ORCID Profile
0000-0003-1479-3251
Current Organisation
University of Oxford
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Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543768.V1
Abstract: Movie S3 shows CD103- T cell killing HCT116 cancer cell, in brighfield imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543774
Abstract: Movie S1 shows CD103+ T cell killing HCT116 cancer cell, in brighfield imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543762
Abstract: Supplementary Figures and Tables
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543765
Abstract: Movie S4 shows CD103- T cell killing HCT116 cancer cell, by calcium flux imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.C.6550399.V1
Abstract: Abstract Enrichment of CD103 sup + /sup tumor-infiltrating T lymphocytes (TIL) is associated with improved outcomes in patients. However, the characteristics of human CD103 sup + /sup cytotoxic CD8 sup + /sup T cells (CTL) and their role in tumor control remain unclear. We investigated the features and antitumor mechanisms of CD103 sup + /sup CTLs by assessing T-cell receptor (TCR)–matched CD103 sup + /sup and CD103 sup − /sup cancer-specific CTL immunity i in vitro /i and its immunophenotype i ex vivo /i . Interestingly, we found that differentiated CD103 sup + /sup cancer-specific CTLs expressed the active form of TGFβ1 to continually self-regulate CD103 expression, without relying on external TGFβ1-producing cells. The presence of CD103 on CTLs improved TCR antigen sensitivity, which enabled faster cancer recognition and rapid antitumor cytotoxicity. These CD103 sup + /sup CTLs had elevated energetic potential and faster migration capacity. However, they had increased inhibitory receptor coexpression and elevated T-cell apoptosis following prolonged cancer exposure. Our data provide fundamental insights into the properties of matured human CD103 sup + /sup cancer-specific CTLs, which could have important implications for future designs of tissue-localized cancer immunotherapy strategies. /
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543765.V1
Abstract: Movie S4 shows CD103- T cell killing HCT116 cancer cell, by calcium flux imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543771.V1
Abstract: Movie S2 shows CD103+ T cell killing HCT116 cancer cell, by calcium flux imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543768
Abstract: Movie S3 shows CD103- T cell killing HCT116 cancer cell, in brighfield imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543774.V1
Abstract: Movie S1 shows CD103+ T cell killing HCT116 cancer cell, in brighfield imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 02-2020
DOI: 10.1158/2326-6066.CIR-19-0554
Abstract: Enrichment of CD103+ tumor-infiltrating T lymphocytes (TIL) is associated with improved outcomes in patients. However, the characteristics of human CD103+ cytotoxic CD8+ T cells (CTL) and their role in tumor control remain unclear. We investigated the features and antitumor mechanisms of CD103+ CTLs by assessing T-cell receptor (TCR)–matched CD103+ and CD103− cancer-specific CTL immunity in vitro and its immunophenotype ex vivo. Interestingly, we found that differentiated CD103+ cancer-specific CTLs expressed the active form of TGFβ1 to continually self-regulate CD103 expression, without relying on external TGFβ1-producing cells. The presence of CD103 on CTLs improved TCR antigen sensitivity, which enabled faster cancer recognition and rapid antitumor cytotoxicity. These CD103+ CTLs had elevated energetic potential and faster migration capacity. However, they had increased inhibitory receptor coexpression and elevated T-cell apoptosis following prolonged cancer exposure. Our data provide fundamental insights into the properties of matured human CD103+ cancer-specific CTLs, which could have important implications for future designs of tissue-localized cancer immunotherapy strategies.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543771
Abstract: Movie S2 shows CD103+ T cell killing HCT116 cancer cell, by calcium flux imaging.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.C.6550399
Abstract: Abstract Enrichment of CD103 sup + /sup tumor-infiltrating T lymphocytes (TIL) is associated with improved outcomes in patients. However, the characteristics of human CD103 sup + /sup cytotoxic CD8 sup + /sup T cells (CTL) and their role in tumor control remain unclear. We investigated the features and antitumor mechanisms of CD103 sup + /sup CTLs by assessing T-cell receptor (TCR)–matched CD103 sup + /sup and CD103 sup − /sup cancer-specific CTL immunity i in vitro /i and its immunophenotype i ex vivo /i . Interestingly, we found that differentiated CD103 sup + /sup cancer-specific CTLs expressed the active form of TGFβ1 to continually self-regulate CD103 expression, without relying on external TGFβ1-producing cells. The presence of CD103 on CTLs improved TCR antigen sensitivity, which enabled faster cancer recognition and rapid antitumor cytotoxicity. These CD103 sup + /sup CTLs had elevated energetic potential and faster migration capacity. However, they had increased inhibitory receptor coexpression and elevated T-cell apoptosis following prolonged cancer exposure. Our data provide fundamental insights into the properties of matured human CD103 sup + /sup cancer-specific CTLs, which could have important implications for future designs of tissue-localized cancer immunotherapy strategies. /
Publisher: Cold Spring Harbor Laboratory
Date: 23-02-2021
DOI: 10.1101/2021.02.20.21252126
Abstract: The use of immunohistochemistry in the reporting of prostate biopsies is an important adjunct when the diagnosis is not definite on haematoxylin and eosin (H& E) morphology alone. The process is however inherently inefficient with delays while waiting for pathologist review to make the request and duplicated effort reviewing a case more than once. In this study, we aimed to capture the workflow implications of immunohistochemistry requests and demonstrate a novel artificial intelligence tool to identify cases in which immunohistochemistry (IHC) is required and generate an automated request. We conducted audits of the workflow for prostate biopsies in order to understand the potential implications of automated immunohistochemistry requesting and collected prospective cases to train a deep neural network algorithm to detect tissue regions that presented ambiguous morphology on whole slide images. These ambiguous foci were selected on the basis of the pathologist requesting immunohistochemistry to aid diagnosis. A gradient boosted trees classifier was then used to make a slide level prediction based on the outputs of the neural network prediction. The algorithm was trained on annotations of 219 immunohistochemistry-requested and 80 control images, and tested by 3-fold cross-validation. Validation was conducted on a separate validation dataset of 212 images. Non IHC-requested cases were diagnosed in 17.9 minutes on average, while IHC-requested cases took 33.4 minutes over multiple reporting sessions. We estimated 11 minutes could be saved on average per case by automated IHC requesting, by removing duplication of effort. The tool attained 99% accuracy and 0.99 Area Under the Curve (AUC) on the test data. In the validation, the average agreement with pathologists was 0.81, with a mean AUC of 0.80. We demonstrate the proof-of-principle that an AI tool making automated immunohistochemistry requests could create a significantly leaner workflow and result in pathologist time savings.
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543759.V1
Abstract: Titles and Legends for Movies 1-4
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543762.V1
Abstract: Supplementary Figures and Tables
Publisher: American Association for Cancer Research (AACR)
Date: 04-04-2023
DOI: 10.1158/2326-6066.22543759
Abstract: Titles and Legends for Movies 1-4
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Nasullah Khalid Alham.