CONCLUSION: The progress of developing a cancer treatment that may successfully and efficiently target mutant p53 is on the verge of development. Mutant p53 proteins not only initiate oncogenesis but also cause resistance in cancer cells to certain chemo or radiotherapies, further endorse cancer cell survival and promote migration as well as metastasis of cancerous cells. With this regard, many mutant p53 inhibitors have been developed, some of which are currently being evaluated at the pre-clinical level and have been identified and discussed. To date, APR-246 is the most prominent one that has progressed to the Phase III clinical trial.
METHODS: We collected responses to an online and physical survey from people living with T2D through a quantitative cross-sectional study. First, we tested the contextual validity and cultural preciseness of ASQ-DM-EX prototype through a preliminary pilot testing phase. These processes culminated in the development of a 91-item version of the questionnaire which was disseminated widely to evaluate the predictive strength of the ASQ-DM-EX.
RESULTS: All constructs within ASQ-DM-EX showed internal consistencies within good to excellent range (Cronbach's ⍺ = 0.70-0.94), except for the Influence construct (Cronbach's ⍺ = 0.33). An increase in ASQ-DM-EX scores was associated with a reduction in HbA1c control (r = -0.17, P