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Sven Diederichs

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    MS22 - Biology of the Lung and Lung Cancer (ID 800)

    • Event: WCLC 2018
    • Type: Mini Symposium
    • Track: Biology
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/26/2018, 10:30 - 12:00, Room 206 F
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      MS22.03 - Non-Coding RNA in Lung Cancer (ID 11492)

      11:00 - 11:15  |  Presenting Author(s): Sven Diederichs

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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    P3.13 - Targeted Therapy (Not CME Accredited Session) (ID 979)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.13-32 - Drug Sensitivity of Lung Adenocarcinoma Towards Inducers of Epigenetic Modifications (ID 13779)

      12:00 - 13:30  |  Author(s): Sven Diederichs

      • Abstract


      Over the last decade, epigenetic regulation of gene expression emerged as a central mechanism in tumorigenesis and metastasis. In contrast to DNA mutations, epigenetic modifications are reversible and therefore suitable targets for pharmacological therapy.

      To understand which patients will benefit the most from which drug regime remains a challenge in everyday clinical practice. The aim of this study is to characterize the tumor drug sensitivity and epigenetic modifications on a molecular level induced by different compounds, in order to improve tumor-specific treatment for patients.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We tested a total of 40 epigenetically active compounds (partly known and partly unknown/unpublished) in two different concentrations in 56 lung adenocarcinoma cell lines and 3 control cell lines for cell viability.

      4c3880bb027f159e801041b1021e88e8 Result

      The resulting 14000 data points were split according to sensitivity of the tumor cells to the compounds into three different groups (high sensitivity: < 25% viable cells, medium sensitivity: 25%-75 viable cells and low sensitivity: >75% viable cells). Six compounds showed broad effectiveness with high sensitivity in more than half of the cell lines while 15 compounds inhibited proliferation in only a few cell lines and are therefore of special interest for the discovery of new predictive biomarkers. The remaining compounds did not show high sensitivity in any cell line.

      Notably, we found that different compounds targeting the class of histone acetyltransferases (HAT) can have very different impacts on the survival of the tumor cells, and that the epigenetic modification of opposing mechanisms (e.g. HAT- and HDAC-inhibitors) may give rise to similar results

      8eea62084ca7e541d918e823422bd82e Conclusion

      Taken together, we demonstrate the differential effectivity of drugs inducing epigenetic modifications in lung adenocarcinoma cells in vitro. By combining the sensitivity data with molecular profiles of RNA and protein expression which we have generated, we are identifying molecular determinants for the individual sensitivity of the tumor to the respective drugs, which could be further developed in vivointo predictive biomarkers for drug response.