Search

Introduction A diverse workforce improves health care, educational outcomes, and research agendas. Currently, faculty from historically excluded groups remain underrepresented in academic medicine. Resources are needed in academic medical centers for those charged with recruiting and retaining a diverse and talented workforce. Methods Informed by the successful use of holistic review in medical student admissions, the Association of American Medical Colleges (AAMC) developed and piloted a toolkit for use in faculty recruitment and retention at five academic medical centers. Institutions led toolkit-guided holistic review workshops ranging from 2.5 to 3 hours in duration for leaders and faculty to identify and prioritize selection criteria used to modify faculty recruitment and retention materials and processes. AAMC surveys at pilot initiation and at two time points during implementation assessed satisfaction with and perceptions of the toolkit. Results At the first survey time point, the average toolkit rating across five institutions ranged from 3.2 to 4.4 (out of a maximum of 5.0) for helpfulness and from 3.5 to 4.9 for ease of use. At the second survey time point, the helpfulness of the tools received average ratings of 3.0–4.8. In respondents’ qualitative comments, we identified varying strategies for implementation and few barriers to implementation other than reluctance of some faculty to use scripted tools and concerns about anonymity in the exit interviews. Discussion The toolkit was well received and easy to implement. It will be important to study the use of these materials across other institutions, with attention to their impact on faculty diversity.

Micro-ribonucleic acid-155 (miR-155) is one of the first described oncogenic miRNAs. Although multiple direct targets of miR-155 have been identified, it is not clear how it contributes to the pathogenesis of acute myeloid leukemia. We found miR-155 to be a direct target of Meis1 in murine Hoxa9/Meis1 induced acute myeloid leukemia. The additional overexpression of miR-155 accelerated the formation of acute myeloid leukemia in Hoxa9 as well as in Hoxa9/Meis1 cells in vivo. However, in the absence or following the removal of miR-155, leukemia onset and progression were unaffected. Although miR-155 accelerated growth and homing in addition to impairing differentiation, our data underscore the pathophysiological relevance of miR-155 as an accelerator rather than a driver of leukemogenesis. This further highlights the complexity of the oncogenic program of Meis1 to compensate for the loss of a potent oncogene such as miR-155. These findings are highly relevant to current and developing approaches for targeting miR-155 in acute myeloid leukemia.