Improving Blood Donor Diversity Through Focused Recruitment Interventions

Study Design: Beginning in May 2016, the Jefferson Blood Donor Center began collecting donor self-identified race/ethnicity: White, Black or African American, Hispanic, Asian or Pacific Islander, American Indian or Alaskan Native, Multiracial, Other, Unknown (Figure 1). We retrospectively quantified the racial/ethnic groups represented in each month’s donor population. In January 2017,the following intervention strategies were implemented: Emailing donors who self-identified as part of a racial/ethnic minority group Contacting racially/ethnically-focused student groups to organize blood drives with the Jefferson Blood Donor Center Partnering with the Jefferson Medical Oncology Society MarrowthonDrive to encourage blood donations Presentation to the local chapter of the National Association of Hispanic Nurses Interventions still to come Featuring the Jefferson Blood Donor Center in the Office of Diversity and Inclusion’s Diversity Newsletter The quantification of racial/ethnic groups were stratified to pre-intervention months and post-intervention months. Poster presented at Thomas Jefferson University Hospital Housestaff Quality Improvement and Patient Safety conference.https://jdc.jefferson.edu/patientsafetyposters/1038/thumbnail.jp

t(3;8)(q26;q24) with MYC Rearrangement in Acute Myeloid Leukemia: A Case Report

Rearrangements of 3q26 have been described in 5% of de novo or therapy related acute myeloid leukemia, myelodysplastic syndrome (MDS), and blast phase of chronic myeloid leukemia. The most common translocations involving 3q26 are t(3;12)(q26;p13), t(3;21)(q26;q22), t(3;3)(q21;q26), t(2;3)(p15∼23;q26∼27) and rarely t(3;7)(q26;q21). However, t(3;8)(q26;q24) with or without monosomy 7 is a rare phenomenon and has been reported in only 10 patients so far. Hereby, we describe a 58 year old patient who was diagnosed with refractory anemia with multilineage dysplasia. Cytogenetic studies revealed monosomy 7. He was then lost to follow-up. A year later he was found to have worsening cytopenias and circulating blasts. He was started on azacytidine. A month later, follow-up bone marrow biopsy showed progression to acute myeloid leukemia (76% blasts). The blasts showed following immunophenotypic profile: CD7+, CD10-, CD13+, CD14-, CD16-, CD33+, CD38+, CD56-, CD64-, CD117-, HLA-DR+, MPO-, cCD3-, cCD22-, cCD79- and TdT-. His karyotype showed evolution with additional finding of t(3;8) which involved MYC gene at 8q24 which was confirmed with metaphase FISH. The breakpoint on 3q26 is most likely the EVI1 fusing with MYC. Even though monosomy 7 has been frequently described to be associated with t(3;8), it is not described as a predecessor of t(3;8). Patient failed first induction chemotherapy. He is currently finishing up his re-induction chemotherapy. This case describes a case of AML arising from MDS with monosomy 7 and involving MYC gene as a partner for 3q26 (EVI1)