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Accurately identifies the cellular composition of complex tissues, which is critical for understanding disease pathogenesis, early diagnosis, and prevention. However, current methods for deconvoluting bulk RNA sequencing (RNA‐seq) typically rely on matched single‐cell RNA sequencing (scRNA‐seq) as a reference, which can be limiting due to differences in sequencing distribution and the potential for invalid information from single‐cell references. Hence, a novel computational method named SCROAM is introduced to address these challenges. SCROAM transforms scRNA‐seq and bulk RNA‐seq into a shared feature space, effectively eliminating distributional differences in the latent space. Subsequently, cell‐type‐specific expression matrices are generated from the scRNA‐seq data, facilitating the precise identification of cell types within bulk tissues. The performance of SCROAM is assessed through benchmarking against simulated and real datasets, demonstrating its accuracy and robustness. To further validate SCROAM's performance, single‐cell and bulk RNA‐seq experiments are conducted on mouse spinal cord tissue, with SCROAM applied to identify cell types in bulk tissue. Results indicate that SCROAM is a highly effective tool for identifying similar cell types. An integrated analysis of liver cancer and primary glioblastoma is then performed. Overall, this research offers a novel perspective for delivering precise insights into disease pathogenesis and potential therapeutic strategies. [ABSTRACT FROM AUTHOR]

Repopulation of residual tumor cells impedes curative radiotherapy, yet the mechanism is not fully understood. It is recently appreciated that cancer cells adopt a transient persistence to survive the stress of chemo-or targeted therapy and facilitate eventual relapse. Here, it is shown that cancer cells likewise enter a "radiation-tolerant persister" (RTP) state to evade radiation pressure in vitro and in vivo. RTP cells are characterized by enlarged cell size with complex karyotype, activated type I interferon pathway and two gene patterns represented by CST3 and SNCG. RTP cells have the potential to regenerate progenies via viral budding-like division, and type I interferon-mediated antiviral signaling impaired progeny production. Depleting CST3 or SNCG does not attenuate the formation of RTP cells, but can suppress RTP cells budding with impaired tumor repopulation. Interestingly, progeny cells produced by RTP cells actively lose their aberrant chromosomal fragments and gradually recover back to a chromosomal constitution similar to their unirradiated parental cells. Collectively, this study reveals a novel mechanism of tumor repopulation, i.e., cancer cell populations employ a reversible radiation-persistence by poly- and de-polyploidization to survive radiotherapy and repopulate the tumor, providing a new therapeutic concept to improve outcome of patients receiving radiotherapy. [ABSTRACT FROM AUTHOR]