Back

Multi-lineage natural gene therapy mediated by embryonic triploid mosaicism in the context of Fanconi anaemia

Sharp, M. F.; Harris, C.; Mukherjee, C.; Novakovic, S.; Granger, E.; Pujol, R.; Munoz-Pujol, G.; Shi, E.; Dun, K.; Salinas-La Rosa, C.; Xu, Z. H.; Pertile, M.; Standen, K.; Walsh, R.; Deans, A. J.; Velleuer-Carlberg, E.; Moses, J.; Nandini, A.; Nelson, A.; Worgan, L.; Surralles, J.; Crismani, W.

2025-11-04 genetic and genomic medicine
10.1101/2025.10.29.25337140 medRxiv
Show abstract

Fanconi anemia is a rare inherited bone marrow failure syndrome caused by inactivation of genes in the Fanconi anemia/BRCA DNA repair pathway. We report a patient with X-linked Fanconi anemia, and atypical physical features whose genetic diagnosis was initially inconclusive. Over time, his bone marrow karyotype shifted from diploid (46,XY) to triploid (69,XXY). The triploid cells lacked the Fanconi anemia cellular phenotype, enabling sustained hematopoiesis and providing an unexpected route to phenotypic rescue. Genomic analysis indicated early post-zygotic incorporation of the second polar body as the triploid origin. These findings suggest that the selective advantage of restored DNA repair in hematopoietic stem cells, outweigh the potentially deleterious effects of triploidy.

Matching journals

The top 3 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.