Colloidal quantum dot materials for next-generation near-infrared optoelectronics.

Colloidal quantum dots (CQDs) are a promising class of materials for next-generation optoelectronic devices, such as displays, LEDs, lasers, photodetectors, and solar cells. CQDs can be obtained at low cost and in large quantities using wet chemistry. CQDs have also been produced using various materials, such as CdSe, InP, perovskites, PbS, PbSe, and InAs. Some of these CQD materials absorb and emit photons in the visible region, making them excellent candidates for displays and LEDs, while others interact with low-energy photons in the near-infrared (NIR) region and are intensively utilized in NIR lasers, NIR photodetectors, and solar cells. In this review, we have focused on NIR CQD materials and reviewed the development of CQD materials for solar cells, NIR lasers, and NIR photodetectors since the first set of reports on CQD materials in these particular applications.

CHD4 R975H mutant activates tumorigenic pathways and promotes stemness and M2-like macrophage polarization in endometrial cancer.

Endometrial cancer (EC), one of the most prevalent carcinomas in females, is associated with increasing mortality. We identified the CHD4 R975H mutation as a high-frequency occurrence in EC patients through a comprehensive survey of EC databases. Computational predictions suggest that this mutation profoundly impacts the structural and functional integrity of CHD4. Functional assays revealed that the CHD4 R975H mutation enhances EC cell invasion, proliferation, and colony formation, promoting a cancer stem cell (CSC)-like phenotype. RNA-seq analysis of cells expressing CHD4 R975H mutant revealed a transcriptomic landscape marked by the activation of several cancer-promoting signaling pathways, including TNF-α signaling via NF-κB, KRAS, P53, mTOR, TGF-ß, EGFR, Myc and growth factor signaling. Validation assays confirmed the activation of these pathways, further demonstrating that CHD4 R975H mutation induces stemness in EC cells and M2-like polarization of tumor-associated macrophages (TAMs). Our study elucidated the oncogenic role of CHD4 R975H mutation, highlighting its dual impact on facilitating cancer stemness and transforming TAMs into an immunosuppressive subtype. These findings contribute valuable insights into the molecular mechanisms driving EC progression and open avenues for targeted therapeutic interventions.