Results 111 to 120 of about 1,204,389 (301)

PARP inhibition and pharmacological ascorbate demonstrate synergy in castration‐resistant prostate cancer

open access: yesMolecular Oncology, EarlyView.
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon   +13 more
wiley   +1 more source

P1327: INHIBITING TELOMERIC DNA DAMAGE RESPONSE AS A NEW THERAPEUTIC STRATEGY TO REJUVENATE THE AGEING HEMATOPOIETIC SYSTEM

open access: yesHemaSphere, 2023
Alessia Oppezzo   +17 more
doaj   +1 more source

Correction: Corrigendum: DNA damage response inhibition at dysfunctional telomeres by modulation of telomeric DNA damage response RNAs

open access: yesNature Communications, 2017
Nature Communications 8: Article number: 13980 (2017); Published: 27 February 2017; Updated: 13 April 2017 In Supplementary Fig. 3d, the two columns of DAPI images associated with pATM and pS/TQ images were inadvertently swapped.
Francesca Rossiello   +7 more
doaj   +1 more source

The DNA-damage signature in is associated with single-strand breaks in DNA [PDF]

open access: yes, 2006
Background Upon exposure to agents that damage DNA, Saccharomyces cerevisiae undergo widespread reprogramming of gene expression. Such a vast response may be due not only to damage to DNA but also damage to proteins, RNA, and lipids.
Begley Thomas J   +5 more
core   +1 more source

Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin

open access: yesMolecular Oncology, EarlyView.
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla   +10 more
wiley   +1 more source

DNA single-strand break-induced DNA damage response causes heart failure

open access: yesNature Communications, 2017
DNA damage response (DDR) is activated in cardiomyocytes of the failing heart, but the type of DNA damage leading to DDR is unclear. Higoet al. show that in mice heart failure is caused in part by unrepaired DNA single-strand breaks in cardiomyocytes ...
Tomoaki Higo   +18 more
doaj   +1 more source

DNA Damage Response in Plants: Conserved and Variable Response Compared to Animals

open access: yesBiology, 2013
The genome of an organism is under constant attack from endogenous and exogenous DNA damaging factors, such as reactive radicals, radiation, and genotoxins. Therefore, DNA damage response systems to sense DNA damage, arrest cell cycle, repair DNA lesions,
Kaoru Okamoto Yoshiyama   +2 more
doaj   +1 more source

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

open access: yesMolecular Oncology, EarlyView.
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li   +10 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala   +15 more
wiley   +1 more source

Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity

open access: yesMolecular Oncology, EarlyView.
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung   +17 more
wiley   +1 more source

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