Bringing together the RegenSeq community across multiplexed imaging, spatial transcriptomics, and optical pooled screening.

QED Science says that its metrics reduce bias by assessing papers solely on the basis of their originality and validity.

Researchers show how the senescent state induced by sarcoma and breast cancer drugs drives inflammation—and how it could be suppressed.

The p16-3MR mouse model, designed to express Renilla luciferase, mRFP, and herpes simplex virus 1 thymidine kinase (HSV-TK) under the p16INK4a promoter, has been widely used to visualize and ablate senescent cells in vivo, but our analyses revealed critical limitations. Bioluminescence signals in p16-3MR mice were extremely weak and virtually indistinguishable from those of wild-type mice injected with coelenterazine-h, indicating that previously reported signals largely reflected substrate background rather than authentic reporter expression. Signal intensity remained unchanged with aging, doxorubicin treatment, or cutaneous wound healing, failing to replicate earlier observations. Furthermore, RFP signals were undetectable in senescent fibroblasts from p16-3MR mice, and senescent cells were not eliminated by ganciclovir treatment, suggesting poor expression and lack of functional activity of the mRFP and HSV-TK transgenes. These results demonstrate functional deficiencies in all three transgenes, highlighting the importance of using wild-type controls and calling for careful reevaluation of studies employing this system.

Parents want accountability after study went disastrously wrong, Science and Retraction Watch investigation reveals