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Gallagher, W. M.

Publications and source records attributed to Gallagher, W. M..

4 recordsLinked to original sources

A multi-step filtering pipeline for human read removal enhances detection of Fusobacterium in WGS datasets with immunohistochemical confirmation in mucinous rectal cancer.

The study of tumour-associated microbiomes using whole-genome sequencing (WGS) has attracted considerable attention, but microbial signal detection remains controversial due to host contamination and methodological artefacts. As the necessity of human-read removal becomes increasingly evident, many groups now include this step in their data pre-processing workflows. In this work, we introduce an open-source tool designed for rigorous host-read removal and apply it to the reanalysis of WGS data from ten mucinous rectal adenocarcinoma cases originally published by Reynolds et al. The workflow integrates k-mer-based classification (Kraken2), quality and adapter trimming (Trim Galore), vector filtering (BBDuk/UniVec_Core), and duplicate-removal (FastUniq). After reducing data complexity, a multi-aligner, multi-reference approach (BWA-MEM/GRCh38, Bowtie2/T2T-CHM13, Minimap2/HPRC v1.1) removes remaining host sequences, collectively eliminating more than 99.9% of human-derived reads. Although the additional alignment steps eliminated only a small fraction of total reads, they consistently removed millions of residual sequences per sample, underscoring the importance of rigorous filtering in datasets where non-human reads are a small minority. Taxonomic profiling with PathSeq and MetaPhlAn revealed reproducible enrichment of Fusobacterium species in tumour versus matched normal tissues, with stricter filtering reducing overall microbial signal compared to prior results. Cross-validation with immunofluorescence analysis using pan-Fusobacterium (detecting both F. animalis and F. nucleatum) and F. nucleatum-specific antibodies showed a strong concordance with Fusobacterium subspecies detected by WGS. Compared to the unfiltered analysis, host depletion markedly reduced artificial microbial signals in normal samples while preserving tumour-associated Fusobacterium, resulting in a more reliable microbial profile. ImportanceWe developed an open-source tool that enables rapid removal of human-derived sequences and applied it to rectal cancer WGS data. This approach reduced false microbial signals while preserving true tumour-associated Fusobacterium, and we confirmed these findings in tissue using immunofluorescence staining. Our method provides a more reliable foundation for studying tumour-bacteria interactions.

bioinformatics↗

Identification of druggable targets from the interactome of the Androgen Receptor and Serum Response Factor pathways in prostate cancer.

ObjectivesThe Androgen Receptor (AR) is crucial for prostate cancer (PCa) progression. Despite the introduction of second-generation AR antagonist, majority of patients develop resistance. The Serum Response Factor (SRF) was identified as a player involved in a crosstalk with AR signalling pathway and associated resistance. Elevated SRF levels in PCa patients were associated with disease progression and resistance to enzalutamide. However, the molecular mediators of the crosstalk between SRF and AR still need to be elucidated. The objective of this study was to identify common interactors of the AR/SRF crosstalk as therapeutic targets. MethodsHere we used affinity purification mass spectrometry (MS) to identify proteins that interact with both SRF and AR. ResultsSeven common interactors were identified, including HSP70, HSP0AA1, HSP90AB1, HSAP5, PRDX1 and GAPDH. Pathway analysis revealed that the PI3k/AKT pathway was the most enriched in the AR/SRF network. Moreover, pharmacological inhibition of several proteins in this network, including HSP70, HSP90, PI3k and AKT, significantly decreased cellular viability of PCa cells. ConclusionsThis study identified a list of AR/SRF common interactors that represent a pipeline of druggable targets for the treatment of PCa.

cancer biology↗

High Cysteinyl Leukotriene Receptor 1 Expression Correlates with Poor Survival of Uveal Melanoma Patients and Cognate Antagonist Drugs Modulate the Growth, Cancer Secretome, and Metabolism of Uveal Melanoma Cells.

Uveal melanoma (UM) is a rare, but often lethal, form of ocular cancer arising from melanocytes within the uveal tract. UM has a high propensity to spread hematogenously to the liver, with up to 50% of patients developing liver metastases. Unfortunately, once liver metastasis occurs, patient prognosis is extremely poor with as few as 8% of patients surviving beyond two years. There are no standard-of-care therapies available for the treatment of metastatic uveal melanoma, hence it is a clinical area of urgent unmet need. Here, the clinical relevance and therapeutic potential of cysteinyl leukotriene receptors (CysLT1 and CysLT2) in UM was evaluated. High expression of CYSLTR1 or CYSLTR2 transcripts is significantly associated with poor disease-free survival and poor overall survival in UM patients. Digital pathology analysis identified high expression of CysLT1 in primary UM is associated with reduced disease-specific survival (p = 0.012) and overall survival (p = 0.011). High CysLT1 expression shows a statistically significant (p = 0.041) correlation with ciliary body involvement, a poor prognostic indicator in UM. Small molecule drugs targeting CysLT1 were vastly superior at exerting anti-cancer phenotypes in UM cell lines and zebrafish xenografts than drugs targeting CysLT2. Quininib, a selective CysLT1 antagonist, significantly inhibits survival (p < 0.0001), long-term proliferation (p < 0.0001), and oxidative phosphorylation (p < 0.001), but not glycolysis, in primary and metastatic UM cell lines. Quininib exerts opposing effects on the secretion of inflammatory markers in primary versus metastatic UM cell lines. Quininib significantly downregulated IL-2 and IL-6 in Mel285 cells (p < 0.05), but significantly upregulated IL-10, IL-1{beta}, IL-2 (p < 0.0001), IL-13, IL-8 (p < 0.001), IL-12p70 and IL-6 (p < 0.05) in OMM2.5 cells. Finally, quininib significantly inhibits tumour growth in orthotopic zebrafish xenograft models of UM. These preclinical data suggest that antagonism of CysLT1, but not CysLT2, may be of therapeutic interest in the treatment of UM.

cancer biology↗

1,4-dihydroxy Quininib Attenuates Growth of Colorectal Cancer Cells and Xenografts and Regulates the TIE-2 Signaling Pathway in Patient Tumours

Colorectal cancer (CRC) is the second leading cause of cancer associated deaths in developed countries. Cancer progression and metastatic spread is reliant on new blood vasculature, or angiogenesis. Tumour-related angiogenesis is regulated by pro- and anti-angiogenic factors secreted from malignant tissue in a stepwise process. Previously we structurally modified the small anti-angiogenic molecule quininib and discovered a more potent anti-angiogenic compound 1, 4 dihydroxy quininib (Q8), an antagonist of cysteinyl leukotriene receptor-1 with VEGF-independent bioactivity. Here, Q8, quininib (Q1) and five structural analogues were assayed for anti-tumorigenic effects in pre-clinical cancer models. Q8 reduced clone formation of the human colorectal cancer cell line HT29-Luc2. Gene silencing of CysLT1 in HT29-Luc2 cells significantly reduced expression of calpain-2. In human ex vivo colorectal cancer tumour explants, Q8 significantly decreased the secretion of both TIE-2 and VCAM-1 expression. In vivo Q8 was well tolerated up to 50 mg/kg by Balb/C mice and significantly more effective at reducing tumour volume in colorectal tumour xenografts compared to the parent drug quininib. In tumour xenografts, Q8 significantly reduced expression of the angiogenic marker calpain-2 in. In summary, we propose Q8 may act on the TIE-2-Angiopoietin signalling pathway to significantly inhibit the process of tumour angiogenesis in colorectal cancer.

cancer biology↗