SUMMARY Disparities in cancer care have been a long-standing challenge. We estimated the genetic ancestry of The Cancer Genome Atlas patients, and performed a pan-cancer analysis on the influence of genetic ancestry on genomic alterations. Compared with European Americans, African Americans (AA) with breast, head and neck, and endometrial cancers exhibit a higher level of chromosomal instability, while a lower level of chromosomal instability was observed in AAs with kidney cancers. The frequencies of TP53 mutations and amplification of CCNE1 were increased in AAs in the cancer types showing higher levels of chromosomal instability. We observed lower frequencies of genomic alterations affecting genes in the PI3K pathway in AA patients across cancers. Our result provides insight into genomic contribution to cancer disparities.

Despite the development of medical technology, cancer still remains a great threat to the survival of people all over the world. Photothermal therapy (PTT) is a minimally invasive method for selective photothermal ablation of cancer cells without damages to normal cells. Recently, copper chalcogenide semiconductors have emerged as a promising photothermal agent attributed to strong absorbance in the near-infrared (NIR) region and high photothermal conversion efficiency. An earlier study witnessed a rapid increase in their development for cancer therapy, including CuS, CuSe and CuTe nanocrystals. However, a barrier is that the minimum laser power intensity for effective PTT is still significantly higher than the conservative limit for human skin exposure. Improving the photothermal conversion efficiency and reducing the laser power density has become a direction for the development of PTT. Furthermore, in an effort to improve the therapeutic efficacy, many multimode therapeutic nanostuctures have been formulated by integrating the photothermal agents with antitumor drugs, photosensitizers, or radiosensitizers, resulting in a synergistic effect. Various functional materials also have been absorbed, attached, encapsulated, or coated on the photothermal nanostructures, including fluorescence, computed tomography, magnetic resonance imaging, realizing cancer diagnosis, tumor location, site-specific therapy, and evaluation of therapeutic responses via incorporation of diagnosis and treatment. In this Account, we present an overview of the NIR-responsive photothermal semiconductor nanomaterials for cancer theranostics with a focus on their design and functionalization based on our own work. Our group has developed a series of chalcogenides with greatly improved NIR photoabsorption as photothermal agents, allowing laser exposure within regulatory limits. We also investigated the photothermal bioapplications of hypotoxic oxides including WO, MoO, and RuO, expanding their applications into a new field of photothermal materials. Furthermore, considering a much more enhanced therapeutic effect of multifunctional nanoagents, our group elaborately designed many nanocomposites, such as core-shell nanoparticles of FeO@CuS and CuS@mSiO, based on the integration of photothermal agents with contrast agents or other anticancer medicines, achieving cancer theranostic and synergistic treatment. Ternary compound nanocrystals were also prepared with synthetic simplicity for multimodal imaging-guided therapy for cancer. This Account summarizes our past work, including the design and concept, synthesis, and characterization for in vitro and in vivo applications. Then, we analyzed the tendencies of the NIR-responsive photothermal semiconductor nanomaterials for clinical applications, highlighting their prospects and challenges. We believe that the photothermal technology from the NIR-responsive photothermal semiconductor nanomaterials would promote cancer theranostics to result in giant strides forward in the future.

Objective. Macrophages release cytokines, such as tumor necrosis factor ␣ (TNF␣), interleukin-1 (IL-1), and IL-6, which modulate the symptoms of rheumatoid arthritis (RA). Macrophage release of these cytokines can be modulated by estrogen. Fc␥ receptor type IIIA (CD16a) is a receptor expressed on macrophages that selectively binds IgG molecules, an important rheumatoid factor in RA. Binding of CD16 by anti-CD16 monoclonal antibodies stimulates macrophage cytokine release. We undertook this study to test the hypothesis that decreased concentrations of estrogen (17␤-estradiol) directly cause an increase in CD16 expression, resulting in increased release of proinflammatory cytokines from monocytes and/or macrophages upon receptor binding.Methods. THP-1 cells and female human primary monocytes and monocyte-derived macrophages were treated with no 17␤-estradiol, physiologic levels (1 ؋ 10 ؊8 M) of 17␤-estradiol, or 1 ؋ 10 ؊8 M 17␤-estradiol followed by withdrawal of 17␤-estradiol. Surface expression of CD16 and CD16 messenger RNA was measured using fluorescence-activated cell sorting (FACS) and semiquantitative reverse transcription-polymerase chain reaction, respectively. Cytokine release from 17␤-estradiol-treated or untreated monocytes was then quantitated by enzyme-linked immunosorbent assay and FACS after crosslinking the receptor with anti-CD16 antibodies.Results. CD16 transcript significantly increased in macrophage-like THP-1 cells and in primary, peripheral blood macrophages in the absence of 17␤-estradiol, and the observed increase in message was dependent on transcription. CD16 receptor levels on CD14؉, transforming growth factor ␤-treated primary monocytes also increased in cells deprived of 17␤-estradiol. Analysis of the cytokines released showed that CD16 crosslinking stimulated significant increases in TNF␣, IL-1␤, and IL-6 due to the absence of estrogen.Conclusion. Estrogen can modulate proinflammatory cytokine release from activated monocytes and/or macrophages, in part through modulation of CD16 expression.

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MnO@C microsphere are designed as anodes to alleviate volume changes and enhance conductivity, showing improved lithium ion battery performance.