Ankush Sharma

• Gherardini, Lisa; Sharma, Ankush; Taranta, Monia & Cinti, Caterina (2025). Epigenetic Reprogramming by Decitabine in Retinoblastoma. Frontiers in Bioscience-Landmark (FBL). ISSN 2768-6701. 30(4). doi: 10.31083/fbl33386. Fulltekst i vitenarkiv Vis sammendrag

  Introduction: Retinoblastoma (Rb) is a rare cancer, yet it is the most common eye tumor in children. It can occur in either a familial or sporadic form, with the sporadic variant being more prevalent, though its downstream effects on epigenetic markers remain largely unclear. Currently, the treatment for retinoblastoma typically involves aggressive chemotherapy and surgical resection. The identification of specific epigenetic characteristics of non-hereditary (sporadic) Rb has led to the development of advanced, high-throughput methods to explore its epigenetic profile. Our previous research demonstrated that treatment with the demethylating agent 5-Aza-2′-deoxycytidine (decitabine; DAC) induced cell cycle arrest and apoptosis in a well-characterized retinoblastoma model (WERI-Rb-1). Our analysis of time-dependent gene expression in WERI-Rb-1 cells following DAC exposure has led to the development of testable hypotheses to further investigate the epigenetic impact on the initiation and progression of retinoblastoma tumors. Methods: Gene expression analysis of publicly available datasets from patients’ primary tumors and normal retina have been compared with those found in WERI-Rb-1 cells to assess the relevance of DAC-driven genes as markers of primary retinoblastoma tumors. The effect of DAC treatment has been evaluated in vivo, both in subcutaneous xenografts and in orthotopic models. qPCR analysis of gene expression and Methylation-Specific PCR (MSP) was performed. Results: Our analysis of network maps for differentially expressed genes in primary tumors compared to DAC-driven genes identified 15 hub/driver genes that may play a pivotal role in the genesis and progression of retinoblastoma. DAC treatment induced significant tumor growth arrest in vivo in both subcutaneous and orthotopic xenograft retinoblastoma models. This was associated with changes in gene expression, either through the direct switching-on of epigenetically locked genes or through the indirect regulation of linked genes, suggesting the potential use of DAC as an epigenetic anti-cancer drug for the treatment of retinoblastoma patients. Conclusion: There is a pressing need to develop innovative treatments for retinoblastoma. Our research revealed that DAC can effectively suppress the growth and progression of retinoblastoma in in vivo models, offering a potential new therapeutic approach to battle this destructive disease. This discovery highlights the impact of this epigenetic therapy in reprogramming tumor dynamics, and thus its potential to preserve both the vision and lives of affected children.

• Spildrejorde, Mari Roberts; Leithaug, Magnus; Samara, Athina; Aass, Hans Christian; Sharma, Ankush & Acharya, Ganesh [Vis alle 9 forfattere av denne artikkelen] (2024). Citalopram exposure of hESCs during neuronal differentiation identifies dysregulated genes involved in neurodevelopment and depression. Frontiers in Cell and Developmental Biology. 12. doi: 10.3389/fcell.2024.1428538. Fulltekst i vitenarkiv Vis sammendrag

  Selective serotonin reuptake inhibitors (SSRIs), including citalopram, are widely used antidepressants during pregnancy. However, the effects of prenatal exposure to citalopram on neurodevelopment remain poorly understood. We aimed to investigate the impact of citalopram exposure on early neuronal differentiation of human embryonic stem cells using a multi-omics approach. Citalopram induced time- and dose-dependent effects on gene expression and DNA methylation of genes involved in neurodevelopmental processes or linked to depression, such as BDNF, GDF11, CCL2, STC1, DDIT4 and GAD2. Single-cell RNA-sequencing analysis revealed distinct clusters of stem cells, neuronal progenitors and neuroblasts, where exposure to citalopram subtly influenced progenitor subtypes. Pseudotemporal analysis showed enhanced neuronal differentiation. Our findings suggest that citalopram exposure during early neuronal differentiation influences gene expression patterns associated with neurodevelopment and depression, providing insights into its potential neurodevelopmental impact and highlighting the importance of further research to understand the long-term consequences of prenatal SSRI exposure.

• Akshay, Akshay; Katoch, Mitali; Shekarchizadeh, Navid; Abedi, Masoud; Sharma, Ankush & Burkhard, Fiona C. [Vis alle 9 forfattere av denne artikkelen] (2024). Machine Learning Made Easy (MLme): A comprehensive toolkit for machine learning-driven data analysis. GigaScience. 13:giad111, s. 1–9. doi: 10.1093/gigascience/giad111. Fulltekst i vitenarkiv Vis sammendrag

  Background Machine learning (ML) has emerged as a vital asset for researchers to analyze and extract valuable information from complex datasets. However, developing an effective and robust ML pipeline can present a real challenge, demanding considerable time and effort, thereby impeding research progress. Existing tools in this landscape require a profound understanding of ML principles and programming skills. Furthermore, users are required to engage in the comprehensive configuration of their ML pipeline to obtain optimal performance. Results To address these challenges, we have developed a novel tool called Machine Learning Made Easy (MLme) that streamlines the use of ML in research, specifically focusing on classification problems at present. By integrating 4 essential functionalities—namely, Data Exploration, AutoML, CustomML, and Visualization—MLme fulfills the diverse requirements of researchers while eliminating the need for extensive coding efforts. To demonstrate the applicability of MLme, we conducted rigorous testing on 6 distinct datasets, each presenting unique characteristics and challenges. Our results consistently showed promising performance across different datasets, reaffirming the versatility and effectiveness of the tool. Additionally, by utilizing MLme’s feature selection functionality, we successfully identified significant markers for CD8+ naive (BACH2), CD16+ (CD16), and CD14+ (VCAN) cell populations. Conclusion MLme serves as a valuable resource for leveraging ML to facilitate insightful data analysis and enhance research outcomes, while alleviating concerns related to complex coding scripts. The source code and a detailed tutorial for MLme are available at https://github.com/FunctionalUrology/MLme.

• Bai, Baoyan; Wise, Jillian Frances; Vodak, Daniel; Nakken, Sigve; Sharma, Ankush & Blaker, Yngvild Nuvin [Vis alle 23 forfattere av denne artikkelen] (2024). Multi-omics profiling of longitudinal samples reveals early genomic changes in follicular lymphoma. Blood Cancer Journal. 14:147(1), s. 1–12. doi: 10.1038/s41408-024-01124-5. Fulltekst i vitenarkiv Vis sammendrag

  Follicular lymphoma (FL) is the most common indolent type of B-cell non-Hodgkin lymphoma. Advances in treatment have improved overall survival, but early relapse or transformation to aggressive disease is associated with inferior outcome. To identify early genetic events and track tumor clonal evolution, we performed multi-omics analysis of 94 longitudinal biopsies from 44 FL patients; 22 with transformation (tFL) and 22 with relapse without transformation (nFL). Deep whole-exome sequencing confirmed recurrent mutations in genes encoding epigenetic regulators (CREBBP, KMT2D, EZH2, EP300), with similar mutational landscape in nFL and tFL patients. Calculation of genomic distances between longitudinal samples revealed complex evolutionary patterns in both subgroups. CREBBP and KMT2D mutations were identified as genetic events that occur early in the disease course, and cases with CREBBP KAT domain mutations had low risk of transformation. Gains in chromosomes 12 and 18 (TCF4), and loss in 6q were identified as early and stable copy number alterations. Identification of such early and stable genetic events may provide opportunities for early disease detection and disease monitoring. Integrative analysis revealed that tumors with EZH2 mutations exhibited reduced gene expression of numerous histone genes, including histone linker genes. This might contribute to the epigenetic dysregulation in FL.

• Spildrejorde, Mari; Samara, Athina; Sharma, Ankush; Leithaug, Magnus; Falck, Martin Bengt Alfred & Modafferi, Stefania [Vis alle 12 forfattere av denne artikkelen] (2023). Multi-omics approach reveals dysregulated genes during hESCs neuronal differentiation exposure to paracetamol. iScience. 26:107755(10), s. 1–29. doi: 10.1016/j.isci.2023.107755. Fulltekst i vitenarkiv Vis sammendrag

  Prenatal paracetamol exposure has been associated with neurodevelopmental outcomes in childhood. Pharmacoepigenetic studies show differences in cord blood DNA methylation between unexposed and paracetamol-exposed neonates, however, causality and impact of long-term prenatal paracetamol exposure on brain development remain unclear. Using a multi-omics approach, we investigated the effects of paracetamol on an in vitro model of early human neurodevelopment. We exposed human embryonic stem cells undergoing neuronal differentiation with paracetamol concentrations corresponding to maternal therapeutic doses. Single-cell RNA-seq and ATAC-seq integration identified paracetamol-induced chromatin opening changes linked to gene expression. Differentially methylated and/or expressed genes were involved in neurotransmission and cell fate determination trajectories. Some genes involved in neuronal injury and development-specific pathways, such as KCNE3, overlapped with differentially methylated genes previously identified in cord blood associated with prenatal paracetamol exposure. Our data suggest that paracetamol may play a causal role in impaired neurodevelopment.

• Spasevska, Ivana; Sharma, Ankush; Steen, Chloe Beate; Josefsson, Sarah Elisabet; Blaker, Yngvild Nuvin & Kolstad, Arne [Vis alle 26 forfattere av denne artikkelen] (2023). Diversity of intratumoral regulatory T cells in B-cell non-Hodgkin lymphoma. Blood Advances. ISSN 2473-9529. 7(23), s. 7216–7230. doi: 10.1182/bloodadvances.2023010158. Fulltekst i vitenarkiv Vis sammendrag

  Abstract Tumor-infiltrating regulatory T cells (Tregs) contribute to an immunosuppressive tumor microenvironment. Despite extensive studies, the prognostic impact of tumor-infiltrating Tregs in B-cell non-Hodgkin lymphomas (B-NHLs) remains unclear. Emerging studies suggest substantial heterogeneity in the phenotypes and suppressive capacities of Tregs, emphasizing the importance of understanding Treg diversity and the need for additional markers to identify highly suppressive Tregs. Here, we applied single-cell RNA sequencing and T-cell receptor sequencing combined with high-dimensional cytometry to decipher the heterogeneity of intratumoral Tregs in diffuse large B-cell lymphoma and follicular lymphoma (FL), compared with that in nonmalignant tonsillar tissue. We identified 3 distinct transcriptional states of Tregs: resting, activated, and unconventional LAG3+FOXP3− Tregs. Activated Tregs were enriched in B-NHL tumors, coexpressed several checkpoint receptors, and had stronger immunosuppressive activity compared with resting Tregs. In FL, activated Tregs were found in closer proximity to CD4+ and CD8+ T cells than other cell types. Furthermore, we used a computational approach to develop unique gene signature matrices, which were used to enumerate each Treg subset in cohorts with bulk gene expression data. In 2 independent FL cohorts, activated Tregs was the major subset, and high abundance was associated with adverse outcome. This study demonstrates that Tregs infiltrating B-NHL tumors are transcriptionally and functionally diverse. Highly immunosuppressive activated Tregs were enriched in tumor tissue but absent in the peripheral blood. Our data suggest that a deeper understanding of Treg heterogeneity in B-NHL could open new paths for rational drug design, facilitating selective targeting to improve antitumor immunity.

• Huang, Chengqun; Sharma, Ankush; Thakur, Reetu; Rai, Deepika; Katiki, Madhusudhanarao & Germano, Juliana de Freitas [Vis alle 15 forfattere av denne artikkelen] (2022). Asporin, an extracellular matrix protein, is a beneficial regulator of cardiac remodeling. Matrix Biology. ISSN 0945-053X. 110, s. 40–59. doi: 10.1016/j.matbio.2022.04.005. Fulltekst i vitenarkiv
• Samara, Athina; Spildrejorde, Mari; Sharma, Ankush; Falck, Martin; Leithaug, Magnus & Modafferi, Stefania [Vis alle 11 forfattere av denne artikkelen] (2022). A multi-omics approach to visualize early neuronal differentiation from hESCs in 4D. iScience. 25(11). doi: 10.1016/j.isci.2022.105279. Fulltekst i vitenarkiv Vis sammendrag

  Neuronal differentiation of pluripotent stem cells is an established method to study physiology, disease, and medication safety. However, the sequence of events in human neuronal differentiation and the ability of in vitro models to recapitulate early brain development are poorly understood. We developed a protocol optimized for the study of early human brain development and neuropharmacological applications. We comprehensively characterized gene expression and epigenetic profiles at four timepoints, because the cells differentiate from embryonic stem cells towards a heterogeneous population of progenitors, immature and mature neurons bearing telencephalic signatures. A multi-omics roadmap of neuronal differentiation, combined with searchable interactive gene analysis tools, allows for extensive exploration of early neuronal development and the effect of medications.

• Sharma, Ankush & Capobianco, Enrico (2022). Non-Coding RNAs Are Brokers in Breast Cancer Interactome Networks and Add Discrimination Power between Subtypes. Journal of Clinical Medicine. 11(8). doi: 10.3390/jcm11082103. Fulltekst i vitenarkiv Vis sammendrag

  Despite the power of high-throughput genomics, most non-coding RNA (ncRNA) biotypes remain hard to identify, characterize, and validate. This is a clear indication that intensive next-generation sequencing research has led to great efficiency and accuracy in detecting ncRNAs, but not in their functionalization. Computational scientists continue to support the discovery process by spotting significant data features (expression or mutational profiles), elucidating phenotype uncertainty, and delineating complex regulation landscapes for biological pathways and pathophysiological processes. With reference to transcriptome regulation dynamics in cancer, this work introduces a novel network-driven inference approach designed to reveal the potential role of computationally identified ncRNAs in discriminating between breast cancer (BC) subtypes beyond the traditional gene expression signatures. As heterogeneity cast in the subtypes is a characteristic of most cancers, the proposed approach is generalizable beyond BC. Expression profiles of a wide transcriptome spectrum were obtained for a number of BC patients (and controls) listed in TCGA and processed with RNA-Seq. The well-known PAM50 subtype signature was available for the samples and used to move from differentially expressed transcript profiles to subtype-specific biclusters associating gene patterns with patients. Co-expressed gene networks were then generated and annotations were provided, focusing on the biclusters with basal and luminal signatures. These were used to build template maps, i.e., networks in which to embed the ncRNAs and contextually functionalize them based on their interactors. This inference approach is able to assess the influence of ncRNAs at the level of BC subtype. Network topology was considered through the brokerage measure to account for disruptiveness effects induced by the removal of nodes corresponding to ncRNAs. Equivalently, it is shown that ncRNAs can act as brokers of network interactome dynamics, and removing them allows the refinement of subtype-related characteristics previously obtained by gene signatures only. The results of the study elucidate the role of pseudogenes in two major BC subtypes, considering the contextual annotations. Put into a wider perspective, ncRNA brokers may help predictive functionalization studies targeted to new disease phenotypes, for instance those linked to the tumor microenvironment or metabolism, or those specifically involving metastasis. Overall, the approach may represent an in silico prioritization strategy toward the systems identification of new diagnostic and prognostic biomarkers.

• Germano, Juliana de Freitas; Sharma, Ankush; Stastna, Miroslava; Huang, Chengqun; Aniag, Marianne & Aceves, Angie [Vis alle 11 forfattere av denne artikkelen] (2021). Proteomics of mouse heart ventricles reveals mitochondria and metabolism as major targets of a post-infarction short-acting glp1ra-therapy. International Journal of Molecular Sciences. ISSN 1661-6596. 22(16), s. 1–21. doi: 10.3390/ijms22168711. Fulltekst i vitenarkiv Vis sammendrag

  Cardiovascular disease is the main cause of death worldwide, making it crucial to search for new therapies to mitigate major adverse cardiac events (MACEs) after a cardiac ischemic episode. Drugs in the class of the glucagon-like peptide-1 receptor agonists (GLP1Ra) have demonstrated benefits for heart function and reduced the incidence of MACE in patients with diabetes. Previously, we demonstrated that a short-acting GLP1Ra known as DMB (2-quinoxalinamine, 6,7-dichloro-N-[1,1-dimethylethyl]-3-[methylsulfonyl]-,6,7-dichloro-2-methylsulfonyl-3-N-tert-butylaminoquinoxaline or compound 2, Sigma) also mitigates adverse postinfarction left ventricular remodeling and cardiac dysfunction in lean mice through activation of parkin-mediated mitophagy following infarction. Here, we combined proteomics with in silico analysis to characterize the range of effects of DMB in vivo throughout the course of early postinfarction remodeling. We demonstrate that the mitochondrion is a key target of DMB and mitochondrial respiration, oxidative phosphorylation and metabolic processes such as glycolysis and fatty acid beta-oxidation are the main biological processes being regulated by this compound in the heart. Moreover, the overexpression of proteins with hub properties identified by protein–protein interaction networks, such as Atp2a2, may also be important to the mechanism of action of DMB. Data are available via ProteomeXchange with identifier PXD027867.

• Sharma, Ankush; Akshay, Akshay; Rogne, Marie & Eskeland, Ragnhild (2021). ShinyArchR.UiO: user-friendly,integrative and open-source tool for visualization of single-cell ATAC-seq data using ArchR. Bioinformatics. ISSN 1367-4803. 38(3), s. 834–836. doi: 10.1093/bioinformatics/btab680. Fulltekst i vitenarkiv Vis sammendrag

  Motivation: Mapping of chromatin accessibility landscapes in single-cells and the integration with gene expression enables a better understanding of gene regulatory mechanisms defining cell identities and cell-fate determination in development and disease. Generally, raw data generated from single-cell Assay for Transposase-Accessible Chromatin sequencing (scATAC-seq) are deposited in repositories that are generally inaccessible due to lack of in-depth knowledge of computational programming. Results: We have developed ShinyArchR.UiO, an R-based shiny app, that facilitates scATAC-seq data accessibility and visualisation in a user-friendly, interactive, and open-source web interface. ShinyArchR.UiO is an application that can streamline collaborative efforts for interpretation of massive chromatin accessibility datasets and allow for open access data sharing for wider audiences.

• Sharma, Ankush & Colonna, Giovanni (2021). System-Wide Pollution of Biomedical Data: Consequence of the Search for Hub Genes of Hepatocellular Carcinoma Without Spatiotemporal Consideration. Molecular Diagnosis & Therapy. ISSN 1177-1062. 25(1), s. 9–27. doi: 10.1007/s40291-020-00505-3. Fulltekst i vitenarkiv
• Piplani, Honit; Marek-Iannucci, Stefanie; Sin, Jon; Hou, Jean; Takahashi, Toshimasa & Sharma, Ankush [Vis alle 17 forfattere av denne artikkelen] (2019). Simvastatin induces autophagic flux to restore cerulein-impaired phagosome-lysosome fusion in acute pancreatitis. Biochimica et Biophysica Acta - Molecular Basis of Disease. ISSN 0925-4439. 1865(11), s. 1–14. doi: 10.1016/j.bbadis.2019.08.006. Fulltekst i vitenarkiv Vis sammendrag

  Background During pancreatitis, autophagy is activated, but lysosomal degradation of dysfunctional organelles including mitochondria is impaired, resulting in acinar cell death. Retrospective cohort analyses demonstrated an association between simvastatin use and decreased acute pancreatitis incidence. Methods We examined whether simvastatin can protect cell death induced by cerulein and the mechanisms involved during acute pancreatitis. Mice were pretreated with DMSO or simvastatin (20 mg/kg) for 24 h followed by 7 hourly cerulein injections and sacrificed 1 h after last injection to harvest blood and tissue for analysis. Results Pancreatic histopathology revealed that simvastatin reduced necrotic cell death, inflammatory cell infiltration and edema. We found that cerulein triggered mitophagy with autophagosome formation in acinar cells. However, autophagosome-lysosome fusion was impaired due to altered levels of LAMP-1, AMPK and ULK-1, resulting in autophagosome accumulation (incomplete autophagy). Simvastatin abrogated these effects by upregulating LAMP-1 and activating AMPK which phosphorylated ULK-1, resulting in increased formation of functional autolysosomes. In contrast, autophagosomes accumulated in control group during pancreatitis. The effects of simvastatin to promote autophagic flux were inhibited by chloroquine. Mitochondria from simvastatin-treated mice were resistant to calcium overload compared to control, suggesting that simvastatin induced mitochondrial quality control to eliminate susceptible mitochondria. Clinical specimens showed a significant increase in cell-free mtDNA in plasma during pancreatitis compared to normal controls. Furthermore, genetic deletion of parkin abrogated the benefits of simvastatin. Conclusion Our findings reveal the novel role of simvastatin in enhancing autophagic flux to prevent pancreatic cell injury and pancreatitis.

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• Spasevska, Ivana; Kongsrud, Karoline; Sharma, Ankush; Scherer, Eveline; Hoel, Hanna Julie & Vincenti, Marianna [Vis alle 11 forfattere av denne artikkelen] (2025). Beyond Helpers: Unraveling the Potential of CD4+ Cytotoxic T Cells in B cell lymphoma. Vis sammendrag

  CD4+ T cells are heterogeneous and consist of several subsets. While most CD4+ T cells exhibit either helper or immunoregulatory function, emerging evidence suggest the existence of a unique subset of CD4+ T cells with direct cytotoxic potential. Recently, there has been growing interest in these CD4+ cytotoxic T lymphocytes (CTLs) due to their potential involvement in anti-tumor immune responses and their relevance in immunotherapy. We reanalyzed our prior single-cell RNA sequencing (scRNA-seq) dataset (Spasevska et al, Blood Adv 2023) to unravel the landscape of CD4+ T cell states in diffuse large B-cell lymphoma (DLBCL, n = 3), follicular lymphoma (FL, n = 3) and non-malignant tonsils (n = 3). Among 13 clusters, one was annotated CD4 cytotoxic (CTL) due to high expression of a cytotoxic gene signature (GZMK, NKG7, CST7, GZMA, GZMB). CD4+ CTLs represented over 20 % of CD4+ T cells in DLBCL and over 10% in FL tumors but were nearly absent in non-malignant tonsils. Their tumor-specific nature was further highlighted by a shared TCR observed in more than 45% of CD4+ CTLs in DLBCL. This suggests a clonal expansion of CD4+ T cells recognizing tumor antigens. To place the CD4 CTL in the context of other cytotoxic cells (CD8 and NK cells), we performed scRNA-seq of live cells from matched tumor and PBMC from two FL patients and one healthy donor PBMC (>50 000 single cells). Clustering and analysis of cytotoxic genes confirmed high similarity between CD4 CTL, CD8 Temra, CD8Tem and NK cells. We validated these findings using multiparameter flow cytometry, revealing that CD4+ CTLs comprised from 1-23% of intratumoral CD4+ T cells in DLBCL. The CD4+ CTLs were identified as Granzyme B+ and Perforin+ cells within the CD4+ CD8- FOXP3- CD56- population, thereby excluding CD8+ T cells, regulatory T cells and NK cells. Using a 41-marker antibody panel for spectral flow cytometry, we have further validated that CD4+ CTL share a cytotoxic signature with NK cells and CD8 T cells. We will alto test if CD4 CTLs have comparable killing capacity to CD8 T cells by employing cell sorting and functional assays. By employing state-of-the-art technologies, we have characterized CD4+ CTLs in lymphoma and demonstrated substantial clonal expansion in DLBCL. Our findings contribute to the understanding of immune cell heterogeneity and might have implications for therapeutic strategies that leverage the potential of CD4+ CTLs in cancer immunotherapy.

• Sharma, Ankush; Kongsrud, Karoline; Spasevska, Ivana; Lamont, Colin Harry; Steen, Chloe Beate & Lorenz, Susanne [Vis alle 10 forfattere av denne artikkelen] (2025). Deciphering Tumor Microenvironment Complexity in Lymphoma Using Spatial Transcriptomics. Fulltekst i vitenarkiv Vis sammendrag

  The tumor microenvironment (TME) in lymphomas, such as Diffuse Large B-cell Lymphoma (DLBCL) and Follicular Lymphoma (FL), is highly heterogeneous and plays a critical role in modulating therapeutic outcomes, including responses to CD19 CAR T-cell therapy. To unravel the spatial complexity of the TME, we employed an integrative approach combining spatial transcriptomics (Visium, 10x Genomics) and spatial proteomics (imaging mass cytometry, IMC) on FFPE tissue sections from FL and DLBCL patients. Using tools such as CytoSPACE and CARD, we mapped single-cell RNA-seq data to spatial coordinates and validated cellular compositions with IMC data. We identified spatially distinct immune and stromal cell populations, including GC B cells, Tregs, macrophages, dendritic cells, and endothelial cells, across follicular and T-cell rich regions. CytoSPACE-based mapping revealed consistent enrichment of key markers (e.g., CD79B, FOXP3, GRZA) with corresponding protein expression profiles. We also developed R based ShinySpatial framework to visualize spatial data enhancing the accessibility and interpretability of complex spatial datasets. This pilot study lays the groundwork for identifying spatial biomarkers that predict therapeutic responses and resistance in lymphoma, with ongoing integration of data from patients enrolled in the JULIET, BELINDA, and ELARA trials.

• Huse, Kanutte; Blaker, Yngvild Nuvin; Wise, Jillian Frances; Sharma, Ankush; Enemark, Marie Beck Hairing & Meriranta, Leo [Vis alle 12 forfattere av denne artikkelen] (2025). Mapping the Tumor Microenvironment of DLBCL by Imaging Mass Cytometry. Fulltekst i vitenarkiv
• Sharma, Ankush (2024). ShinySpatial : Advancing Spatial Transcriptomics Atlases Through Interactive Visualization. Fulltekst i vitenarkiv
• Sharma, Ankush & Colonna, Giovanni (2021). Correction to: System-Wide Pollution of Biomedical Data: Consequence of the Search for Hub Genes of Hepatocellular Carcinoma Without Spatiotemporal Consideration (Molecular Diagnosis & Therapy, (2021), 25, 1, (9-27), 10.1007/s40291-020-00505-3). Molecular Diagnosis & Therapy. ISSN 1177-1062. 25(3), s. 387–387. doi: 10.1007/s40291-021-00527-5. Fulltekst i vitenarkiv

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