Publications by authors named "K P Nephew"
Article Synopsis
- The study investigates how cancer cells influence the fitness of surrounding tumor microenvironment (TME) cells through a mechanism involving a long non-coding RNA called Tu-Stroma, which alters the expression of Flower isoforms, impacting their growth advantage.
- The expression of Flower Win isoforms in cancer cells enhances their dominance over TME cells that express Flower Lose isoforms, leading to reduced fitness in the TME.
- Targeting Flower proteins with a humanized monoclonal antibody in mice has shown promising results, significantly reducing cancer growth and metastasis while improving survival rates and protecting organs from potential lesions.
Article Synopsis
- - The relationship between the nucleus and cell cycle changes during cancer progression causes genomic instability, which tumor cells exploit to avoid cell death and treatment resistance.
- - In epithelial ovarian cancer, the overexpression of claudin-4 is linked to increased therapy resistance and helps stabilize the genome by modifying both the nuclear structure and the cell cycle dynamics.
- - Intervention using a claudin mimic peptide and forskolin shows that disrupting claudin-4 enhances the effectiveness of PARP inhibitors by altering the oxidative stress response and impacting genomic stability.
Article Synopsis
- Black women experience higher mortality rates from high grade serous ovarian cancer compared to White women, prompting a study to explore biological differences in their tumors.
- Analysis of tumor samples revealed significant differences in DNA methylation (191 sites) and gene expression (277 genes) between Black and White patients, with pathways related to DNA damage response and metabolism being particularly affected.
- Tumors from Black women showed lower levels of specific immune cells, and the study suggests these biological differences may influence treatment responses, warranting further research.
DNA methyltransferase and poly(ADP-ribose) polymerase inhibitors (DNMTis, PARPis) induce a stimulator of interferon (IFN) genes (STING)-dependent pathogen mimicry response (PMR) in ovarian (OC) and other cancers. We now show that combining DNMTis and PARPis upregulates expression of a little-studied nucleic-acid sensor, NFX1-type zinc finger-containing 1 protein (ZNFX1). We demonstrate that ZNFX1 is a novel master regulator for PMR induction in mitochondria, serving as a gateway for STING-dependent PMR.
View Article and Find Full Text PDFDuring cancer development, the interplay between the nucleus and the cell cycle leads to a state of genomic instability, often accompanied by observable morphological aberrations. These aberrations can be controlled by tumor cells to evade cell death, either by preventing or eliminating genomic instability. In epithelial ovarian cancer (EOC), overexpression of the multifunctional protein claudin-4 is a key contributor to therapy resistance through mechanisms associated with genomic instability.
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