bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.10.12.758609

AI-ASSISTED NANOMEDICINE REVEALS SYSTEMIC IMMUNE IMPACT IN OVARIAN CANCER METASTASIS

Abstract

Ovarian cancer, a gynecological malignancy, poses a significant challenge as researchers struggle to comprehend how tumor cells communicate with the immune system. Ovarian tumors contain both bulk cancer cells and cancer stem cells (CSCs), which are linked to chemoresistance, relapse, and immune escape. However, it remains unclear whether these two populations affect immune cells differently. To investigate this, a study used surface-enhanced Raman spectroscopy (SERS) combined with machine learning to examine the biochemical changes in peripheral blood mononuclear cells (PBMCs) after co-culture with OVCAR4 ovarian cancer cells or OVCAR4-derived CSC-enriched populations. PBMCs and tumor cells were co-cultured for 48 hours in an indirect Transwell system, allowing exchange of soluble factors without direct cell contact. SERS spectra were acquired on gold-coated nickel substrates and analyzed using principal component analysis, t-test, and a linear support vector machine (SVM). The results showed that PBMCs co-cultured with CSCs and PBMCs co-cultured with OVCAR4 cells exhibited distinct spectral profiles. Moreover, the SVM demonstrated a high cross-validated accuracy of 98.9% in separating these two populations. PBMCs exposed to CSCs exhibited higher adenine and carbohydrate signals, while those exposed to OVCAR4 cells displayed higher protein and lipid signals. Interestingly, the tumor cells themselves exhibited the same pattern at baseline. Moreover, six out of the ten most discriminating bands were shared between the tumor and PBMC comparisons, indicating a consistent direction of change. These findings suggest that tumor-derived soluble factors leave a distinct biochemical signature on PBMCs. Label-free SERS combined with machine learning offers a sensitive approach for studying tumor-immune communication and developing blood-based tools to monitor ovarian cancer.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Manandhar, R., Tchalabi, H., Kesavan, Y., Koroma, S., Holman, L., Haldavnekar, R.. 2026-10-14. AI-ASSISTED NANOMEDICINE REVEALS SYSTEMIC IMMUNE IMPACT IN OVARIAN CANCER METASTASIS. https://doi.org/10.64898/2026.10.12.758609

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

KEEP EXPLORING

Related preprints

Spatial epigenomics reveals ancestry-associated regulatory states linked to aggressive prostate cancer biology

Prostate cancer (PCa) exhibits substantial biological heterogeneity, including population associated differences in tumor aggressiveness and clinical outcomes. Although socioeconomic and environmental factors contribute to these disparities, intrinsic tumor regulatory programs may also influence disease behavior. Here, we investigated whether differences in chromatin regulation contribute to distinct tumor states in Black and White men with localized PCa. We performed spatial chromatin accessibility profiling (ATAC-seq) of prostatectomy specimens from Black and White patients receiving equal healthcare access at the Center for Prostate Disease Research (USUHS) and Walter Reed National Military Medical Center. Tumors showed distinct chromatin accessibility landscapes between the two populations, with tumors from Black patients exhibiting reduced accessibility of motifs associated with the chromatin architectural regulator CTCF and enrichment of motifs linked to epithelial-mesenchymal transition and inflammatory programs. Reduced CTCF expression was independently validated by immunohistochemistry in 99 prostatectomy specimens. These findings identify population-associated differences in chromatin regulation in localized PCa and suggest that altered CTCF-associated regulation, inflammatory signaling, and epithelial plasticity may contribute to the biological heterogeneity underlying ancestry-dependent PCa disparities.

cancer biology↗

Domain-resolved epitope mapping of B7-H3-targeting VHH-Fcs defines isoform-selective binders for antibody-drug conjugate development

The immune checkpoint molecule B7-H3 has emerged as one of the most actively pursued therapeutic targets in solid tumors, and multiple B7-H3-targeting antibody-drug conjugates have entered clinical evaluation. B7-H3 occurs as a 2Ig isoform carrying a single IgV-IgC domain pair and a predominant 4Ig isoform carrying two tandem pairs of near-identical sequence in their extracellular domains. Resolving which pair an antibody engages, or how antibodies distinguish the two isoforms, requires epitope mapping at residue level. Here we generated a panel of six B7-H3-targeting VHH-Fcs and characterized them by surface plasmon resonance, epitope binning, domain-resolved deep mutational scanning and receptor internalization, benchmarked against the clinically advanced antibodies ifinatamab, mirzotamab and vobramitamab. Most VHH-Fcs bound the membrane-proximal pair more tightly than the distal pair, and 4Ig 10- to 100-fold more tightly than 2Ig, whereas the three clinical antibodies showed no such discrimination. Displaying each domain pair independently on yeast identified the residues that account for this selectivity. Internalization varied several-fold among binders, including between VHH-Fc 620 and 636, which have near-identical footprints and comparable affinities. VHH-Fc 620 internalized most efficiently, also compared to ifinatamab, and was conjugated to exatecan through a protease-cleavable linker. The conjugate showed B7-H3-dependent cytotoxicity that scaled with B7-H3 cell surface density, though it was less potent than ifinatamab-exatecan. Affinity, epitope and internalization therefore behaved as independent characteristics rather than integrating to predict antibody-drug conjugate potency. Together, these results define the molecular basis for isoform-selective recognition of B7-H3 and identify VHH-Fc 620 as a starting point for isoform-selective targeting.

cancer biology↗

Bioenergetic and Proteomic Profiling of ARID1A-Deficient Ovarian Clear Cell Carcinoma under Metabolic Challenge

ARID1A loss is associated with increased mitochondrial respiration in ovarian clear cell carcinoma (OCCC), but whether this phenotype is maintained under metabolic challenge remains unclear. Here, we examined mitochondrial function and electron transport chain (ETC) protein abundance in isogenic ARID1A wild-type (WT) and ARID1A-knockout (KO) OCCC cells cultured under physiological glucose, galactose, or the Complex I inhibitor IACS-010759. Across all conditions, KO cells maintained higher basal, ATP-linked, and maximal respiration, greater spare respiratory capacity, and higher coupling efficiency than WT cells, despite lower steady-state ATP levels. In human OCCC tumors, ARID1A-negative cases showed a higher bioenergetic cellular (BEC) index than ARID1A-positive cases, and high BEC was associated with poorer cancer-specific survival. Quantitative proteomics revealed a trend toward higher ETC complex abundance in KO cells, although whole-complex differences did not reach statistical significance. ARID1A loss was associated with selective increases in Complex III and V proteins, whereas metabolic challenge was associated with increases in Complex I and IV proteins. Together, these findings show that the ARID1A-associated mitochondrial phenotype persists across distinct metabolic challenges and is not explained simply by coordinated increases in ETC protein abundance. The association of mitochondrial bioenergetics with clinical outcomes further supports its relevance in human OCCC.

cancer biology↗