bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.05.21.726767

Label-Free Multimodal Volumetric Imaging of Colon Cancer Tissue via Registration of Propagation-Based Phase-Contrast CT, Light-Sheet, and Three-Photon Microscopy

Abstract

Multimodal 3D imaging has emerged as a powerful approach for investigating complex tissue architecture in pathological specimens. Techniques such as propagation-based phase-contrast computed tomography (PCT), light-sheet microscopy (LSM), and three-photon microscopy (3PM) provide complementary information on unlabeled tissue morphology based on distinct intrinsic contrast mechanisms. However, integrating these heterogeneous datasets into a unified spatial framework remains challenging due to differences in imaging geometry, spatial resolution, and modality-specific distortions. In this study, we present a registration pipeline for spatially aligning volumetric datasets acquired with PCT, LSM, and 3PM from formalin-fixed paraffin-embedded (FFPE) human colon cancer specimens. Biopsies from theses specimens were optically cleared and imaged sequentially using the three high-resolution modalities. To compensate for large positional differences between acquisitions, a three-stage cascade registration strategy was developed, consisting of coarse global alignment on down-sampled data, followed by rigid refinement at intermediate resolution. Mutual information was used as the similarity metric to ensure robust multimodal registration. The resulting framework enables the generation of spatially aligned multi-channel 3D datasets that combine structural information from X-ray phase-contrast imaging with complementary optical contrast signals. Beyond registration, we demonstrate that the fused six-dimensional feature space can be further exploited for unsupervised tissue characterization using a Gaussian Mixture Model (GMM), enabling data-driven identification of spatially coherent tissue regions without manual annotation. Qualitative evaluation confirms consistent alignment of major anatomical structures across modalities, while the unsupervised clustering reveals biologically meaningful patterns despite modality-specific noise and resolution differences. While further optimization and validation across larger datasets will enhance its computational efficiency and breadth of application, the approach already demonstrates strong potential for comprehensive tissue analysis and enables scalable, label-free 3D characterization of colon cancer tissue architecture.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dullin, C., Schroeter, M., Pinkert-Leetsch, D., Ramos-Gomes, F., Markus, A., Missbach-Guentner, J., Bohnenberger, H., Stroebel, P., Alves, F.. 2026-05-25. Label-Free Multimodal Volumetric Imaging of Colon Cancer Tissue via Registration of Propagation-Based Phase-Contrast CT, Light-Sheet, and Three-Photon Microscopy. https://doi.org/10.64898/2026.05.21.726767

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Identification of Novel Inhibitors of JEV RdRp as Potent Antiviral Drugs: Targeting NS5-NS3 Protein Interaction

Japanese Encephalitis Virus (JEV) belongs to the Flavivirus family, and the RNA dependent RNA polymerase (RdRp) domain located at the C terminus of non structural protein 5 (NS5) regulates de novo viral genome synthesis. The conserved priming loop inserted in the thumb domain of RDRP initiates de novo genome synthesis. Interestingly, the reported replication process initiates with an interaction between NS5 (methyltransferase/RDRP) and NS3 (protease/helicase), and inhibiting this interaction directly correlates with the inhibition of viral replication. The function of the priming loop in the context of the NS5 NS3 interaction is not yet known. In this study, we studied the priming loop function in the NS5 NS3 interaction and viral replication. Using a structure based drug design approach, we screened the Maybridge compound library against the RdRp priming loop and identified 15 candidate compounds based on binding energy. Among them, DSHS00151 showed significant dose dependent inhibition of the NS5 NS3 interaction with an IC50 of 3.5 micromolar in the mammalian two hybrid assay, inhibited viral infectivity with an IC50 of 2.54 micromolar, and reduced viral RNA load with an IC50 of 2.9 micromolar, compared to CD10712. Molecular Dynamics (MD) simulations revealed that DSHS00151 exhibits stronger and more stable binding with the priming loop residues (790 to 812) compared to CD10712. The molecular mechanism suggested by the docking of the NS5 and NS3 proteins showed that the priming loop tends to rotate toward the NS3 protein to stabilize the complex, and compound binding restricts this loop rotation, thus compromising the stability of the NS5 and NS3 complex and affecting viral replication. Overall, our study validated the function of the NS5 priming loop as an allosteric site, and compounds binding to this allosteric site belong to the Non Nucleoside Reverse Transcriptase Inhibitors (NNRTI) class of inhibitors, which disrupt the NS5 and NS3 interaction and could be developed as novel anti JEV therapeutics.

pathology↗

Autophagic flux is increased in peripheral blood mononuclear cells in atherosclerotic vascular disease and associates inversely with adverse cardiovascular events

Background: Autophagy is a homeostatic pathway supporting stress adaptation and is dysregulated in atherosclerosis. Its potential as a biomarker or therapeutic target in atherosclerotic vascular disease (ASVD) remains incompletely defined. We measured autophagic flux in peripheral blood mononuclear cells (PBMCs) from patients with peripheral arterial disease (PAD) or carotid stenosis (CS), compared with healthy controls, and explored clinical outcome associations. Methods: Ninety-four patients with PAD or CS and 19 healthy controls were studied. Autophagic flux was quantified from fresh blood using a validated ex vivo chloroquine inhibition ELISA measuring LC3BII accumulation. Major adverse cardiovascular events (MACE) and major adverse limb events (MALE) were ascertained over a median follow up of 828 days. Results: The ASVD cohort comprised claudication (n = 16), chronic limb threatening ischemia (CLTI; n = 49), and CS (n = 29). Autophagic flux was higher in ASVD than controls (mean 281.4 vs. 182.3 ng LC3BII/mg protein/h; p < 0.0001) and remained independently associated after multivariable adjustment. Within CLTI, concurrent infection was associated with lower flux (p = 0.001), approaching control levels (p = 0.327). In CLTI, higher flux quartiles were associated with lower MACE risk, most strongly for quartile 3 (hazard ratio 0.07 vs. quartile 1, 95% CI 0.01 to 0.50; p = 0.009). Conclusion: Autophagic flux is elevated in PBMCs from ASVD patients, independent of age and sex. Attenuated flux in CLTI with concurrent infection may indicate autophagic exhaustion in advanced disease. The association between higher flux and lower MACE in CLTI suggests prognostic utility, warranting evaluation in larger prospective studies.

pathology↗

Quantitative Model of the Ocular Immune Response during Seasonal Allergic Conjunctivitis

Allergic conjunctivitis is an inflammation of the conjunctiva caused by allergen; it is common disorder affecting up to 40% of the population. In this work, we study seasonal allergic conjunctivitis (SAC), also called "hay fever eyes", which is caused by exposure to airborne pollens. We develop a mathematical model quantifying the ocular immune system response to the allergens. First, we present a simplified qualitative description of the immunopathogenesis of SAC. Then, we express each chosen immunopathological mechanism mathematically to construct a system of thirty-one ordinary differential equations. We compare summary statistics of the predicted observable immune signals to experimental measurements and find our model captures key qualitative features of SAC progression. We then compare our predicted time series of histamine concentration to symptom scores and find a strong correlation suggesting the model predicts relevant clinically trends. Next, we calibrate the model through multi-step process. We find the most influential parameters are the production and depletion rates of IL-4, and the production rates of IL-5 and IL-8. These cytokines are targeted in treatments for asthma, atopic dermatitis, and severe eosinophilic associated disorder and suggest potential therapeutic targets for SAC. Our calibrated model mimics most of the summary statistics of the experimentally observable immune signals with discrepancies for IL-5 and IL-13 indicating that additional immunopathological mechanisms could be important.

pathology↗