A novel, simple, soft, and fast microwave-assisted hydrothermal method was used for the preparation of single-crystal nanorods of hexagonal rhabdophane-type La 1 -x Sr x PO 4 -x/2 ÁnH 2 O (x = 0 or 0.02) from commercially available La(NO 3 ) 3 Á6H 2 O, Sr(NO 3 ) 2 , and H 3 PO 4 . The synthesis was conducted at 130°C for 20 min in a sealed-vessel microwave reactor specifically designed for synthetic applications, and the resulting products were characterized using a wide battery of analytical techniques. Highly uniform, well-shaped nanorods of LaPO 4 ÁnH 2 O and La 0.98 Sr 0.02 PO 3.99 ÁnH 2 O were readily obtained, with average length of 213 ± 41 nm and 102 ± 25 nm, average aspect ratio (ratio between length and diameter) of 21 ± 9 and 12 ± 5, and specific surface area of 45 ± 2 and 51 ± 1 m 2 /g, respectively. In both cases, the single-crystal nanorods grew anisotropically along their c crystallographic-axis direction. At 700°C, the hexagonal rhabdophane-type phase has already transformed into the monoclinic monazite-type structure, although the undoped and Sr-doped nanorods retain their morphological features and specific surface area during calcination.

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TP53 mutations are present in all molecular subtypes of breast cancer and often correlate with de-creased survival; however, few therapeutic options exist for patients with TP53-mutant breast can-cers. To discover therapeutic strategies for these patients, we investigated the sensitivity of 129 FDA-approved chemotherapies to TP53-KO and TP53-WT MCF7 breast adenocarcinoma cells and found p53 loss to confer sensitivity to 5-fluorouracil (5-FU). We then treated the p53-null cells and isogenic controls with F10, a second-generation polymeric fluoropyrimidine, and found this preferential cytotoxicity of TP53-KO cells to be significantly magnified. F10 killing could only minimally be rescued by addition of exogenous uridine, whereas it was completely abrogated by addition of exogenous thymidine, suggesting DNA incorporation to be central to the cytotoxic mechanism of action. Furthermore, F10 killing of p53-null cells was persistent even in heterogeneous cellular mixtures more reflective of natural tumor evolution. Together, our results suggest F10 may widen the therapeutic window for TP53-mutant breast cancer by enhancing genotoxicity in cells resistant to apoptosis.