ArticlebioRxiv : the preprint server for biology2026
Mapping breast cancer lineage in radiation and immunotherapy using the REMAP mouse.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
We present REMAP (Recording Evolution in Mammary tumors via Active PyMT), a lineage-tracing mouse model that integrates inducible CRISPR recording with the MMTV-PyMT model of hormone receptor-positive (HR+) breast cancer. Inducible Cas9 drives editing of MARC1 homing guide RNAs (hgRNAs), generating heritable lineage marks, and enables reconstruction of clonal relationships. Using REMAP, we profiled tumor evolution and response to radiation combined with anti-PD1 immunotherapy. Treatment reduced tumor burden locally and systemically, and single-cell RNA sequencing revealed remodeling of the tumor microenvironment (TME). We identified metastatic clones present across primary tumors and distant sites, which exhibited elevated epithelial-mesenchymal transition (EMT) programs as a heritable clonal state. Treatment reduced EMT-associated transcriptional programs and reshaped immune composition, with radiation driving clonal expansion of T cells and reduced repertoire diversity. In contrast, cancer-associated fibroblast clones spanned multiple transcriptional states, indicating substantial stromal plasticity. Together, REMAP enables high-resolution coupling of clonal history and cellular state in vivo, revealing that tumor progression, metastasis, and therapeutic response are governed by heritable lineage programs.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.