The Christie Research Publications Repository

The repository contains the research outputs from staff and students at The Christie NHS Foundation Trust and Cancer Research UK Manchester Institute.

Current Repository Content:

Over 7000 peer reviewed articles, reviews and selected publications from 1933 onwards.

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We upload data monthly to the repository. To find out more about the repository, article submission or for advice on how to search it:

Please contact The Christie Library and Knowledge Service at the-christie.library@nhs.net.

Recent Submissions

  • ItemMetadata only
    Induction chemotherapy and molecular MRD influence outcomes in KMT2A-rearranged AML
    (2025) Othman, J.; Potter, N.; Freeman, S. D.; McCarthy, N.; Jovanovic, J.; Runglall, M.; Canham, J.; Thomas, I.; Johnson, S.; Gilkes, A.; Cavenagh, J.; Kottaridis, P.; Taussig, D.; Arnold, C.; Hemmaway, C.; Culligan, D.; Overgaard, U. M.; Dennis, M.; Burnett, A. K.; Russell, N. H.; Dillon, R.; Haematology and Transplant Unit, The Christie NHS Foundation Trust, Manchester, United Kingdom.
    We analyzed 217 patients with KMT2A-rearranged acute myeloid leukemia (AML) in 2 large sequential randomized trials. Those randomized to FLAG-Ida (fludarabine, cytarabine, granulocyte colony-stimulating factor, idarubucin) had markedly lower rates of relapse than other chemotherapy regimens. Molecular measurable residual disease assessment after cycle 2 was strongly prognostic for relapse and death. The trials were registered at the ISRCTN Registry as AML17 ISRCTN55675535 and AML19 ISRCTN78449203.
  • ItemMetadata only
    Infection rate profile of etentamig monotherapy in patients with relapsed/refractory multiple myeloma
    (2025) Valdes, C. R.; Lichtman, E.; Voorhees, P.; D'Souza, A.; Chung, A.; Tuchman, S.; Gatt, M.; Weisel, K.; Teipel, R.; Vij, R.; Korde, N.; Searle, E.; McKay, J.; Avivi, I.; Svensson, A.; Pothacamury, R.; Talati, C.; Doerr, T.; Ross, J.; Ahsan, A.; Polepally, A.; Rosenberg, T.; Jin, Z. Y.; Kumar, S.; Christie NHS Fdn Trust, Manchester, England
  • ItemMetadata only
    Initial estimate of the carbon footprint of UK proton beam therapy services
    (2025) Chuter, R.; Smith, A.; Newton-Sullivan, V.; Fathi, K.; Waring, E.; Gohil, P.; Hardy, M.; Christie NHS FT, Christie Med Phys & Engn, Manchester, England Univ Manchester, Fac Biol Med & Hlth, Sch Med Sci, Div Canc Sci, Manchester, England
  • ItemOpen Access
    Radiation-induced extracellular matrix remodelling drives prognosis and predicts radiotherapy response in muscle-invasive bladder cancer
    (2025) Guerrero Quiles, C.; Fahy, S.; Bartak, M.; Gonzalez Abalos, J.; Powell, E.; Lodhi, T.; Reed, R.; Reeves, K.; Baker, A.; James, N. D.; Hall, E.; Huddart, R. A.; Porta, N.; Hoskin, P.; West, C.; Biolatti, L. V.; Choudhury, A.; Division of Cancer Sciences, The University of Manchester, The Christie Hospital National Health Service (NHS) Foundation Trust, Manchester, United Kingdom. Institute Curie, Immunity and Cancer Unit (U932), Paris, France. Cancer Research UK Manchester Institute, The University of Manchester, Manchester, United Kingdom. Clinical Trials & Statistics Unit, The Institute of Cancer Research, London, United Kingdom.
    Muscle-invasive bladder cancer (MIBC) is a prevalent disease that can be treated with radiotherapy, but has a poor prognosis. Radiation-induced extracellular matrix (ECM) remodelling and fibrosis can induce tumour resistance and recurrence, but have not been studied in MIBC. Here, we aimed to characterise the impact of radiation on the ECM composition of MIBC. Three MIBC cell lines (T24, UMUC3, J82) were treated with fractionated radiation. We used proteomics to analyse the ECM composition produced by surviving cancer cells and immunofluorescence to investigate changes in the morphology and number of ECM fibres. We evaluated the RNA expression of identified ECM proteins (FN1, COL5A1, COL1A1, TNF6AIP6, FLG) in one cystectomy (TCGA-BLCA, n=397) and two radiotherapy (BC2001, n=313; BCON, n=151) cohorts. There were 613 proteins affected by radiation (p(adj)<0.05, fold change >2 or <-2), 68 of which were ECM-associated proteins. There was a general increase in proteases and protease regulators but heterogeneity across cell lines. Enrichment analysis showed ECM organisation was the primary pathway affected. Immunofluorescence confirmed radiation affected ECM structure, generally, reducing the number, length and width of fibres. Five ECM genes of interest were identified (COL1A1, COL5A2, FN1, FLG, TNFAIP6), constituting an ECM signature. High FN1, COL1A1, TNF6AIP6 mRNA levels and ECM signature scores were independent poor prognostic markers, while FLG mRNA expression independently predicted radiotherapy benefit in a meta-analysis (n=861). We found high COL1A1 expression levels predicted hypoxia-modifying treatment benefit. Prognostic significance of COL5A2, FN1 and the ECM signature was dependent on patients harbouring TP53-mutations. Radiation alters the composition and structure of the ECM produced by MIBC. As a proof-of-concept, we showed that radiation-affected ECM genes are independent prognostic and predictive markers of radiotherapy benefit in MIBC. Future studies should validate these radiation-induced ECM changes in clinical samples, and explore the role of FLG in radioresistance.
  • ItemOpen Access
    Impaired plasma membrane calcium ATPase activity and mitochondrial dysfunction contribute to calcium dysregulation in Fabry disease-related painful neuropathy
    (2025) Formaggio, F.; Pizzi, A.; Delprete, C.; Pasqualini, D.; Mataloni, I.; Rimondini, R.; Campolongo, L.; Donadio, V.; Ghelli, A. M.; Liguori, R.; Caprini, M.; Univ Bologna, Dept Pharm & Biotechnol FaBiT, Lab Cellular & Mol Physiol, Bologna, Italy Univ Bologna, Dept Med & Clin Sci DIMEC, Bologna, Italy IRCCS Ist Sci Neurolog Bologna, Bologna, Italy Univ Bologna, Dept Biomed & Neuromotor Sci DIBINEM, Bologna, Italy Univ Manchester, Canc Res UK Manchester Inst, Skin Canc & Ageing Lab, Manchester, England
    Neuropathic pain is a hallmark symptom in Fabry disease (FD), a hereditary X-linked lysosomal storage disorder caused by a reduced activity of alpha-galactosidase A (alpha-Gal A). The alpha-Gal A deficiency results in the progressive accumulation of globotriaosylceramide (Gb3) and globotriaosylsphingosine (lyso-Gb3) in the body fluids and lysosomes of various cell types, including sensory ganglia. The FD neuropathy affects the small thinly myelinated A delta fibers and unmyelinated C fibers leading to the loss of intra-epidermal neuronal terminations, along with altered thermal and mechanical perception. Lipid accumulation, such as Gb3 and lyso-Gb3, is implicated in various cellular dysfunctions, including the alteration of ionic currents. It has been shown that administration of Gb3 to human umbilical vein endothelial cells leads to the downregulation of the calcium (Ca2+)-activated K+ channel KCa3.1, whereas lyso-Gb3 evokes cytosolic Ca2+ transients and an enhancement of voltage-activated Ca2+ currents in murine dorsal root ganglia. Therefore, we examined the mechanism underlying Ca2+ regulation in primary afferent neurons from the alpha-Gal A (-/0) mouse model. The obtained results suggest that other transport proteins participate in Ca2+ homeostasis in FD and their dysfunction may be directly involved in nociception. In this context, plasma-membrane Ca2+ ATPases exhibited reduced activity in FD, leading to an increased resting [Ca2+]i in sensory neurons. The reduced activity was associated with a decrease of cytosolic pH which weakened the PMCA-dependent calcium extrusion. We finally evaluated the contribution of mitochondria to the Ca2+ signalling and we observed impairment of the mitochondrial buffer capacity, as well as dysfunctional mitochondria and enhanced autophagy/mitophagy. These findings provide a basis for future insights into the alterations of calcium signalling underlying the onset of neuropathic symptoms in FD.
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