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Kanannejad, S.

Publications and source records attributed to Kanannejad, S..

3 recordsLinked to original sources

scINTILLA: Single-Cell Integrated Inference, Labelling, and Landscape Analysis for Cell-Type Annotation Quality Assessment

Single-cell RNA sequencing has enabled the construction of comprehensive cell atlases, yet the quality and coherence of the cell-type annotations within these atlases remain largely unexamined. When a label is applied to a transcriptionally heterogeneous population, the downstream analyses that depend on it, and automated label transfer in particular, become unreliable. We present scINTILLA (Single-Cell Integrated Inference, Labelling, and Landscape Analysis), a computational framework that combines supervised and unsupervised machine learning to score the learnability and internal consistency of cell-type labels in single-cell datasets. The unsupervised arm benchmarks a broad panel of clustering algorithms and derives a neighbourhood confusion score for every cell, whilst the supervised arm trains up to twelve classifiers and extracts prediction agreement, entropy, and confidence. These signals are normalised and aggregated into a single composite score per cell type, where a low score flags label ambiguity or concealed heterogeneity. As a by-product, scIN-TILLA also reports which clustering and classification algorithms perform best on a given dataset, offering practical guidance for downstream label transfer. We applied it to five Human Cell Atlas datasets spanning the adult brain, lung, eye, and two organoid atlases, and recovered clear differences in the learnability and internal consistency of annotations across atlases that were not driven by the number of annotated cell types. Focused re-analysis of lowscoring populations in the lung and endoderm-organoid atlases resolved biologically coherent sub-populations, in some cases with context-specific enrichment, much of it recovered from cells that had been assigned broad or catch-all labels. scINTILLA is advisory rather than prescriptive, guiding principled, data-driven re-annotation at atlas scale.

bioinformatics↗

Targeting GL-Lect driven endocytosis to suppress cell plasticity in breast cancer

Aberrant endocytosis has long been associated with epithelial plasticity and tumorigenesis, but direct in vivo evidence of its causal role in tumor progression and metastasis has been lacking. Here, we identify and molecularly characterize a previously unrecognized form of E-cadherin (ECAD) internalization in mammary epithelial cells. This process is mediated by the endocytic adaptor Epsin 3 (EPN3) through glycolipid-lectin (GL-Lect) driven endocytosis requiring galectin-3 and Eps15-family adaptors. Leveraging an EPN3 knock-in mouse model, we show that dysregulation of GL-Lect driven endocytosis disrupts mammary gland morphogenesis and activates epithelial-to-mesenchymal plasticity (EMP), synergizing with the ERBB2/Neu breast oncogene to drive metastasis. Pharmacologic inhibition of the GL-Lect mechanism suppresses morphogenetic and invasive phenotypes ex vivo, providing proof-of-concept for therapeutic targeting. These findings establish the GL-Lect mechanism as a driver of metastatic plasticity and uncover a tractable vulnerability in BC.

cancer biology↗

Integrated in silico and in vitro approaches identify SNX.2112 as a drug vulnerability in t(7;12) AML stem-like cells

The t(7;12) translocation is a chromosomal rearrangement characteristic of infant Acute Myeloid Leukemia (AML). It arises in utero and results in ectopic overexpression of homeobox gene MNX1. Using a 3-dimensional (3D) model of blood development, we recently showed that t(7;12)-AML originates at the endothelial-to-hematopoietic transition, explaining its characteristic gene expression signature. Herein, we employ that signature to interrogate the transcriptional profiles of hundreds of human cell lines against the GDSC database of drug sensitivities to identify candidate drugs against t(7;12)-AML. We employ a cell line in which we engineered t(7;12) and systematically test the candidate drugs by cell surface phenotype and clonogenic assays. Importantly, we identify HSP90 inhibitor SNX.2112 as a potential therapeutic agent against t(7;12)-AML. SNX.2112 selectively eliminates colony-initiating leukemia progenitors in vitro and decreases MNX1 expression, effects recapitulated by other HSP90 inhibitors. SNX.2112 acts at least partly through destabilisation of STAT5 signalling. Critically, SNX.2112-differential signatures uniquely map to progenitors with hemato-endothelial characteristics in t(7;12)-AML patient blasts, suggesting targeting of leukemia-initiating cells. Combinatorial treatment with chemotherapeutic agents indicates synergy, suggesting SNX.2112 potential as a targeted and cytotoxicity-sparing therapeutic approach. Overall, we successfully use an integrated computational and multi-model experimental approach to identify a drug vulnerability of t(7;12)-AML. Key pointsO_LIClassifier-based in silico drug screening identifies vulnerabilities of t(7;12)-infant leukemia C_LIO_LI2D and 3D models of t(7;12)-leukemia match HSP90 inhibition cellular and molecular responses to candidate leukemia stem cells in t(7;12) patient analysis. C_LI

cancer biology↗