (95%) and brief intervention (90%) at their next appointment, while 91% and 88% were willing to talk with their provider or a cessation counselor, respectively, about the subsequent results. Results persisted across age, sex, and race/ethnicity. Openness to technology-based interventions in this population provides support for future work that may ultimately reduce disparities

The CK1 family: contribution to cellular stress response and its role in carcinogenesis

Members of the highly conserved and ubiquitously expressed pleiotropic CK1 family play major regulatory roles in many cellular processes including DNA-processing and repair, proliferation, cytoskeleton dynamics, vesicular trafficking, apoptosis, and cell differentiation. As a consequence of cellular stress conditions, interaction of CK1 with the mitotic spindle is manifold increased pointing to regulatory functions at the mitotic checkpoint. Furthermore, CK1 is able to alter the activity of key regulatory proteins and signal integration molecules and is tightly connected to the regulation of β-catenin, p53- and MDM2-specific functions and degradation. Considering the importance of CK1 for accurate cell division and regulation of tumor suppressor functions it is not surprising that mutations and alterations in the expression and/or activity of CK1 isoforms are often detected in various tumor entities including cancer of the kidney, choriocarcinomas, breast carcinomas, oral cancer, adenocarcinomas of the pancreas, and ovarian cancer. Therefore, effort has enormously increased (i) to understand the regulation of CK1 and its involvement in tumorigenesis- and tumor progression-related signal transduction pathways and (ii) to develop CK1-specific inhibitors for the use in personalized therapy concepts. In this review we summarize the current knowledge regarding the regulation, functions, and interactions of CK1 family members with cellular proteins playing central roles in cellular stress-responses and carcinogenesis