Special considerations for the use of AI tools by PEERs as a learning and communication aid.

There is no doubt that navigating academia is a formidable challenge, particularly for those from underrepresented backgrounds who face additional barriers at every turn. In such an environment, efforts to create learning and training environments that are diverse, equitable, and inclusive can feel like an uphill battle. We believe that harnessing the power of artificial intelligence (AI) tools can help in leveling the playing field. While AI cannot supplant the need for supportive mentorship, it can serve as a vital supplement, offering guidance and assistance to those who may lack access to adequate avenues of support. Embracing AI in this context should not be stigmatized, as it may represent a vital lifeline for underrepresented individuals who often face systemic biases while forging their own paths in pursuit of success and belonging in academia. AI tools should not be gatekept from these individuals, particularly by those in positions of power and privilege within the scientific community. Instead, we argue, institutions should make a strong commitment to educating their community members on how to ethically harness these tools.

Chemotherapy induces myeloid-driven spatial T-cell exhaustion in ovarian cancer.

To uncover the intricate, chemotherapy-induced spatiotemporal remodeling of the tumor microenvironment, we conducted integrative spatial and molecular characterization of 97 high-grade serous ovarian cancer (HGSC) samples collected before and after chemotherapy. Using single-cell and spatial analyses, we identify increasingly versatile immune cell states, which form spatiotemporally dynamic microcommunities at the tumor-stroma interface. We demonstrate that chemotherapy triggers spatial redistribution and exhaustion of CD8+ T cells due to prolonged antigen presentation by macrophages, both within interconnected myeloid networks termed "Myelonets" and at the tumor stroma interface. Single-cell and spatial transcriptomics identifies prominent TIGIT-NECTIN2 ligand-receptor interactions induced by chemotherapy. Using a functional patient-derived immuno-oncology platform, we show that CD8+T-cell activity can be boosted by combining immune checkpoint blockade with chemotherapy. Our discovery of chemotherapy-induced myeloid-driven spatial T-cell exhaustion paves the way for novel immunotherapeutic strategies to unleash CD8+ T-cell-mediated anti-tumor immunity in HGSC.