Food Access Support Technology (FAST): a Centralized City-Wide Platform for Rapid Response to Food Insecurity.

BACKGROUND: Food access for patients remains a critical need for health systems to address given varying resource availability and inefficient coordination among health and food services. AIM: Develop and evaluate the Food Access Support Technology (FAST), a centralized digital platform for food access that pairs health systems with food and delivery community-based organizations (CBOs). SETTING AND PARTICIPANTS: Two health systems, 12 food partners, and 2 delivery partners in Philadelphia, PA. PROGRAM DESCRIPTION: Using FAST, referrers can post requests for food delivery on recipients' behalf, which are reviewed and claimed by eligible CBOs that can prepare food boxes for delivery to people's homes. PROGRAM EVALUATION: Between March 2021 and July 2022, FAST received 364 requests, representing 207 food insecure households in 51 postal codes. The platform facilitated the completion of 258 (70.9%) requests, with a median completion time of 5 (IQR 0-7) days and a median of only 1.5 days (IQR 0-5) for requests marked "urgent." Qualitative interviews with FAST end-users endorsed the usability of the FAST platform and its effectiveness in facilitating resource-sharing between partners. DISCUSSION: Our findings suggest that centralized platforms can address household food insecurity by (1) streamlining partnerships between health systems and CBOs for food delivery and (2) facilitating the real-time coordination of resources among CBOs.

The c-Rel-c-Myc axis controls metabolism and proliferation of human T leukemia cells.

Genome-wide association studies have established that human REL is a susceptibility gene for lymphoid cancers and inflammatory diseases. REL is the hematopoietic member of the nuclear factor-κB (NF-κB) family and is frequently amplified in human lymphomas. However, the mechanism through which REL and its encoded protein c-Rel affect human lymphoma is largely unknown. Using both loss-of-function and gain-of-function approaches, we studied the roles of REL gene in human Jurkat leukemia cells. Compared with control Jurkat cells, REL knockout cells exhibited significant defects in cell growth and mitochondrial respiration. Genome-wide transcriptome analyses revealed that T cells lacking c-Rel had selective defects in the expression of inflammatory and metabolic genes including c-Myc. We found that c-Rel controlled the expression of c-Myc through its promotor, and expressing c-Myc in c-Rel-deficient lymphoma cells rescued their proliferative and metabolic defects. Thus, the human c-Rel-c-Myc axis controls lymphoma growth and metabolism and could be a therapeutic target for lymphomas.

c-Rel Is a Myeloid Checkpoint for Cancer Immunotherapy.

Immunotherapy that targets lymphoid cell checkpoints holds great promise for curing cancer. However, a majority of cancer patients do not respond to this form of therapy. In addition to lymphoid cells, myeloid cells play essential roles in controlling immunity to cancer. Whether myeloid checkpoints exist that can be targeted to treat cancer is not well established. Here we show that c-Rel, a member of the nuclear factor (NF)-B family, specified the generation of myeloid-derived suppressor cells (MDSCs) by selectively turning on pro-tumoral genes while switching off anti-tumoral genes through a c-Rel enhanceosome. c-Rel deficiency in myeloid cells markedly inhibited cancer growth in mice, and pharmaceutical inhibition of c-Rel had the same effect. Combination therapy that blocked both c-Rel and the lymphoid checkpoint protein PD1 was more effective in treating cancer than blocking either alone. Thus, c-Rel is a myeloid checkpoint that can be targeted for treating cancer.