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1. Updates on radiotherapy-immunotherapy combinations: Proceedings of 6th annual ImmunoRad conference.

Author

Gregucci, Fabiana, Spada, Sheila, Barcellos-Hoff, Mary Helen, Bhardwaj, Nina, Chan Wah Hak, Charleen, Fiorentino, Alba, Guha, Chandan, Guzman, Monica L, Harrington, Kevin, Herrera, Fernanda G, Honeychurch, Jamie, Hong, Theodore, Iturri, Lorea, Jaffee, Elisabeth, Karam, Sana D, Knott, Simon RV, Koumenis, Constantinos, Lyden, David, Marciscano, Ariel E, Melcher, Alan, Mondini, Michele, Mondino, Anna, Morris, Zachary S, Pitroda, Sean, Quezada, Sergio A, Santambrogio, Laura, Shiao, Stephen, Stagg, John, Telarovic, Irma, Timmerman, Robert, Vozenin, Marie-Catherine, Weichselbaum, Ralph, Welsh, James, Wilkins, Anna, Xu, Chris, Zappasodi, Roberta, Zou, Weiping, Bobard, Alexandre, Demaria, Sandra, Galluzzi, Lorenzo, Deutsch, Eric, and Formenti, Silvia C

Subjects
Humans, Neoplasms, Immunotherapy, Combined Modality Therapy, FLASH radiotherapy, dose and fractionation, immune checkpoint inhibitors, immunomodulators, lymph node sparing, tumor-associated macrophages, Immunization, Cancer, Vaccine Related, Immunology, Oncology and Carcinogenesis
Abstract

Focal radiation therapy (RT) has attracted considerable attention as a combinatorial partner for immunotherapy (IT), largely reflecting a well-defined, predictable safety profile and at least some potential for immunostimulation. However, only a few RT-IT combinations have been tested successfully in patients with cancer, highlighting the urgent need for an improved understanding of the interaction between RT and IT in both preclinical and clinical scenarios. Every year since 2016, ImmunoRad gathers experts working at the interface between RT and IT to provide a forum for education and discussion, with the ultimate goal of fostering progress in the field at both preclinical and clinical levels. Here, we summarize the key concepts and findings presented at the Sixth Annual ImmunoRad conference.

Published
2023

5. Reprogramming the immunosuppressive tumor microenvironment results in successful clearance of tumors resistant to radiation therapy and anti-PD-1/PD-L1

Author

Mukherjee, Debayan, primary, Romano, Erminia, additional, Walshaw, Richard, additional, Zeef, Leo A. H., additional, Banyard, Antonia, additional, Kitcatt, Stephen J., additional, Cheadle, Eleanor J., additional, Tuomela, Karoliina, additional, Pendharkar, Swati, additional, Al-Deka, Aws, additional, Salerno, Beatrice, additional, Raby, Sophie, additional, Mills, Ian G., additional, Honeychurch, Jamie, additional, and Illidge, Tim M., additional

Published
2023
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6. Reprogramming the immunosuppressive tumor microenvironment results in successful clearance of tumors resistant to radiation therapy and anti-PD-1/PD-L1

Author

Mukherjee, Debayan, Romano, Erminia, Walshaw, Richard, Zeef, Leo A H, Banyard, Antonia, Kitcatt, Stephen J, Cheadle, Eleanor J, Tuomela, Karoliina, Pendharkar, Swati, Al-Deka, Aws, Salerno, Beatrice, Raby, Sophie, Mills, Ian G, Honeychurch, Jamie, and Illidge, Tim M

Subjects
SDG 3 - Good Health and Well-being
Abstract

Despite breakthroughs in immune checkpoint inhibitors (ICI), the majority of tumors, including those poorly infiltrated by CD8+ T cells or heavily infiltrated by immunosuppressive immune effector cells, are unlikely to result in clinically meaningful tumor responses. Radiation therapy (RT) has been combined with ICI to potentially overcome this resistance and improve response rates but reported clinical trial results have thus far been disappointing. Novel approaches are required to overcome this resistance and reprogram the immunosuppressive tumor microenvironment (TME) and address this major unmet clinical need. Using diverse preclinical tumor models of prostate and bladder cancer, including an autochthonous prostate tumor (Pten-/-/trp53-/-) that respond poorly to radiation therapy (RT) and anti-PD-L1 combinations, the key drivers of this resistance within the TME were profiled and used to develop rationalized combination therapies that simultaneously enhance activation of anti-cancer T cell responses and reprogram the immunosuppressive TME. The addition of anti-CD40mAb to RT resulted in an increase in IFN-y signaling, activation of Th-1 pathways with an increased infiltration of CD8+ T-cells and regulatory T-cells with associated activation of the CTLA-4 signaling pathway in the TME. Anti-CTLA-4mAb in combination with RT further reprogrammed the immunosuppressive TME, resulting in durable, long-term tumor control. Our data provide novel insights into the underlying mechanisms of the immunosuppressive TME that result in resistance to RT and anti-PD-1 inhibitors and inform therapeutic approaches to reprogramming the immune contexture in the TME to potentially improve tumor responses and clinical outcomes.

Published
2023

8. The CD40 agonist HERA-CD40L results in enhanced activation of antigen presenting cells, promoting an anti-tumor effect alone and in combination with radiotherapy

Author

Frankish, Jamie, primary, Mukherjee, Debayan, additional, Romano, Erminia, additional, Billian-Frey, Katharina, additional, Schröder, Matthias, additional, Heinonen, Karl, additional, Merz, Christian, additional, Redondo Müller, Mauricio, additional, Gieffers, Christian, additional, Hill, Oliver, additional, Thiemann, Meinolf, additional, Honeychurch, Jamie, additional, Illidge, Tim, additional, and Sykora, Jaromir, additional

Published
2023
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11. Supplemental Figure 4 from Fractionated Radiation Therapy Stimulates Antitumor Immunity Mediated by Both Resident and Infiltrating Polyclonal T-cell Populations when Combined with PD-1 Blockade

Author

Dovedi, Simon J., primary, Cheadle, Eleanor J., primary, Popple, Amy L., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Yusko, Erik C., primary, Sanders, Catherine M., primary, Vignali, Marissa, primary, Emerson, Ryan O., primary, Robins, Harlan S., primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Timothy M., primary

Published
2023
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12. Supplemental Figure 1 from Fractionated Radiation Therapy Stimulates Antitumor Immunity Mediated by Both Resident and Infiltrating Polyclonal T-cell Populations when Combined with PD-1 Blockade

Author

Dovedi, Simon J., primary, Cheadle, Eleanor J., primary, Popple, Amy L., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Yusko, Erik C., primary, Sanders, Catherine M., primary, Vignali, Marissa, primary, Emerson, Ryan O., primary, Robins, Harlan S., primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Timothy M., primary

Published
2023
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13. Supplemental Figure Legends from Fractionated Radiation Therapy Stimulates Antitumor Immunity Mediated by Both Resident and Infiltrating Polyclonal T-cell Populations when Combined with PD-1 Blockade

Author

Dovedi, Simon J., primary, Cheadle, Eleanor J., primary, Popple, Amy L., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Yusko, Erik C., primary, Sanders, Catherine M., primary, Vignali, Marissa, primary, Emerson, Ryan O., primary, Robins, Harlan S., primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Timothy M., primary

Published
2023
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14. Supplemental Figure 6 from Fractionated Radiation Therapy Stimulates Antitumor Immunity Mediated by Both Resident and Infiltrating Polyclonal T-cell Populations when Combined with PD-1 Blockade

Author

Dovedi, Simon J., primary, Cheadle, Eleanor J., primary, Popple, Amy L., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Yusko, Erik C., primary, Sanders, Catherine M., primary, Vignali, Marissa, primary, Emerson, Ryan O., primary, Robins, Harlan S., primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Timothy M., primary

Published
2023
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15. Supplemental Figure 5 from Fractionated Radiation Therapy Stimulates Antitumor Immunity Mediated by Both Resident and Infiltrating Polyclonal T-cell Populations when Combined with PD-1 Blockade

Author

Dovedi, Simon J., primary, Cheadle, Eleanor J., primary, Popple, Amy L., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Yusko, Erik C., primary, Sanders, Catherine M., primary, Vignali, Marissa, primary, Emerson, Ryan O., primary, Robins, Harlan S., primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Timothy M., primary

Published
2023
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16. Supplemental Figure 3 from Fractionated Radiation Therapy Stimulates Antitumor Immunity Mediated by Both Resident and Infiltrating Polyclonal T-cell Populations when Combined with PD-1 Blockade

Author

Dovedi, Simon J., primary, Cheadle, Eleanor J., primary, Popple, Amy L., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Yusko, Erik C., primary, Sanders, Catherine M., primary, Vignali, Marissa, primary, Emerson, Ryan O., primary, Robins, Harlan S., primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Timothy M., primary

Published
2023
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17. Supplemental Figure 2 from Fractionated Radiation Therapy Stimulates Antitumor Immunity Mediated by Both Resident and Infiltrating Polyclonal T-cell Populations when Combined with PD-1 Blockade

Author

Dovedi, Simon J., primary, Cheadle, Eleanor J., primary, Popple, Amy L., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Yusko, Erik C., primary, Sanders, Catherine M., primary, Vignali, Marissa, primary, Emerson, Ryan O., primary, Robins, Harlan S., primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Timothy M., primary

Published
2023
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18. Data from Acquired Resistance to Fractionated Radiotherapy Can Be Overcome by Concurrent PD-L1 Blockade

Author

Dovedi, Simon J., primary, Adlard, Amy L., primary, Lipowska-Bhalla, Grazyna, primary, McKenna, Conor, primary, Jones, Sherrie, primary, Cheadle, Eleanor J., primary, Stratford, Ian J., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Jones, Hazel, primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Tim M., primary

Published
2023
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22. Supplemental Figures 1 - 7 from Acquired Resistance to Fractionated Radiotherapy Can Be Overcome by Concurrent PD-L1 Blockade

Author

Dovedi, Simon J., primary, Adlard, Amy L., primary, Lipowska-Bhalla, Grazyna, primary, McKenna, Conor, primary, Jones, Sherrie, primary, Cheadle, Eleanor J., primary, Stratford, Ian J., primary, Poon, Edmund, primary, Morrow, Michelle, primary, Stewart, Ross, primary, Jones, Hazel, primary, Wilkinson, Robert W., primary, Honeychurch, Jamie, primary, and Illidge, Tim M., primary

Published
2023
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24. Engineered antibodies in the treatment of B cell lymphoma

Author

Honeychurch, Jamie

Subjects
610, Bispecific, BsAb, T cells
Abstract

The incidence of lymphoma is rising, now representing 3% of cancers in the UK alone. Current treatments include chemotherapy and radiotherapy, but whilst significant remission is often observed, responses frequently prove not to be durable. Thus, alternative treatments are sought. One such alternative is the use of bispecific antibodies (BsAb), which show dual specificity for both a target antigen on the tumour cell, and a cytotoxic trigger molecule on an effector cell. To further investigate these issues, we have designed a panel of F(ab')₂ BsAb against a range of murine B cell lymphoma antigens (idiotype, MHC class II, CD19, CD22 and D40). We have assessed the relative merits in targeting both T cells and neutrophils against these antigens. In the first case, BsAb were directed towards the CD3 and CD2 molecules of the T cell receptor. In the second, a transgenic mouse was utilised, to investigate the therapeutic potential of targeting G-CSF primed neutrophils via human FcγRI. Extensive analysis of these derivatives both in vitro and in vivo has revealed that it is the nature of the tumor antigen itself that has most bearing on therapy. This work indicates that effector mechanisms such as antibody-dependent cellular cytotoxicity, whilst certainly contributing to tumor removal, are not sufficient to eradicate the malignant clone. Instead, it appears likely that a combination of growth inhibitory signals, and generation of T cell immunity are more important to successful therapy. In light of this, Ab dimers were produced in an effort to increase the signalling potential of mAb. Following dimerisation, mAb were able to induce growth arrest and cell death in human lymphoma lines, as well as showing increased complement activation. Dimers were also able to protect against in vivo tumor challenge.

Published
2000

27. Updates on radiotherapy-immunotherapy combinations: Proceedings of 6th annual ImmunoRad conference.

Author

Gregucci, Fabiana, Spada, Sheila, Barcellos-Hoff, Mary Helen, Bhardwaj, Nina, Chan Wah Hak, Charleen, Fiorentino, Alba, Guha, Chandan, Guzman, Monica L., Harrington, Kevin, Herrera, Fernanda G., Honeychurch, Jamie, Hong, Theodore, Iturri, Lorea, Jaffee, Elisabeth, Karam, Sana D., Knott, Simon R.V., Koumenis, Constantinos, Lyden, David, Marciscano, Ariel E., and Melcher, Alan

Subjects
RADIOTHERAPY, IMMUNE checkpoint inhibitors, CONFERENCES & conventions, DISCUSSION in education
Abstract

Focal radiation therapy (RT) has attracted considerable attention as a combinatorial partner for immunotherapy (IT), largely reflecting a well-defined, predictable safety profile and at least some potential for immunostimulation. However, only a few RT-IT combinations have been tested successfully in patients with cancer, highlighting the urgent need for an improved understanding of the interaction between RT and IT in both preclinical and clinical scenarios. Every year since 2016, ImmunoRad gathers experts working at the interface between RT and IT to provide a forum for education and discussion, with the ultimate goal of fostering progress in the field at both preclinical and clinical levels. Here, we summarize the key concepts and findings presented at the Sixth Annual ImmunoRad conference. [ABSTRACT FROM AUTHOR]

Published
2023
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30. The suitability of micronuclei as markers of relative biological effect

Author

Heaven, Charlotte J, primary, Wanstall, Hannah C, additional, Henthorn, Nicholas T, additional, Warmenhoven, John-William, additional, Ingram, Samuel P, additional, Chadwick, Amy L, additional, Santina, Elham, additional, Honeychurch, Jamie, additional, Schmidt, Christine K, additional, Kirkby, Karen J, additional, Kirkby, Norman F, additional, Burnet, Neil G, additional, and Merchant, Michael J, additional

Published
2022
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34. Monoclonal antibodies directed to CD20 and HLA-DR can elicit homotypic adhesion followed by lysosome-mediated cell death in human lymphoma and leukemia cells

Author

Ivanov, Andrei, Beers, Stephen A., Walshe, Claire A., Honeychurch, Jamie, Alduaij, Waleed, Cox, Kerry L., Potter, Kathleen N., Murray, Stephen, Chan, Claude H.T., Klymenko, Tetyana, Erenpreisa, Jekaterina, Glennie, Martin J., Illidge, Tim M., and Cragg, Mark S.

Subjects
Cell death -- Causes of, Cell death -- Control, Lymphomas -- Genetic aspects, Lymphomas -- Drug therapy, Lymphomas -- Research, Monoclonal antibodies -- Usage, Monoclonal antibodies -- Health aspects
Abstract

mAbs are becoming increasingly utilized in the treatment of lymphoid disorders. Although Fc-Fc[gamma]R interactions are thought to account for much of their therapeutic effect, this does not explain why certain mAb specificities are more potent than others. An additional effector mechanism underlying the action of some mAbs is the direct induction of cell death. Previously, we demonstrated that certain CD20-specific mAbs (which we termed type II mAbs) evoke a nonapoptotic mode of cell death that appears to be linked with the induction of homotypic adhesion. Here, we reveal that peripheral relocalization of actin is critical for the adhesion and cell death induced by both the type II CD20-specific mAb tositumomab and an HLA-DR--specific mAb in both human lymphoma cell lines and primary chronic lymphocytic leukemia cells. The cell death elicited was rapid, nonapoptotic, nonautophagic, and dependent on the integrity of plasma membrane cholesterol and activation of the V-type ATPase. This cytoplasmic cell death involved lysosomes, which swelled and then dispersed their contents, including cathepsin B, into the cytoplasm and surrounding environment. The resulting loss of plasma membrane integrity occurred independently of caspases and was not controlled by Bcl-2. These experiments provide what we believe to be new insights into the mechanisms by which 2 clinically relevant mAbs elicit cell death and show that this homotypic adhesion--related cell death occurs through a lysosome-dependent pathway., Introduction mAbs are becoming increasingly utilized in the treatment of lymphoid disorders (1), (2). In particular, mAb directed to cell-surface antigens on malignant B cells has proven the most clinically [...]

Published
2009

37. Investigating Radiotherapy Response in a Novel Syngeneic Model of Prostate Cancer

Author

Haughey, Charles M., primary, Mukherjee, Debayan, additional, Steele, Rebecca E., additional, Popple, Amy, additional, Dura-Perez, Lara, additional, Pickard, Adam, additional, Patel, Mehjabin, additional, Jain, Suneil, additional, Mullan, Paul B., additional, Williams, Rich, additional, Oliveira, Pedro, additional, Buckley, Niamh E., additional, Honeychurch, Jamie, additional, S. McDade, Simon, additional, Illidge, Timothy, additional, Mills, Ian G., additional, and Eddie, Sharon L., additional

Published
2020
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38. suitability of micronuclei as markers of relative biological effect.

Author

Heaven, Charlotte J, Wanstall, Hannah C, Henthorn, Nicholas T, Warmenhoven, John-William, Ingram, Samuel P, Chadwick, Amy L, Santina, Elham, Honeychurch, Jamie, Schmidt, Christine K, Kirkby, Karen J, Kirkby, Norman F, Burnet, Neil G, and Merchant, Michael J

Subjects
BIOMARKERS, NUCLEOLUS, IONIZING radiation, DNA damage, CYTOKINESIS
Abstract

Micronucleus (MN) formation is routinely used as a biodosimeter for radiation exposures and has historically been used as a measure of DNA damage in cells. Strongly correlating with dose, MN are also suggested to indicate radiation quality, differentiating between particle and photon irradiation. The "gold standard" for measuring MN formation is Fenech's cytokinesis-block micronucleus (CBMN) cytome assay, which uses the cytokinesis blocking agent cytochalasin-B. Here, we present a comprehensive analysis of the literature investigating MN induction trends in vitro , collating 193 publications, with 2476 data points. Data were collected from original studies that used the CBMN assay to quantify MN in response to ionizing radiation in vitro. Overall, the meta-analysis showed that individual studies mostly have a linear increase of MN with dose [85% of MN per cell (MNPC) datasets and 89% of percentage containing MN (PCMN) datasets had an R 2 greater than 0.90]. However, there is high variation between studies, resulting in a low R 2 when data are combined (0.47 for MNPC datasets and 0.60 for PCMN datasets). Particle type, species, cell type, and cytochalasin-B concentration were suggested to influence MN frequency. However, variation in the data meant that the effects could not be strongly correlated with the experimental parameters investigated. There is less variation between studies when comparing the PCMN rather than the number of MNPC. Deviation from CBMN protocol specified timings did not have a large effect on MN induction. However, further analysis showed less variation between studies following Fenech's protocol closely, which provided more reliable results. By limiting the cell type and species as well as only selecting studies following the Fenech protocol, R 2 was increased to 0.64 for both measures. We therefore determine that due to variation between studies, MN are currently a poor predictor of radiation-induced DNA damage and make recommendations for futures studies assessing MN to improve consistency between datasets. [ABSTRACT FROM AUTHOR]

Published
2022
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39. Abstract 2781: Diffusion weighted MRI evaluation of response to immunotherapy and radiotherapy in CT26 and 4T1 syngeneic mouse models of cancer

Author

Lipowska-Bhalla, Grazyna, primary, McHugh, Damien J., additional, Babur, Muhammad, additional, Martin, Isabel Peset, additional, Berks, Michael, additional, Little, Ross A., additional, Cheung, Susan, additional, Watson, Yvonne, additional, Alferez, Denis G., additional, Williams, Kaye J., additional, Honeychurch, Jamie, additional, and O'Connor, James P., additional

Published
2020
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40. Development of a novel allograft model of prostate cancer: a new tool to inform clinical translation

Author

Haughey, Charles M., primary, Mukherjee, Debayan, additional, Steele, Rebecca E., additional, Popple, Amy, additional, Dura-Perez, Lara, additional, Pickard, Adam, additional, Jain, Suneil, additional, Mullan, Paul B., additional, Williams, Rich, additional, Oliveira, Pedro, additional, Buckley, Niamh E., additional, Honeychurch, Jamie, additional, McDade, Simon, additional, Illidge, Timothy, additional, Mills, Ian G., additional, and Eddie, Sharon L., additional

Published
2020
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41. Diffusion model comparison identifies distinct tumor sub‐regions and tracks treatment response

Author

McHugh, Damien J., primary, Lipowska‐Bhalla, Grazyna, additional, Babur, Muhammad, additional, Watson, Yvonne, additional, Peset, Isabel, additional, Mistry, Hitesh B., additional, Hubbard Cristinacce, Penny L., additional, Naish, Josephine H., additional, Honeychurch, Jamie, additional, Williams, Kaye J., additional, O'Connor, James P. B., additional, and Parker, Geoffrey J. M., additional

Published
2020
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42. Additional file 1: of Evaluation of apoptosis imaging biomarkers in a genetic model of cell death

Author

Vassileva, Vessela, Stribbling, Stephen, Barnes, Chris, Carroll, Laurence, Braga, Marta, Abrahams, Joel, Heinzmann, Kathrin, Haegeman, Caroline, MacFarlane, Marion, Simpson, Kathryn, Dive, Caroline, Honeychurch, Jamie, Illidge, Timothy, and Aboagye, Eric

Abstract

Figure S1. PET imaging with apoptotic radiotracers. Representative PET images with (A) 18F-ICMT-11 at 6 and 24â h and (B) 18F-ML-10 at 24â h, after doxycycline administration in mice bearing B16ova and B16ovaRevC3 tumours. (PDF 560 kb)

Published
2019
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