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@sigtrans-sttt.bsky.socialOct 10, 2026, 2:45 AM

#TumorHeterogeneity challenges antigen-specific #Vaccination.

This review explores how in situ #CancerVaccines combine immunogenic cell death, advanced delivery, microenvironment modulation, and checkpoint blockade to broaden antitumor immunity.
#STTT #OpenAccess: doi.org/10.1038/s413...

Combinatorial in situ cancer vaccines: unlocking broad and enhanced antitumor responses
@sigtrans-sttt.bsky.socialSep 24, 2026, 7:30 AM

#TumorHeterogeneity fuels #Cancer progression and treatment resistance through clonal evolution, stem cell plasticity, and microenvironmental crosstalk, highlighting the need for dynamic monitoring and precision therapies.

#STTT #OpenAccess: doi.org/10.1038/s413...

Tumor heterogeneity: development, mechanisms, and therapeutic implications
@sigtrans-sttt.bsky.socialSep 22, 2026, 3:00 AM

#TumorHeterogeneity and #Immunosuppressive microenvironments hinder the treatment of #SolidTumors.

This review explores diverse immune and stem-cell platforms, alongside allogeneic and in vivo engineering strategies for broader cancer treatment.

#STTT #OpenAccess: doi.org/10.1038/s413...

Advances and prospects in cell therapy for cancer: explorations from T cells to stem cells
@alicefrolov.bsky.socialSep 10, 2026, 5:07 PM

Sharing a visualization from ongoing work on cancer stem cell (CSC) clonal dynamics under therapeutic pressure.

#CancerStemCells #TumorHeterogeneity #ClonalEvolution #MinimalResidualDisease #TumorPlasticity #DrugTolerantPersisters #SingleCellGenomics #PhylogeneticReconstruction

Sharing a visualization from ongoing work on cancer stem cell (CSC) clonal dynamics under therapeutic pressure.

Figure: "Therapy reshapes clonal hierarchy via stem-like subclone selection"
Subtitle: "Ranked clonal fraction of tumor subclones across treatment phases; stem-marked clones rise under selective pressure"

The chart is a phylogenetic bump plot (Muller-style ranked clonal flow) tracking the relative clonal fraction of individual subclones across sequential treatment phases: baseline, on-treatment, minimal residual disease (MRD), and relapse. Each ribbon corresponds to a distinct subclone, with vertical band thickness encoding clonal fraction and vertical ordering encoding rank. Subclones carrying stem-associated marker states (e.g., high ALDH activity, CD133/CD44 enrichment, quiescence-linked transcriptional programs) are highlighted to distinguish them from bulk proliferative lineages.

The illustrated trajectory recapitulates a well-documented pattern: cytotoxic selection preferentially depletes proliferative, differentiation-committed subclones while sparing slow-cycling, stem-marked populations. During the MRD window, stem-like ribbons ascend in rank despite overall tumor contraction, consistent with therapy-tolerant persister states buffered by quiescence, enhanced drug efflux, and reinforced self-renewal signaling (WNT, NOTCH, Hedgehog). At relapse, these ascended subclones seed the reconstituted hierarchy, producing a repopulated tumor with an altered clonal architecture rather than a faithful reconstruction of the baseline composition.

I want to emphasize that the underlying data here are simulated. The intent is to render a literature-grounded trend in an interpretable topological format, not to present empirical measurements. The parameterization draws on reported CSC plasticity and selection dynamics, but ribbon values are synthetic.