Association of Funding and Meal Preparation Time With Nutritional Quality of Meals of Supplemental Nutritional Assistance Program Recipients.

Importance: The Supplemental Nutrition Assistance Program (SNAP) is a federal program that provides food-purchasing assistance to low-income people; however, its current design does not account for the time availability of SNAP recipients to prepare meals.

Objective: To evaluate the association of the availability of funding for food purchases and time for meal preparation with the nutritional quality of meals of SNAP recipients.

Design, Setting, And Participants: This study used decision analytical modeling to evaluate the nutritional quality of meals of SNAP recipients.

Correction: Modeling differentiation-state transitions linked to therapeutic escape in triple-negative breast cancer.

[This corrects the article DOI: 10.1371/journal.pcbi.

Modeling differentiation-state transitions linked to therapeutic escape in triple-negative breast cancer.

Drug resistance in breast cancer cell populations has been shown to arise through phenotypic transition of cancer cells to a drug-tolerant state, for example through epithelial-to-mesenchymal transition or transition to a cancer stem cell state. However, many breast tumors are a heterogeneous mixture of cell types with numerous epigenetic states in addition to stem-like and mesenchymal phenotypes, and the dynamic behavior of this heterogeneous mixture in response to drug treatment is not well-understood. Recently, we showed that plasticity between differentiation states, as identified with intracellular markers such as cytokeratins, is linked to resistance to specific targeted therapeutics.

Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer.

Intratumoral heterogeneity in cancers arises from genomic instability and epigenomic plasticity and is associated with resistance to cytotoxic and targeted therapies. We show here that cell-state heterogeneity, defined by differentiation-state marker expression, is high in triple-negative and basal-like breast cancer subtypes, and that drug tolerant persister (DTP) cell populations with altered marker expression emerge during treatment with a wide range of pathway-targeted therapeutic compounds. We show that MEK and PI3K/mTOR inhibitor-driven DTP states arise through distinct cell-state transitions rather than by Darwinian selection of preexisting subpopulations, and that these transitions involve dynamic remodeling of open chromatin architecture.