Photothermal ablation (PTA) therapy has a great potential to revolutionize conventional therapeutic approaches for cancers, but it has been limited by difficulties in obtaining biocompatible photothermal agents that have low cost, small size (<100 nm), and high photothermal conversion efficiency. Herein, we have developed hydrophilic plate-like Cu(9)S(5) nanocrystals (NCs, a mean size of ∼70 nm × 13 nm) as a new photothermal agent, which are synthesized by combining a thermal decomposition and ligand exchange route. The aqueous dispersion of as-synthesized Cu(9)S(5) NCs exhibits an enhanced absorption (e.g., ∼1.2 × 10(9) M(-1) cm(-1) at 980 nm) with the increase of wavelength in near-infrared (NIR) region, which should be attributed to localized surface plasmon resonances (SPR) arising from p-type carriers. The exposure of the aqueous dispersion of Cu(9)S(5) NCs (40 ppm) to 980 nm laser with a power density of 0.51 W/cm(2) can elevate its temperature by 15.1 °C in 7 min; a 980 nm laser heat conversion efficiency reaches as high as 25.7%, which is higher than that of the as-synthesized Au nanorods (23.7% from 980 nm laser) and the recently reported Cu(2-x)Se NCs (22% from 808 nm laser). Importantly, under the irradiation of 980 nm laser with the conservative and safe power density over a short period (∼10 min), cancer cells in vivo can be efficiently killed by the photothermal effects of the Cu(9)S(5) NCs. The present finding demonstrates the promising application of the Cu(9)S(5) NCs as an ideal photothermal agent in the PTA of in vivo tumor tissues.

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Over 90% of chondroblastomas contain a heterozygous mutation replacing lysine 36 with methionine (K36M) in the histone H3 variant H3.3. Here, we show that H3K36 methylation is reduced globally in chondroblastomas and in chondrocytes harboring the same genetic mutation due to inhibition of at least two H3K36 methyltransferases, MMSET and SETD2, by the H3.3K36M mutant proteins. Genes with altered expression as well as H3K36 di- and trimethylation in H3.3K36M cells are enriched in cancer pathways. In addition, H3.3K36M chondrocytes exhibit several hallmarks of cancer cells including increased ability to form colonies, resistance to apoptosis and defects in differentiation. Thus, H3.3K36M proteins reprogram H3K36 methylation landscape and contribute to tumorigenesis in part through altering the expression of cancer-associated genes.