Results 71 to 80 of about 55,108 (306)

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

Molecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura, Tadahiro Kuribayashi, Johannes Brägelmann, Sachi Okawa, Masataka Taoka, Shunta Mori, Tomoka Nishimura, Takaaki Tanaka, Go Makimoto, Kiichiro Ninomiya, Kammei Rai, Eiki Ichihara, Ryohei Katayama, Katsuyuki Hotta, Masahiro Tabata, Yosuke Togashi, Yoshinobu Maeda, Martin L. Sos, Katsuyuki Kiura, Kadoaki Ohashi   +19 more
wiley   +1 more source

Evaluating the efficacy of DNA repair biomarkers to assess human cell response to chemotherapy using imaging flow cytometry [PDF]

, 2013
This thesis was submitted for the degree of Doctor of Philosophy and awarded by Brunel University.Chemotherapy and radiotherapy are widely accepted as common forms of treatment for cancers. The majority of cancer patients receive chemotherapy alone or in
Zahir, Sheba Adam
core  

NF-κB regulates DNA double-strand break repair in conjunction with BRCA1-CtIP complexes [PDF]

, 2011
NF-κB is involved in immune responses, inflammation, oncogenesis, cell proliferation and apoptosis. Even though NF-κB can be activated by DNA damage via Ataxia telangiectasia-mutated (ATM) signalling, little was known about an involvement in DNA repair ...
Salles, Daniela, Bernd Baumann, Lisa Wiesmüller, Volcic, Meta, Fulda, Simone, Meta Volcic, Volcic, M., Wiesmueller, L., Baumann, B., Daniel, P., Sabine Karl, Simone Fulda, Daniela Salles, Peter Daniel, Karl, Sabine, Baumann, Bernd, Fulda, S., Salles, D., Karl, S., Daniel, Peter, Wiesmüller, Lisa   +20 more
core   +1 more source

c-Myc Suppression of DNA Double-strand Break Repair

Neoplasia: An International Journal for Oncology Research, 2012
c-Myc is a transcriptional factor that functions as a central regulator of cell growth, proliferation, and apoptosis. Overexpression of c-Myc also enhances DNA double-strand breaks (DSBs), genetic instability, and tumorigenesis. However, the mechanism(s)
Zhaozhong Li, Taofeek K. Owonikoko, Shi-Yong Sun, Suresh S. Ramalingam, Paul W. Doetsch, Zhi-Qiang Xiao, Fadlo R. Khuri, Walter J. Curran, Xingming Deng   +8 more
doaj   +1 more source

Short-term calorie restriction enhances DNA repair by non-homologous end joining in mice

npj Aging and Mechanisms of Disease, 2020
Calorie restriction (CR) improves health, reduces cancer incidence and extends lifespan in multiple organisms including mice. CR was shown to enhance base excision repair and nucleotide excision repair pathways of DNA repair, however, whether CR improves
Zhonghe Ke, Denis Firsanov, Brianna Spencer, Andrei Seluanov, Vera Gorbunova   +4 more
doaj   +1 more source

Regulation of repair choice: Cdk1 suppresses recruitment of end joining factors at DNA breaks [PDF]

DNA Repair, 2009
Cell cycle plays a crucial role in regulating the pathway used to repair DNA double-strand breaks (DSBs). In Saccharomyces cerevisiae, homologous recombination is primarily limited to non-G(1) cells as the formation of recombinogenic single-stranded DNA requires CDK1-dependent 5' to 3' resection of DNA ends.
Yu, Zhang, Eun Yong, Shim, Melody, Davis, Sang Eun, Lee   +3 more
openaire   +2 more sources

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

Retinoblastoma family proteins: New players in DNA repair by non-homologous end-joining [PDF]

Molecular & Cellular Oncology, 2015
Loss of retinoblastoma protein (RB1) function is a major driver in cancer development. We have recently reported that, in addition to its well-documented functions in cell cycle and fate control, RB1 and its paralogs have a novel role in regulating DNA repair by non-homologous end joining (NHEJ).
Paul H, Huang, Rebecca, Cook, Georgia, Zoumpoulidou, Maciej T, Luczynski, Sibylle, Mittnacht   +4 more
openaire   +2 more sources

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

Molecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu, Nicolas J. Niklaus, Anna M. Schläfli, Igor Tokarchuk, Magali Humbert, Federico La Manna, Bich Vu, David Maul, Ramin Radpour, Marianna Kruithof‐de Julio, Inti Zlobec, Jörn Dengjel, Bruce E. Torbett, Mario P. Tschan   +13 more
wiley   +1 more source

PAXX and its paralogs synergistically direct DNA polymerase λ activity in DNA repair

Nature Communications, 2018
PAXX functions as part of the nonhomologous end-joining pathway to repair double-strand DNA breaks. Here the authors show PAXX and its paralogs interact with polymerase lambda to promote joining of incompatible ends.
Andrew Craxton, Deeksha Munnur, Rebekah Jukes-Jones, George Skalka, Claudia Langlais, Kelvin Cain, Michal Malewicz   +6 more
doaj   +1 more source