Back

Tumor-myeloid crosstalk drives therapy resistance in localized bladder cancer

Carvalho, F. L.; Lee, J.; Kalavros, N.; Zhou, Y.; Michaud, D.; Stelter, I.; Siddiqui, H.; Stawiski, K.; Bel, J. P.; Wang, S.; Garza, A.; Bi, K.; Park, J.; Egan, J. M.; Hirohashi, Y.; Epstein, I.; Vlachos, I.; Jia, L.; Kibel, A. S.; Hirsch, M.; Bellmunt, J.; Guerriero, J. L.; Mouw, K. W.; Van Allen, E. M.

2025-09-13 cancer biology
10.1101/2025.09.08.674862 bioRxiv
Show abstract

Neoadjuvant cisplatin-based chemotherapy results in pathologic complete response for only a minority of patients with muscle-invasive bladder cancer (MIBC), and mechanisms of resistance and the effects of chemotherapy on the MIBC microenvironment remain incompletely understood. Here, we defined the single-cell and spatial transcriptomes of cancer and immune cells from MIBC patients with resistance to cisplatin-based chemotherapy. Tumors with persistent MIBC after chemotherapy harbored cancer cells expressing epithelial-to-mesenchymal programs that were associated with worse overall survival in independent cisplatin-treated bladder cancer cohorts. These cisplatin-resistant tumor cells were infiltrated by macrophages that upregulated tumor permissive programs defined by increased PARP14 expression in spatially resolved multicellular niches. Macrophage reprogramming through PARP14 inhibition sensitized tumors to cisplatin via downregulation of tumor cell pathways implicated in resistance. Our results demonstrate that cancer cells and macrophages cooperate to promote cisplatin resistance and identify macrophage-directed PARP14 inhibition as a novel therapeutic strategy to sensitize MIBC to cisplatin.

Matching journals

The top 7 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.