K. M. Aird

Deoxyuridine-rich cytoplasmic DNA antagonizes STING-dependent innate immune responses and sensitizes resistant tumors to anti-PD-L1 therapy

The paper shows that dU-rich cytoplasmic DNA inhibits STING-dependent immune responses and enhances anti-PD-L1 therapy efficacy in tumors.

αKG-mediated carnitine synthesis promotes homologous recombination via histone acetylation

This study shows that αKG-mediated carnitine synthesis supports HR proficiency by promoting histone acetylation, which enhances DNA repair.

GPX3 supports ovarian cancer tumor progression in vivo and promotes expression of GDF15

This study shows GPX3 is necessary for ovarian cancer growth in vivo and promotes GDF15 expression, linking it to immune checkpoint inhibitor response.

The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming

This study shows that chemotherapy-induced senescence-associated secretome promotes metastasis in ovarian cancer by reprogramming metabolism and increasing cell detachment.

ATR promotes mTORC1 activity via de novo cholesterol synthesis

This study shows ATR enhances mTORC1 activity through cholesterol synthesis via LSS, independent of CHK1 and TSC, and this effect is amplified in p16-deficient cells.

Alternative splice variants of the mitochondrial fission protein DNM1L/Drp1 regulate mitochondrial dynamics and cell fate in ovarian cancer.

This study identifies an alternative splice variant of Drp1 in ovarian cancer that promotes metastasis and chemoresistance by altering mitochondrial dynamics.

Tumor-Associated Macrophages Expand Chemoresistant, Ovarian Cancer Stem-Like Cells

This study shows that tumor-associated macrophages (TAMs) enhance ovarian cancer stem-like cell (OvCSC) proliferation and survival, contributing to chemotherapy resistance and relapse.

De novo purine metabolism is a metabolic vulnerability of cancers with low p16 expression

This study identifies de novo purine metabolism as a vulnerability in cancers with low p16 expression, showing sensitivity to anti-folate drugs like methotrexate.

Thymidine rescues ATR kinase inhibition induced deoxyuridine contamination in genomic DNA, cell death, and Type 1 interferon expression

This study shows that thymidine rescues ATR kinase inhibitor-induced deoxyuridine contamination, cell death, and Type 1 interferon expression in CD8+ T cells.

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

This study shows that DOT1L regulates the senescence-associated secretory phenotype (SASP) through epigenetic control of IL1A expression in oncogene-induced senescence.

Suppression of p16 alleviates the senescence-associated secretory phenotype

This study shows that reducing p16 expression lowers SASP factor and cytokine levels in senescent cells without affecting senescence markers.

ATM Inhibition Synergizes with Fenofibrate in High Grade Serous Ovarian Cancer Cells

This study shows that combining ATM inhibitors with fenofibrate improves treatment in high-grade serous ovarian cancer cells by inducing senescence.

ATM inhibition drives metabolic adaptation via induction of macropinocytosis

This study shows that ATM inhibition promotes cancer cell survival by increasing macropinocytosis, which can be suppressed by BCAA supplementation.

NFATC4 Promotes Quiescence and Chemotherapy Resistance in Ovarian Cancer

This study identifies NFATC4 as a regulator of quiescence and chemotherapy resistance in ovarian cancer, showing its role in promoting a non-proliferative state and poor prognosis.

Suppression of p16 increases nucleotide synthesis via mTORC1

This study shows that p16 suppression increases nucleotide synthesis through mTORC1 activation, promoting tumorigenesis by bypassing senescence.

Context-dependent activation of SIRT3 is necessary for anchorage-independent survival and metastasis of ovarian cancer cells.

This study shows that SIRT3 activation is required for ovarian cancer cell survival and metastasis by regulating mitochondrial antioxidant defenses and metabolic changes during detachment.

Targeting IDH1 as a pro-senescent therapy in high-grade serous ovarian cancer

This study identifies IDH1 as a therapeutic target in HGSC by showing its role in promoting metabolic adaptation and epigenetic repression, leading to senescence when inhibited.

Simultaneous isotope dilution quantification and metabolic tracing of deoxyribonucleotides by liquid chromatography high resolution mass spectrometry

This paper develops a method to simultaneously quantify and trace dNTP metabolites using isotope dilution and high-resolution mass spectrometry, showing improved accuracy and metabolic pathway insights.