New preprint from @BiffiGiulia authored by @eloise_g_lloyd & colleagues: “SMAD4 and KRAS status shape malignant-stromal crosstalk in #PancreaticCancer” This work is a twofer because it dissects two important observations: (1) how the cooperating mutation with oncogenic KRAS alters the tumor microenvironment (most all preclinical studies are based on p53 as the cooperating driver, but SMAD4 status too impacts the TME composition, including fibroblast subtypes & infiltrating myeloid cells). (2) Importantly, the allelic variant of KRAS (G12D v G12V) also has an impact, including divergent therapeutic dependencies induced within the resulting TME. This latter observation is particularly important in the era of “allele agnostic” KRAS inhibitors, as the allelic variants might respond distinctly based on their surrounding ecosystem.