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     Long Response


    DNMTi / HDACi / HKMTi Evidence Matrix β€” Ovarian Chemoresistance (From Provided Paper Text)

    Below is an evidence matrix strictly derived from the paper-text content provided in your research data. Where the provided excerpts contain no explicit HDACi or HKMTi agent / results, I mark cells as β€œNot stated in provided text” rather than inferring.

    1) Evidence Matrix Table

    Columns: therapy class (DNMTi, HDACi, HKMTi) crossed with the ovarian chemoresistance context present in the excerpts (e.g., platinum-resistant/refractory platinum response; epigenetic priming/signals).

    Epigenetic class Representative agent(s) explicitly in provided text Ovarian chemoresistance evidence in provided text Evidence type(s) explicitly mentioned Key reported outcomes / signals Limitations/uncertainty (from provided text)
    DNMTi Azacitidine (explicit) Sequential azacitidine then carboplatin is reported to partially reverse platinum resistance and to prime immune activation in provided ovarian cancer excerpts.
    Clinical (platinum-resistant/refractory) :
    Preclinical (cell lines; platinum-resistant model) : sequential azacitidine then carboplatin slows growth and upregulates immune-related pathways.
    • Clinical: single-arm phase 1b-2a
    • In vitro: ovarian HGSOC cell lines with methylome + RNA-seq integration
    • Biomarkers: DR4 methylation changes reported
    Clinical: ORR 13.8% overall; ORR 22% in platinum-resistant; DR4 methylation decreased in responders (reported mean ~40% drop in 3/4 responders).
    Preclinical: sequential treatment increased immune pathway transcript changes after demethylation; immune-related signaling pathways upregulated; Ξ²2M upregulated (fold-change 5.319).
    • Clinical: small, non-randomized design; PBMC/plasma methylation may not fully mirror tumor tissue methylation; limited subset sizes.
    • Preclinical: lacks tumor microenvironment heterogeneity; methylation/transcript changes may not equal protein/functional immune effects; multiple-testing/FDR thresholds noted in text.
    HDACi Not stated in provided ovarian chemoresistance excerpts Not stated in the provided text for ovarian chemoresistance (within the supplied research excerpts). N/A (no explicit HDAC inhibitor + ovarian chemoresistance results in provided excerpts) N/A This cell is intentionally blank of claims because no HDACi agent-specific findings were included in the provided paper-text dataset.
    HKMTi Not stated in provided ovarian chemoresistance excerpts Not stated in the provided text for ovarian chemoresistance (within the supplied research excerpts). N/A (no explicit HKMT inhibitor + ovarian chemoresistance results in provided excerpts) N/A This cell is intentionally blank of claims because no HKMTi agent-specific findings were included in the provided paper-text dataset.
    Epistemic note: A narrative review excerpt mentions β€œepidrugs (DNMT inhibitors, HDAC inhibitors, BET inhibitors, and others)” as a general concept, but the provided excerpts do not supply agent-specific HDACi/HKMTi ovarian chemoresistance results to populate this matrix for those classes.

    2) Minimal β€œRaw-claim traceability” View (what was explicitly present)

    DNMTi (Azacitidine) β†’ platinum resistance / platinum refractory response signals
    DNMTi (Azacitidine) β†’ methylation + immune pathway activation (cell lines)
    Optional: fill the missing HDACi/HKMTi cells

    To populate the HDACi and HKMTi sections rigorously, we would need paper-text that explicitly names HDAC inhibitors or histone-lysine methyltransferase inhibitors in ovarian chemoresistance contexts (agent names + outcomes/biomarkers).



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    Updated: April 26, 2026

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