Pioneering research to fight
pulmonary fibrosis and lung infection

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Breathing Matters was established in 2011 with the aim of finding better treatments for interstitial lung diseases (ILD) and lung infections. Since that time, we have raised money and awareness into these often neglected conditions.

Looking back, we have come much further than any of us would have anticipated. We have established new theories on the development of ILD or lung fibrosis and the role of the immune system, in particular, how inflammatory cells sense the damaged lung epithelium. We also have better ways of monitoring and diagnosing these conditions and our novel nuclear medicine imaging programme and relatively non-invasive lung biopsy service were the first in the UK. The initial data on a novel therapy in IPF (idiopathic pulmonary fibrosis), C21, which we began working on even before Breathing Matters was conceived, is looking promising and further studies are planned. We are developing another novel therapy for pulmonary fibrosis that targets the blood vessels. We could not have achieved any of this without the support of our funders and our patients, so thank you all. This review highlights our achievements to date and our future directions in ILD

Relatively non-invasive lung cryobiopsy (2014-ongoing):

  • Objective: To find a less invasive and better diagnostic tool for every patient with ILD.
  • Main benefactors:
    • Teresa Timberlake and family – equipment purchase
    • Lawrence Matz Memorial Fund – Clinical Fellow
  • Breathing Matters investment: £52,000 salary; £36,000 (total £88,000)
  • Leveraged funding: £347,000
  • Outcomes:
    • Novel cryobiopsy service, first in the UK including training other centres; presentations at European Respiratory Society (2015 and 2018), British Thoracic Society (2014-6).
    • Completed Lung-INHALE Study (2019) to assess inhaled drug deposition using CLB. This will allow drug companies to develop inhaled therapies for IPF and be sure that they are reaching the part of the lung where they are needed. The use of inhaled therapy will avoid some of the side-effects of anti-fibrotic drugs that are taken as tablets.
  • Publications:
    • Transbronchial cryobiopsy in the diagnosis of interstitial lung disease: a cool new approach. Mikolasch TA, Porter JC. Respirology. 2014 Jul;19(5):623-4. doi: 10.1111/resp.12320. Epub 2014 May 25.
    • Mass spectrometry detection of inhaled drug in distal fibrotic lung. Mikolasch TA, Oballa E, Vahdati-Bolouri M, Jarvis E, Cui Y, Cahn A, Terry RL, Sahota J, Thakrar R, Marshall P, Porter JC. Respir Res. 2022 May 11;23(1):118. doi: 10.1186/s12931-022-02026-5.PMID: 35546672 Free PMC article.
  • Our plans for 2024:
    • Continue a prospective review of patients with CLB and publish our local outcomes
    • Ultimate aim is of a clinical trial to see if early CLB improves outcomes in early ILD that is indeterminate for UIP. This will need inter/national involvement and funding

This project was developed in discussion with a family whose mother had had a surgical lung biopsy towards the end of her life. Her experience was such that her family felt that a less invasive alternative must be available. Dr Theresia Mikolasch, the Lawrence Matz Clinical Fellow, took this on for Breathing Matters to find out about and train in new techniques. Dr Mikolasch then returned to UCLH and established the first and only UK cryoscopic lung biopsy (CLB) service. CLB is a new way of obtaining larger lung biopsies using a flexible bronchoscope passed into the lungs through the mouth. The patient is sedated and surgery is avoided. This is not only better for the patient than a surgical lung biopsy, but also provides a solution to the lack of biopsy samples available for scientific research. GSK were so excited by the technique that they awarded Dr Mikolasch and Professor Jo Porter a grant of over £300,000 to carry on the service for an additional 3 years to see if inhaled drugs were able to reach the lung in ILD. It was hoped that by delivering medication by inhalation we would avoid the side-effects that have limited the ability of many patients to tolerate medication.

Novel FDG-PET imaging to predict prognosis and response to treatment in ILD (2014-ongoing):

  • Objective: To find a new test (biomarker) that will enable us to predict prognosis and response to treatment in each individual patient.
  • Main benefactors: Whitaker family
  • Breathing Matters investment: £34,766
  • Leveraged funding: £173,850

Funding from BLF for clinical trial of FDG-PET in post-transplant bronchiolitis £40,000.

  • Outcomes: Novel FDG-PET imaging programme in ILD – first in the UK; presentations at American Nuclear Medicine Society (2015), British Thoracic Society (2015-23); American Thoracic Society (2017 and 2019); European Respiratory Society (2015-2023)
  • Publications:
    • Pulmonary 18F-FDG uptake helps refine current risk stratification in idiopathic pulmonary fibrosis (IPF). Win T, Screaton NJ, Porter JC, Ganeshan B, Maher TM, Fraioli F, Endozo R, Shortman RI, Hurrell L, Holman BF, Thielemans K, Rashidnasab A, Hutton BF, Lukey PT, Flynn A, Ell PJ, Groves AM. Eur J Nucl Med Mol Imaging. 2018 May;45(5):806-815. doi: 10.1007/s00259-017-3917-8. Epub 2018 Jan 16.
    • Synergistic application of pulmonary 18F-FDG PET/HRCT and computer-based CT analysis with conventional severity measures to refine current risk stratification in idiopathic pulmonary fibrosis (IPF). Fraioli F, Lyasheva M, Porter JC, Bomanji J, Shortman RI, Endozo R, Wan S, Bertoletti L, Machado M, Ganeshan B, Win T, Grove Eur J Nucl Med Mol Imaging. 2019 Sep;46(10):2023-2031s AM.
    • Measurement of hypoxia in the lung in idiopathic pulmonary fibrosis: an F-MISO PET/CT study. Porter JC, Win T, Erlandsson K, Fraioli F, Rashidnasab A, Holman B, Ganeshan B, Screaton NJ, Maher TM, Endozo R, Hoath J, Shortman RI, Emond E, Thielemans K, Hutton BF, Lukey PT, Aigbirhio F, Khan S, Rodriguez-Justo M, Groves AM. Eur Respir J. 2021 Oct 7;58(4):2004584. doi: 10.1183/13993003.04584-2020. Print 2021 Oct.

    • Filtration-histogram based texture analysis and CALIPER based pattern analysis as quantitative CT techniques in idiopathic pulmonary fibrosis: head-to-head comparison. AlDalilah Y, Ganeshan B, Endozo R, Bomanji J, Porter JC, Machado M, Bertoletti L, Lilburn D, Lyasheva M, Groves AM,Fraioli F. Br J Radiol. 2022 Jun;95(1134):20210957. doi: 10.1259/bjr.20210957. Epub 2022 Feb 22. PMID: 35191759.

    • Evolution of 18F-FDG-PET/CT findings in patients following COVID-19 pneumonia: An Initial Investigation. Thornton, A; Fraioli, F; Wan, S; Garthwaite, HS; Ganeshan, B; Shortman, RI; Endozo, R; Voo, S; Kayani, I; Neriman, D; Menezes, L; Bomanji, JB; Hillman, T; Heightman, M; Porter, JC; Groves, AM (2021) Evolution of 18F-FDG-PET/CT findings in patients following COVID-19 pneumonia: An Initial Investigation. Journal of Nuclear Medicine
  • Our plans for 2024:
    • FDG-PET may be used as a response biomarker to see if we can detect which patients benefit from anti-fibrotic therapy and which patients do not benefit. This work has now been completed by Hannah Torlot, our Whitaker Fellow, and has been submitted for publication – end of 2023
    • We have shown that the major lymph-nodes in the lung can tell us which patients will do well or badly with ILD – we hope to understand this more and correlate with lymph-node biopsies. Our first steps will be to analyse and publish our data on lymph-nodes and raise funding for more work.
    • We have finished the analysis of our scleroderma cohort and this will be written up and hopefully published in 2024
    • Publish our work on correlations between FDG-PET signal in IPF and tissue biopsies of the lung to understand how the FDG-PET signal is generated.
    • Start our study on FDG-PET in bronchiolitis obliterans.
    • Discussions to introduce Gallium-labelled fibroblast activating protein inhibitor (Ga-FAPI) as a biomarker of myofibroblasts

Interstitial lung disease (ILD) consists of a heterogeneous group of diseases with varying amounts of interstitial inflammation and fibrosis. Survival in the most severe form of lung fibrosis, idiopathic pulmonary fibrosis or IPF, is particularly poor; however, there is heterogeneity in outcome. Some patients gradually deteriorate; some undergo stepwise progression, whilst others decline rapidly. Moreover, much of the prognostic data heralds from an era when the criteria for diagnosing IPF were less well and differently defined than at present. There is a definite need to find prognostic biomarkers to predict outcome in IPF patients.

Positron emission tomography (PET) offers the ability to non-invasively investigate cellular metabolism in vivo. PET studies in animals have yielded valuable insights into the biology of IPF and ILD and there is potentially encouraging evidence that PET may aid the development of therapeutic interventions to treat these debilitating conditions. It has been recently demonstrated that 18F-Fluorodeoxyglucose (18F-FDG) PET signal is consistently raised and can be objectively measured in patients with IPF. Moreover, these PET signals are shown to be stable and reproducible.

We have shown over several years and imaging hundreds of patients with ILD that the baseline measures of pulmonary 18F-FDG PET signal to predict survival in patients with IPF compared to other more established prognostic data. We have also shown that combing PET data with our clinical scoring system based on gender, age and physiology (GAP) data (“PET modified GAP score”) refined the ability to predict mortality. We took advantage of the COVID-19 pandemic to investigate our findings in patients with post-COVID ILD and made some interesting observations. The FDG-PET signal does reduce with time and most patients will get better. This was published in 2021.

Most excitingly, we have some data that shows a correlation between histology on lung biopsy and the 18FDG-PET signal so that we can find out why these areas of the lung take up so much glucose and perhaps understand what this is telling us about the disease process and therefore how we can change it to be a healing, rather than a destructive, response.

Future studies are to investigate the role of FDG-PET scanning in other ILDs, such as bronchiolitis obliterans (post lung transplant), rheumatoid arthritis (see below) and systemic sclerosis.

Rheumatoid arthritis (RA) associated ILD (2018-ongoing):

  • Objective: To discover why 1:5 patients with rheumatoid arthritis (RA) will develop lung fibrosis and what novel treatment can prevent disease progression.
  • Breathing Matters investment: £94,766
  • Leveraged funding: £414,766 (£312,000 in 2023 Rosetrees and EMINENT-GSK and MRC
  • Outcomes:
    • Novel biomarker test for neutrophils extracellular traps (NETS) in ILD in discussion with UCL business for further development; presentations at American College of Rheumatology (2014-6); British Thoracic Society (2016); British Rheumatology Society (2014-6
  • Publications:
    • The lung in a cohort of rheumatoid arthritis patients-an overview of different types of involvement and treatment. Duarte AC, Porter JC, Leandro MJ. Rheumatology (Oxford). 2019 Nov 1;58(11):2031-2038. doi: 10.1093/rheumatology/kez177.
    • Autoimmune rheumatic disease IgG has differential effects upon neutrophil integrin activation that is modulated by the endothelium. Khawaja AA, Pericleous C, Ripoll VM, Porter JC, Giles IP. Sci Rep. 2019 Feb 4;9(1):1283. doi: 10.1038/s41598-018-37852-5.
    • Identification of a novel HIF-1α-αMβ2 Integrin-NETosis axis in fibrotic interstitial lung disease. Khawaja AK, Chong DLW, Sahota J, Pericleous C, Ripoli VM, Booth HL, Khan S, Rodriguez-Justo M, Giles IP, Porter JC. Frontiers in Immunology; 2020.
  • Our plans for 2024:
    • To work with a group in Cold Spring Harbour, USA, to see if inhibiting NET formation prevents fibrosis. This is ongoing.
    • To see if the autoantibodies in the blood of patients that recognise Mucin-1 can react with epithelium of different organs. Dr Beatson has a long interest in this area and in particular how patients with RA are protected (relatively) from breast cancer (that expresses more Mucin-1). However, these antibodies may also cause damage to epithelia of other organs that express Mucin-1 such as the lung and gut.
    • Understand more about NETs and their impact on the local environment – in particular, how they affect monocytes in the airspace.

RA is a chronic debilitating disease estimated to afflict 13% of the world population. Around 10% of patients with RA will develop an ILD that is very similar to the lung fibrosis that we see with IPF. Dr Akif Khawaja was funded by Rosetrees and UCL to carry out a PhD into the aetiology of RA-ILD. His work proposed that RA is a disease that starts in the lung. That chronic lung damage caused by smoking, infection and other insults causes the immune response to recognize the lungs and joints as “foreign” and

attack them causing chronic damage. His work implicated neutrophils in this process and, in particular, the p38 MAPkinase pathway. Dr Richard Beatson has taken this a step further to show that monocytes and macrophages in the lung are the first to sense lung damage and produce signals that recruit neutrophils. We are hoping to develop a new test using blood or sputum to detect early activation of inflammatory cells that may suggest that a patient is at risk of developing ILD. This same test may act as a biomarker for prognosis and to detect early response to novel therapies.

A trial of anticoagulation in IPF (2016-ongoing):

  • Objective: To assess the potential of anticoagulation as a treatment for IPF
  • Main benefactors: The Hulme Family – The Mark Hulme Clinical Fellow
  • Breathing Matters investment: £40,000
  • Leveraged funding: £100,000 from UCL/H NIHR BRC
  • Our plans for 2024:
    • To write up our study of a trial of anticoagulation with heparin in IPF using FDG-PET as a response biomarker

At present, we do not know the exact cause of idiopathic pulmonary fibrosis (IPF), although research has identified lots of processes that are likely to be involved. Currently, we believe that microscopic injury occurs in patients with IPF and then the body responds to repair this, but does so in a way that leads to more damage and scarring. One of the processes involved in repair pathway is coagulation, which minimises blood loss when tissues are damaged. Patients with IPF are at increased risk of blood clots and this can reduce their already low life expectancy. We also think that these blood clots drive the worsening of their lung disease. Researchers have shown that clotting is over-activated in the lungs of IPF patients and we want to investigate how reducing this might improve the disease. Based on work carried out at UCL, we believe that anticoagulation with heparin is safe and may even prevent disease progression in IPF. Patients will be asked if they would be willing to take the oral anticoagulant, dabigatran, for 3 weeks to reduce clotting. We will perform blood tests and FDG-PET scans before and after taking the drug to judge response. If we find that the heparin is safe and the patients report some improvement that we can confirm with questionnaires lung function and FDG-PET scans, then we will progress to leverage funding for a much bigger trial. We have now recruited to this study and are analysing the results. We hope to have this work reported completely in 2024.

The neutrophil lymphocyte ratio in IPF (2021-ongoing):

  • Objective: To assess the potential of NLR as a biomarker in IPF
  • Main benefactors: NIHR BRC £100,000
  • Breathing Matters investment: £40,000
  • Leveraged funding: NIHR.
  • Publications:
    • Multi-center evaluation of baseline neutrophil-to-lymphocyte (NLR) ratio as an independent predictor of mortality and clinical risk stratifier in idiopathic pulmonary fibrosis
    • eClinicalMedicine, ISSN: 2589-5370, Vol: 55, Page: 101758
    • Theresia A. Mikolasch; Peter M. George; Jagdeep Sahota; Thomas Nancarrow; Shaney L. Barratt; Felix A. Woodhead; Vasilis Kouranos; Victoria S.A. Cope; Andrew W. Creamer; Silan Fidan; Balaji Ganeshan; Luke Hoy; John A. Mackintosh; Robert Shortman; Anna Duckworth; Janet Fallon; Helen Garthwaite; Melissa Heightman; Huzaifa I. Adamali; Sarah Lines; Thida Win; Rebecca Wollerton; Elisabetta A. Renzoni; Matthew Steward; Athol U. Wells; Michael Gibbons; Ashley M. Groves; Bibek Gooptu; Chris J. Scotton; Joanna C. Porter
    • Publication Year 2023
    • https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(22)00487-4/fulltext
  • Our plans for 2024:
    • To use our NETs data to understand what the NLR is telling us about neutrophil dynamics

 

Assessing effectiveness of treatments for IPF is difficult as often they do not make patients feel better, despite decelerating disease. Currently, we are guided by regular breathing tests and special imaging of the lungs, which are insensitive to changes and may be unpleasant for patients. We need better tests like a simple blood test to predict the prognosis for individual patients, and their responses to treatment. Causes of IPF are unknown, but we have found that specific white blood cells, called neutrophils, are increased in the lungs of patients with IPF. We also found that the more neutrophils in the lungs, the faster the decline from IPF. This suggests that neutrophils are actively worsening IPF. We have also shown that a simple measurement from the blood, called the neutrophil:lymphocyte ratio is a power predictor of outcomes in IPF. We have not validated our initial findings in groups of IPF patients from around the country. Our paper was published in one of the prestigious – The Lancet eClinicalMedicine in 2023.

A trial of a novel treatment (C21) in IPF (2021-ongoing):

  • Objective: To assess the potential of C21 as a treatment for IPF
  • Main benefactors: NIHR BRC £100,000
  • Breathing Matters investment: £40,000
  • Leveraged funding: Application to British Thoracic Society, Wellcome Trust and NIHR. Funded by LifeArc/Vicore for around £1Million to study C21 in COVID pneumonits (2020-2022-3).
  • Publications:
    • Seven days treatment with the angiotensin II type 2 receptor agonist C21 in hospitalized COVID-19 patients; a placebo-controlled randomised multi-centre double-blind phase 2 trial. Tornling G, Batta R, Porter JC, Williams B, Bengtsson T, Parmar K, Kashiva R, Hallberg A, Cohrt AK, Westergaard K, Dalsgaard CJ, Raud J. EClinicalMedicine. 2021 Nov;41:101152. doi: 10.1016/j.eclinm.2021.101152. Epub 2021 Oct 24. PMID: 34723163 Free PMC article
  • Our plans for 2024:
    • To work with Vicore Pharma to complete further later phase studies of C21 in IPF

We are currently working with Vicore Pharma to assess the safety and efficacy of twice daily oral C21 in the treatment of IPF. Patients will be treated with active C21 for 9 months. C21 is an oral angiotensin II agonist. It has already been shown to be well tolerated and safe in the treatment of patients with COVID-19 pneumonitis and appears to help the lungs to repair. Initial findings were encouraging and a further study is planned.

Understanding mucin 5b and its role in IPF (2019-ongoing):

  • Objective: To assess the role of Muc5B in IPF
  • Main benefactors: NIHR £300,000
  • Breathing Matters investment: £40,000
  • Next steps: Further investigations in patients with IPF of the effects of blocking neutrophil activation
  • Publications:
    • Mucins and their receptors in chronic lung disease. Denneny E, Sahota J, Beatson R, Thornton D, Burchell J, Porter JC. Clinical and Translational Immunology 2020
  • Our plans for 2024:
    • Analyse and publish our work on imaging and MUC5B genotypes
    • Complete our review on Mucins and Siglecs

It is unclear what causes IPF, but it is thought to be a response to damage to the lining of the airways (epithelium) following an unidentified injury. This results in the formation of excessive scar tissue which disrupts the delicate architecture of the lung and ultimately death follows from respiratory failure. We have shown from research previously sponsored by The Rosetrees Trust that a certain type of white blood cell which is specialised in fighting infections, called neutrophils, may play a role in PF. We have found that neutrophils are increased in the blood and lungs of patients with PF and the more neutrophils you have, the worse the individual’s outcome. In addition, it is recognised that you are more likely to develop IPF if you have a commonly occurring genetic mutation that causes increased mucus production by the lung epithelium, and in particular a protein called Mucin or MUC5B that gives sputum its stringy quality. We propose that the overproduction of MUC5B may stress the epithelium, making it more prone to damage and scarring. In addition, the increased MUC5B will attract and activate neutrophils from the blood and these white blood cells can cause further damage. We hope that, by identifying treatments that limit the

number of neutrophils moving into the lung, we can protect patients from developing PF or from PF progressing. We will use neutrophils and epithelial samples from patients and healthy volunteers to compare differences and see how the MUC5B affects neutrophil activation in the lung. Lastly, we plan to block neutrophil activation and recruitment with a specific treatment that is already being developed for other indications and has an excellent safety profile. If our results are encouraging, we can take this medication into an early clinical trial for patients with IPF.

We have also shown that we can detect very early changes in the CT scans of patients that make too much MUC5B and this might be a very early sign, even before the scan looks abnormal, that these patients are at risk of lung disease.

Remote monitoring of patients with chronic lung disease including IPF (2021-ongoing):

Malik Althobiani, a respiratory therapist, has been sponsored to undertake a PhD with Professor John Hurst and Professor Jo Porter to investigate the potential of remote monitoring or patients with lung diseases including IPF. Our research looked at whether remote monitoring of signs (such as heart rate and oxygen saturation) and symptoms (such as shortness of breath or reduced exercise tolerance) and lung function (such as walk tests and spirometry using wearable sensors and questionnaires is feasible. Malik has already finished recruiting patients to this study and early results are very promising. He is writing his PhD for examination in 2024! Good Luck Malik.

ILD in patients after lung infections (2022-2026):

  • Objective: To assess the development of ILD and lung fibrosis in patients who have had infectious diseases: in particular, COVID-19 and tuberculosis (TB)
  • Main benefactors: NIHR ~£150,000 as part of the UK-ILD post COVID consortium
  • Breathing Matters investment: £30,000
  • Leveraged outcome: £70,000 from Mason Medical Research Trust
  • Outcomes: Presentations at ERS 2023/BTS 2023
  • Publications:
  • Our plans for 2024:
    • Complete and report our systematic review of lung function post TB in early 2024
    • Publish our work on ILD after COVID-19 in 2024

Dr Emma Denneny and Dr Sharenja Ratnakumar are working to investigate the incidence of lung disease after TB infection by carrying out a systematic review of the literature. In addition, we are involved in a much larger national study to investigate the incidence of ILD after COVID-19 infections. Our work is aimed at understanding the mechanisms underlying the development of ILD in the hope of developing novel treatments. We have already published on the radiological changes in FDG-PET seen post-acute COVID-19, but now need to understand what happens with time in patients with these changes. Will they get better completely, will they remain stable or will they worsen?

Developing a novel biomarker in ILD that is improved in specificity and sensitivity from previous biomarkers (2022-ongoing)

  • Objective: To develop a novel mucin-based biomarker in ILD
  • Main benefactors: UCLH Charities Fast Track £40K, MRC TAS Grant £40K
  • Breathing Matters investment: £40,000
  • Next steps: To use our preliminary data for a larger grant proposal
  • Next steps: To use our preliminary data for a larger grant proposal
  • Our plans for 2024:
    • Continue this work and raise further funding into 2024/5

Dr Richard Beatson, an expert in glycobiology in cancer, is working with Dr Megha Sravani-Bondada to develop a biomarker in ILD that is based on mucins. The biology behind this is very complicated and challenging, but if successful, this high-risk project would be a game changer. We already have some exciting preliminary data generated by a Masters student, Osama Alsuhimi, who returned to us as a PhD student in 2023. Welcome back Osama!

NETS in ILD (2018-ongoing)

  • Objective: To discover if inhibiting NETs is feasible and if it will reduce ILD
  • Breathing Matters investment: £34,766
  • Leveraged funding: £602,766 including funding from LIfeArc to inhibit NETs in COVID-19
  • Outcomes:
    • Novel biomarker test for neutrophils extracellular traps (NETS) in ILD in discussion with UCL business for further development; presentations at American College of Rheumatology (2014-6); British Thoracic Society (2016); British Rheumatology Society (2014-6)
    • Completed trial of Dornase Alfa (an inhibitor of NETs) in COVID-19 pneumonitis-the COVASE trial. Awarded David Cooksey Prize in Translational Medicine 2021 for this work
  • Our plans for 2024:
    • Complete the publication of our findings in eLife in 2024

We have been interested in NETs in ILD for many years. During the COVID-19 pandemic, it was also clear that NETS played a role in COVID-19 pneumonitis. We were funded by LifeArc to carry out a study of nebulized Dornase Alfa in patients with COVID-19 pneumonitis. This has now been completed with very positive results and we hope will be published in 2023.

Sarcopenia in ILD (2023-ongoing)

  • Objective: To discover how prevalent sarcopenia (muscle wasting) is in patients with ILD, whether it affects life expectancy and what we can do about it.
  • Breathing Matters investment: £10,000
  • Leveraged funding: £120,000 (2023 funding for Osama Alsuhimi to complete a PhD)
  • Outcomes and publications:
    • Awaited
  • Our plans for 2024:
    • Complete a systematic review of sarcopenia in ILD
    • Get the ethics and approvals in place to screen our patients at UCLH for ILD

We have become very interested in sarcopenia, or muscle wasting, in ILD and how this may impact on outcomes for patients with ILD. We are very excited to have recruited Osama Alsuhimi, a respiratory therapist, to complete a PhD in this area.

Pneumonitis during cancer treatment (2023-ongoing)

  • Objective: To understand more about pneumonitis in patients treated for cancers, especially lung cancer or cancers, such as breast, that have metastasised to the lungs. In particular, why patients with underlying ILD are more at risk of pneumonitis; how we can identify and prevent this; does drug induced pneumonitis give us insights into other ILDs.
  • Breathing Matters investment: £10,000
  • Leveraged funding: To be applied for
  • Publications:

    • Drugs without benefits? Confronting the challenges of drug-induced interstitial lung disease Denneny, Emma K; Porter, Joanna C; (2021) Drugs without benefits? Confronting the challenges of drug-induced interstitial lung disease. Thorax , 76 (12) pp. 1172-1173. 10.1136/thoraxjnl-2021-217373.

  • Our plans for 2024:
    • Identify the incidence of therapy-induced pneumonitis from cancer therapies; identify patients at risk; develop better pathways to minimise the damage to the lungs
    • Apply for further funding to take this work further

We have always had an interest in drug-induced ILD, by which we mean therapeutic drugs often given as part of cancer treatment, but even innocent antibiotics can cause drug-induced pneumonitis or ILD in some patients.

Therapy-Induced pneumonitis is a serious and potentially life-threatening condition estimated to impact 8% of cancer patients undergoing treatment. After immune checkpoint inhibitors, tyrosine kinase inhibitors, antibody-drug conjugates and M-TOR inhibitors are the most associated causative agents. The incidence is particularly pronounced in individuals with pre-existing ILD or previous respiratory issues, and paradoxically, its impact can be most severe in patients showing the most positive response to therapy.

It is anticipated that approximately 1 in 2000 individuals in the UK will experience this condition at some point, potentially limiting their chances of a complete cure from the original cancer, as it may necessitate discontinuation or modification of the drug. This concern becomes particularly significant when the cancer treatment is proving effective. Furthermore, therapy-induced pneumonitis has the potential to independently compromise both the quality and duration of an individual’s life.

If you are a UCLH patient and want to get involved in any of the above studies, please discuss this with your consultant.

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