Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.11.19.684505

Characterization of lymphoma models for the surface ROR1 expression

Abstract

Receptor tyrosine kinase-like orphan receptor 1 (ROR1) is a developmental antigen aberrantly expressed in several B-cell malignancies and represents an attractive therapeutic target. Here, we systematically characterized ROR1 expression in a large panel of B-cell lymphoma cell lines and assessed the activity of a ROR1-targeting antibody-drug conjugate (ADC). ROR1 RNA expression was first evaluated using a previously generated total RNA-Seq dataset from 47 B-cell lymphoma cell lines. ROR1 transcripts were detectable in most models, with 19 cell lines showing moderate to high expression. To determine whether ROR1 is present on the cell surface, we next analyzed 29 cell lines by flow cytometry using a PE-conjugated anti-ROR1 antibody. Only a subset of cell lines expressed appreciable levels of ROR1 on the cell membrane, with the highest expression observed in mantle cell lymphoma (MCL) models compared with other B-cell lymphoma subtypes, and detectable expression in a few diffuse large B-cell lymphoma (DLBCL) and one marginal zone lymphoma (MZL) line. ROR1 RNA and surface protein levels were highly correlated. As a proof of principle, four ROR1-positive DLBCL cell lines and one cell line with low surface protein were exposed to the ROR1-targeting ADC zilovertamab vedotin for 120 hours. All ROR1-positive models were sensitive, with IC50 values ranging from 28 to 58 nM, whereas the remaining one was largely resistant. In summary, we defined a set of well-characterized lymphoma models suitable for preclinical studies of ROR1-directed agents, confirming the functional relevance of ROR1 surface expression for the activity of zilovertamab vedotin. The gene coding for the receptor tyrosine kinase-like orphan receptor 1 (ROR1) was initially identified while looking for genes encoding proteins with tyrosine kinase-like domains 1,2. It is now understood that ROR1 possesses intrinsic tyrosine kinase activity and also functions as a receptor for Wnt5a, which activates {beta}-catenin-independent non-canonical pathways, sustaining cell survival and oncogenesis 2,3. In adult tissues, including normal B lymphocytes, ROR1 is preferentially expressed by cancer cells rather than normal cells and has a role in sustaining the growth and survival of neoplastic cells 2,4. Several therapeutic strategies targeting ROR1 have been developed, including naked monoclonal antibodies, antibody-drug conjugates (ADCs), small molecule inhibitors, bispecific T cell engager (BiTE), and chimeric antigen receptor (CAR) T cells have been developed 2, with some currently in advanced clinical evaluation 2. Here, we characterized a vast panel of lymphoma cell lines for their ROR1 RNA level and ROR1 cell surface protein expression, and showed, using zilovertamab vedotin as proof-of-principle, that these models can be exploited to study this promising class of anti-cancer agents.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Tarantelli, C., Civanelli, E., Spriano, F., Risi, G., Cascione, L., Kaufmann, G., Bertoni, F.. 2025-11-19. Characterization of lymphoma models for the surface ROR1 expression. https://doi.org/10.1101/2025.11.19.684505

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

KEEP EXPLORING

Related preprints

Ex vivo human tumor slices more accurately predict patient responses to an oncolytic virus than in vivo mouse models

Immunotherapies, including oncolytic viruses (OV), are promising therapies that can enhance anti-tumor immune responses. However, preclinical success of immunotherapies in mouse models has not always translated to clinical benefit in cancer patients. This study compared preclinical efficacy and mechanism of action for ASP9801, a vaccinia virus expressing IL-7 and IL-12, using mouse models of colorectal cancer (CRC) in vivo and in human organotypic tumor slice models ex vivo. The murine surrogate for ASP9801 significantly reduced tumor volumes in treated and abscopal tumors in two different CRC models in vivo (MC38 and RO100). Treatment efficacy was accentuated when combined with anti-PD1 treatment, and single-cell RNA sequencing analysis revealed depletion of tumor cells and increased T cell infiltration and activation in both treated and abscopal tumors. However, human tissue analysis ex vivo (E-slices) using PDX models and patient samples showed that ASP9801 is not effective in CRC, consistent with clinical trial results. On the other hand, ASP9801 was highly effective in GBM, indicating indication-specific efficacy of ASP9801, and how E-slice assays can be used to identify treatment-sensitive indications. This study demonstrates the superiority of E-slices over mouse models for predicting clinical response and its utility in planning clinical trials.

cancer biology↗

Immune-cell depleted diffuse large B-cell lymphomas have reduced expression of MHC class I

Immunotherapy has transformed treatment for many cancers. In the aggressive and genetically heterogeneous diffuse large B-cell lymphoma (DLBCL), CD19 CAR T-cell therapy is highly effective, whereas immune checkpoint blockade has shown limited benefit. Loss of MHC expression is a common mechanism to escape T-cell cytotoxicity, and loss of MHC class I (MHC-I) and II are frequent in DLBCL. We applied imaging mass cytometry to diagnostic biopsies from younger, high-risk DLBCL patients to map the tumor microenvironment (TME) spatial architecture in relation to tumor cell MHC expression, mutational status, transcriptomic and proteomic profiles. Neighborhood analyses identified four TME subtypes: immune-cell depleted and three immune-infiltrated types (mixed, CD4 T cell-rich, CD8 T-cell/macrophage-rich). Depleted cases had shorter overall survival (p = 0.033) and increased expression of proteins involved in DNA replication and proliferation markers compared to infiltrated cases. Tumor cell MHC-I expression was heterogeneous. Cases with low frequency of MHC-I-pos tumor cells were enriched for the depleted TME type. MHC-I-pos tumor cells were surrounded by CD4 and CD8 T cells and M1 macrophages, whereas MHC-I-neg tumor cells were closer to other MHC-I-neg tumor cells. These findings suggest that TME-based classification incorporating tumor cell MHC-I status may improve individualized immunotherapy selection.

cancer biology↗

Cross-species analysis links cell-cell communication rewiring to NOTCH2 during serous endometrial carcinogenesis

Cell-cell interactions shape the fate of mutant cells during cancer initiation but how these interactions evolve during progression to pathologically recognizable lesions remain poorly understood. Here, we investigated cell-cell communication during serous endometrial carcinoma (SEC; also known as uterine serous carcinoma) development using a lineage-traceable mouse model and cross-species analyses of the mouse and human neoplastic endometrium. In mice, the early, pre-dysplastic stage was marked by a global decrease in inferred cell-cell interactions, followed by extensive communication network rewiring during neoplastic progression. Pathway-specific analysis revealed a similar pattern for NOTCH signaling, with NOTCH2 emerging as the dominant NOTCH receptor in Trp53/Rb1-mutant immature epithelial cells. Functionally, NOTCH2 promoted the outgrowth of more proliferative mutant organoids. Cross-species transcriptomic analysis identified conserved immature epithelial states in mouse and human neoplastic endometrial epithelium. In human tissues, NOTCH2 was overexpressed in serous endometrial intraepithelial carcinoma, a precursor of SEC, and in overt SEC. Furthermore, elevated NOTCH2 expression was associated with poor patient survival. These findings link cell-cell communication rewiring during experimental SEC development to conserved neoplastic epithelial states and identify NOTCH2 as an early marker and a potential target of disease interception.

cancer biology↗