Mentorship: The necessity of intentionality.

A large body of research exists that is dedicated to exploring and defining mentoring. It is widely recognized that mentorship is a process informed by one's personal experiences. Yet, mentorship literature primarily centers around advancing technical proficiencies, and very little focuses on individual characteristics, such as honesty, consistency, and transparency. Individual wisdom is an invaluable tool for intentional mentorship. Intentional mentors catalyze the ability to understand and tap into one's own power, promote awareness of individual strengths and limitations, and clarify personal vision. Through intentional mentorship, mentors identify, improve, and implement strategies and skills that they acquired throughout their career. After conducting a self-assessment and identifying the personal skills that can be attributed to effective mentoring, mentors advance along the mentorship continuum to improve, and subsequently implement, these skills. Given the changing landscape of the scientific workforce in general, faculty mentors must be intentional about seeking avenues for growth. Beyond individual implementation, it is essential for educational institutions to also take a systemic approach when it comes to supporting faculty advisors and their mentees. A few tools and resources are offered to encourage mentors in taking a proactive role as they intentionally develop and enhance their individual mentoring process. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

E4orf1 limits the oncolytic potential of the E1B-55K deletion mutant adenovirus.

Clinical trials have shown oncolytic adenoviruses to be tumor selective with minimal toxicity toward normal tissue. The virus ONYX-015, in which the gene encoding the early region 1B 55-kDa (E1B-55K) protein is deleted, has been most effective when used in combination with either chemotherapy or radiation therapy. Therefore, improving the oncolytic nature of tumor-selective adenoviruses remains an important objective for improving this form of cancer therapy. Cells infected during the G(1) phase of the cell cycle with the E1B-55K deletion mutant virus exhibit a reduced rate of viral late protein synthesis, produce fewer viral progeny, and are less efficiently killed than cells infected during the S phase. Here we demonstrate that the G(1) restriction imposed on the E1B-55K deletion mutant virus is due to the viral oncogene encoded by open reading frame 1 of early region 4 (E4orf1). E4orf1 has been reported to signal through the phosphatidylinositol 3'-kinase pathway leading to the activation of Akt, mTOR, and p70 S6K. Evidence presented here shows that E4orf1 may also induce the phosphorylation of Akt and p70 S6K in a manner that depends on Rac1 and its guanine nucleotide exchange factor Tiam1. Accordingly, agents that have been reported to disrupt the Tiam1-Rac1 interaction or to prevent phosphorylation of the ribosomal S6 kinase partially alleviated the E4orf1 restriction to late viral protein synthesis and enhanced tumor cell killing by the E1B-55K mutant virus. These results demonstrate that E4orf1 limits the oncolytic nature of a conditionally replicating adenovirus such as ONYX-015. The therapeutic value of similar oncolytic adenoviruses may be improved by abrogating E4orf1 function.