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Bozorgui, B.

Publications and source records attributed to Bozorgui, B..

7 recordsLinked to original sources

Evaluation of Cross-slice Imputation for Spatial Proteomics

Spatial single-cell protein profiling is at the forefront of translational medicine research efforts that try to decipher tissue heterogeneity. However, existing experimental approaches are limited in the number of biomarkers that they measure. This has motivated extensive research into the problem of protein imputation, where proteins or biomarkers not directly measured in a given slice of biopsy tissue are learned from those measured. In this work, we focus on the specific problem of cross-slice protein imputation (CSPI). In the CSPI problem, two sets of biomarker expressions at the single-cell level are known for physically adjacent slices of tissue. Each slice has its own known set of biomarkers, which overlaps with but does not subsume that of the adjacent. For each slice, we wish to learn the expressions of the proteins unique to the adjacent. Existing literature for protein imputation methodologies can be grouped in two categories: learning-based and alignment-based approaches. Learning-based approaches do not account for spatial and structural similarities between the training and the target sets. Alignment based approaches aim to determine an association between cells in adjacent slices, but without the explicit goal of using this alignment for imputation. In this work, we evaluate several methods from both categories and their adaptability to the cross-slice protein imputation problem. We provide a statistical analysis of all methods' performance under varying conditions of implementation. We find that learning-based methods significantly outperform alignment-based methods at the task of cross-slice protein imputation, with the latter more suited to the task of inter-slice interpolation or 3D tissue reconstruction. Moreover, inter-patient imputation is far less accurate than intra-patient imputation for all methods evaluated.

bioinformatics↗

CROCHET: a versatile pipeline for automated analysis and visual atlas creation from single-cell spatialomic data

Spatial biology technologies offer a unique opportunity to link tissue composition with function. However, analytical methods for quantifying and interpreting highly complex spatial data remain limited. We present CROCHET (ChaRacterization Of Cellular HEterogeneity in Tissues), an end-to-end analysis pipeline for construction of spatially resolved cell atlases from raw data covering millions of cells across large sample cohorts. Its modular architecture supports the integration of diverse data modalities and novel analytical methods for image processing and segmentation, spatialomics quantification and downstream analyses. With comprehensive, open-source, user-friendly, interactive, and visual analysis modules, CROCHET aims to democratize spatial omics for a broad community of users.

bioinformatics↗

A spatially resolved single cell proteomic atlas of Small Bowel Adenocarcinoma

Small bowel adenocarcinoma (SBA) is a rare malignancy marked with a poor prognosis. The cellular and proteomic heterogeneity within the tumor immune microenvironment (TIME) of SBA is a likely driver of prognosis, disease progression and response to therapy. We have addressed a major gap in knowledge of the TIME in SBA using highly multiplexed, protein imaging of the SBA tumor-immune ecosystem generating a comprehensive, single-cell level, spatial, proteomic atlas of TIME in > 600,000 cells from 136 tumor and matched normal samples from clinically and genomically annotated SBA patients (N=37). The SBA TIME Atlas informs on spatial distribution and interactions of tumor-intrinsic processes, diverse immune cell types, immune checkpoints, and vascularization. Enrichment of proliferating epithelial tissue, stem cells, and likely pro-tumor immune signatures in the tumor niche is contrasted by the representation of naive and early-effector T-cells in the epithelial compartments of adjacent normal tissues. Epithelial-stem-immune cell spatial architectures within tumor and matched-normal niches were strongly associated with patient survival, suggesting malignancy is driven by spatial architecture beyond the tumor microenvironment. The blueprints of therapeutically actionable immune checkpoints at the interface between epithelial and microenvironmental T-cells as well as macrophages have established a guideline for precision immunotherapies tailored to the TIME composition in SBA. We expect that this SBA atlas will contribute to a deeper understanding of the immune contexture in this rare disease as well as other gastrointestinal cancers and help guide future precision immune-oncology strategies.

cancer biology↗

A prognostic matrix code defines functional glioblastoma phenotypes and niches.

Interactions among tumor, immune and vascular niches play major roles in driving glioblastoma (GBM) malignancy and treatment responses. The composition, heterogeneity, and localization of extracellular core matrix proteins (CMPs) that mediate such interactions, however, are not well understood. Here, we characterize functional and clinical relevance of genes encoding CMPs in GBM at bulk, single cell, and spatial anatomical resolution. We identify a "matrix code" for genes encoding CMPs whose expression levels categorize GBM tumors into matrisome-high and matrisome-low groups that correlate with worse and better survival, respectively, of patients. The matrisome enrichment is associated with specific driver oncogenic alterations, mesenchymal state, infiltration of pro-tumor immune cells and immune checkpoint gene expression. Anatomical and single cell transcriptome analyses indicate that matrisome gene expression is enriched in vascular and leading edge/infiltrative anatomic structures that are known to harbor glioma stem cells driving GBM progression. Finally, we identified a 17-gene matrisome signature that retains and further refines the prognostic value of genes encoding CMPs and, importantly, potentially predicts responses to PD1 blockade in clinical trials for GBM. The matrisome gene expression profiles may provide biomarkers of functionally relevant GBM niches that contribute to mesenchymal-immune cross talk and patient stratification to optimize treatment responses.

cancer biology↗

Mapping the functional interactions at the tumor-immune checkpoint interface

It is challenging to identify the tumor-immune system interactions that modulate immune states and immunotherapy responses due to the prohibitively complex space of possible interactions. Our statistical analysis framework, ImogiMap quantifies tumor-immune interactions based on their synergistic co-associations with immune-associated phenotypes. ImogiMap-based analyses recapitulated known interactions modulating immunotherapy responses and nominated the CD86/CD70 axis as an immunotherapy target that overlaps with IFNG overexpression and patient survival in endometrial carcinoma.

bioinformatics↗

Precision combination therapies from recurrent oncogenic co-alterations

Cancer cells depend on multiple driver alterations whose oncogenic effects can be suppressed by drug combinations. Discovery of effective combination therapies is challenging due to the complexity of the biomolecular landscape of drug responses. Here, we developed the method REFLECT (REcurrent Features Leveraged for Combination Therapies), which integrates machine learning and cancer informatics algorithms. The method maps recurrent co-alteration signatures from multi-omic data across patient cohorts to combination therapies. Using the REFLECT framework, we generated a precision therapy resource matching 2,201 drug combinations to co-alteration signatures across 201 cohorts stratified from 10,392 patients and 33 cancer types. We validated that REFLECT-predicted combinations introduce significantly higher therapeutic benefit through analysis of independent data from comprehensive drug screens. In patient cohorts with immunotherapy response markers, HER2 activation and DNA repair aberrations, we identified therapeutically actionable co-alteration signatures shared across patient sub-cohorts. REFLECT provides a framework to design combination therapies tailored to patient cohorts in data-driven clinical trials.

cancer biology↗

BET inhibition induces an anti-apoptotic adaptive response and therapeutic vulnerability to MCL1 inhibitors in breast cancer

The development of effective targeted therapies for the treatment of basal-like breast cancers remains challenging. Here, we demonstrate that BET inhibition induces a multi-faceted adaptive response program leading to MCL1 protein-driven evasion of apoptosis in breast cancers. Consequently, co-targeting MCL1 and BET is highly synergistic in in vitro and in vivo breast cancer models. Drug response and genomics analyses revealed that MCL1 copy number alterations, including low-level gains, are selectively enriched in basal-like breast cancers and associated with effective BET and MCL1 co-targeting. The mechanism of adaptive response to BET inhibition involves upregulation of critical lipid metabolism enzymes including the rate-limiting enzyme stearoyl-CoA desaturase (SCD). Changes in the lipid metabolism are associated with increases in cell motility and membrane fluidity as well as transitions in cell morphology and adhesion. The structural changes in the cell membrane leads to re-localization and activation of HER2/EGFR which can be interdicted by inhibiting SCD activity. Active HER2/EGFR, in turn, induces accumulation of MCL1 protein and therapeutic vulnerability to MCL1 inhibitors. The BET protein, lipid metabolism and receptor tyrosine kinase activation cascade is observed in patient cohorts of basal-like and HER2-amplified breast cancers. The high frequency of MCL1 chromosomal amplifications (>30%) and gains (>50%) in basal-like breast cancers suggests that BET and MCL1 co-inhibition may have therapeutic utility in this aggressive subtype.

cancer biology↗