(a) Ki67 staining showed similar cell cycle rates for peritoneal (A38Per) and matched lung (A38Lg) metastases from the same patient grown in medium with 10% FBS, and serum-free medium (SFM) greatly slowed growth in both subclones. Scale bars, 100 μm. (b) Serial cell counts for the indicated times confirmed similar growth rates and growth arrest in SFM. (c) GO analysis on RNA–seq data from cells cultured in serum versus SFM further confirmed growth arrest in SFM (lung data; the peritoneal cells gave identical results). (d) Immunoblots showed persistence of reprogrammed chromatin modifications in proliferative (FBS) and growth-arrested (SFM) cells. (e) Treatment of the peritoneal subclone with PDAC chemotherapies (Gem, gemcitabine; G+FU, gemcitabine + 5-fluorouracil) did not induce loss of methylation or gain of acetylation as seen between peritoneal and distant metastases (e.g., Fig. 1c,d), supporting the notion that those changes were independent of chemotherapy treatments. As expected, treatments resulted in increased levels of γH2AX, a signature of activated DNA repair pathways.