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David L. Rimm

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    OA03 - Advances in Lung Cancer Pathology (ID 897)

    • Event: WCLC 2018
    • Type: Oral Abstract Session
    • Track: Pathology
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/24/2018, 10:30 - 12:00, Room 205 BD
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      OA03.08 - Discussant - OA 03.05, OA 03.06, OA 03.07 (ID 14551)

      11:45 - 12:00  |  Presenting Author(s): David L. Rimm

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    P2.04 - Immunooncology (Not CME Accredited Session) (ID 953)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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      P2.04-20 - Immunologic Characterization of Fibrinous Pericarditis as an Immune Checkpoint Blockade Toxicity in NSCLC (ID 14058)

      16:45 - 18:00  |  Author(s): David L. Rimm

      • Abstract


      Immune checkpoint inhibitors have revolutionized the treatment paradigm in number of cancers including Non-Small Cell Lung Cancer (NSCLC) but unrestrained modulation of the immune system remains a challenge. Here, we characterized the immune infiltration in the toxicity site and compared immune profile in primary tumor in three patients treated with PD-1/PD-L1 axis inhibitors and developed fibrinous pericarditis (FP)

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We used the AQUA method of quantitative immunofluorescence (QIF) to assess multiplexed panels identifying immune cell populations and their activation status in pre-treatment, post-treatment primary tumor, post-treatment metastatic tumor and the toxicity sites (including pericardial tissue) from 3 NSCLC patients. We also compared the expression of 730 immune-related genes across sites from the 3 patients with FP and 2 NSCLC patients with different toxicity sites after immunotherapy (hypophysitis and myocarditis) using Nanostring Sprint platform.

      4c3880bb027f159e801041b1021e88e8 Result

      In immune infiltration assessment, TILs markers’ expression (CD4, CD8 and CD20) did not differ between primary tumor and toxicity site. There was a trend towards higher CD3+ expression in the toxicity samples but T-cell activation markers expression, Granzyme B and Ki67, was significantly lower in the pericarditis samples. Interestingly, high Granzyme B expression in CD3- cells and CD56+ cells were seen in the pericarditis samples. CD68+ expression, as well as PD-L1 expression in macrophages, was significantly higher (p<0.0001) in the pericarditis samples. mRNA analysis confirmed the QIF findings, with the chemokine profile indicating an M1 macrophage polarization. Additionally, there was a trend towards higher NCR1, perforin1 and Granzyme B gene expression in the toxicity samples, further supporting a possible role of Natural Killer (NK) cells in the development of toxicity.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Our findings suggest that macrophages and possibly NK cells contribute to inflammatory tissue damage in immune related adverse events. Conversely, T-cells that were infiltrating the toxicity sites had low expression of activation markers, further indicating that toxicity may be mediated by other cellular pathways.