Results 121 to 130 of about 103,862 (301)

SMAD4 Palmitoylation Drives a Metabolic‐Transcriptional Circuit to Promote Tumorigenesis and Confers Radiosensitivity in Pancreatic Cancer

open access: yesAdvanced Science, EarlyView.
This study identifies palmitoylation as a novel regulatory modification of SMAD4, mediated by ZDHHC22/APT2. It activates fatty acid synthesis, creating a self‐reinforcing SMAD4–FASN–palmitate feedback loop that drives pancreatic cancer growth and enhances radiotherapy sensitivity.
Yang Wang   +16 more
wiley   +1 more source

N4‐acetylcytidine in LncRNA Gm26917 Promotes Translation in Female Germline Stem Cells by Recruiting Ribosomal Protein mRNA via EEF1A1

open access: yesAdvanced Science, EarlyView.
This work establishes that ac4C modification on lncRNA Gm26917 governs its spatial interactions with Rpl10 mRNA, and RBP EEF1A1 mediates the interaction between Gm26917 and Rpl10. It elucidates a novel ac4C‐Gm26917‐EEF1A1‐Rpl10 axis in FGSC maintenance both in vitro and in vivo, and provides a potential molecular target for modulating germ cell ...
Xinyue Li, Xiaopeng Hu, Ji Wu
wiley   +1 more source

The underlying mechanism for the PARP and BRCA synthetic lethality: Clearing up the misunderstandings

open access: yesMolecular Oncology, 2011
Poly (ADP‐ribose) polymerase (PARP) inhibitors effectively kill tumours defective in the BRCA1 or BRCA2 genes through the concept of synthetic lethality. It is suggested that PARP inhibitors cause an increase in DNA single‐strand breaks (SSBs), which are
Thomas Helleday
doaj   +1 more source

NUDT21 Drives T‐Cell Acute Lymphoblastic Leukemia Through Dual Regulation of Alternative Polyadenylation and Transcriptional Activation

open access: yesAdvanced Science, EarlyView.
In summary, our study defines a coordinated oncogenic model in which NUDT21 integrates alternative polyadenylation–dependent UBE2D3 stabilization and transcriptional activation to sustain MYC‐driven T‐ALL cell survival, thereby establishing NUDT21 as a central regulatory node and a promising therapeutic target.
Conglian Qiu   +18 more
wiley   +1 more source

Glutamine Deprivation Triggers Tribbles Homolog 3 Dependent G‐Quadruplex Resolution to Maintain DNA Repair and Tumor Survival

open access: yesAdvanced Science, EarlyView.
Glutamine deprivation triggers transient DNA damage yet activates adaptive repair in hepatocellular carcinoma cells. We identify TRIB3 as a stress‐induced nuclear scaffold that associates with DDX5 and G‐quadruplex DNA atBRCA1 andRAD51AP1 promoters. TRIB3 loss increases G4 accumulation, suppresses HR gene transcription, elevates γ‐H2A.X, and sensitizes
Qiang Ji   +10 more
wiley   +1 more source

PARP Inhibitors as a Novel Treatment Strategy for Patients with BRCA-Mutated Metastatic Breast Cancer

open access: yesEuropean Medical Journal Oncology, 2019
Inhibitors of poly(ADP-ribose) polymerase (PARP), such as olaparib and talazoparib, have recently been approved as therapies for BRCA-mutated human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer (BC).
Katarzyna Rygiel
doaj  

Pancancer Fine‐Mapping of Mutational Intolerance Identifies CHEK1 as an Immunosuppressive Driver in Lung Adenocarcinoma

open access: yesAdvanced Science, EarlyView.
This study identifies mutation‐intolerant genes (MIGs), which are mutationally constrained in tumors despite normal‐tissue variability. Using miDriver, the authors pinpoint MIGs essential for tumor‐intrinsic fitness and immune evasion. Focusing on CHEK1, they show it drives tumor fitness and sculpts an immunosuppressive niche via the MIF–CD74 axis ...
Tao Wang   +16 more
wiley   +1 more source

The status of poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitors in ovarian cancer, part 2: extending the scope beyond olaparib and BRCA1/2 mutations [PDF]

open access: yes, 2016
Poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitors have shown clinical activity in epithelial ovarian cancer, leading both the US Food and Drug Administration (FDA) and the European Medicines Agency to approve olaparib for tumors ...
Ledermann, JA, Miller, RE
core  

Detachment‐Induced FAK‐STAT3‐NNMT Inhibits CTCs Anoikis to Promote Breast Cancer Metastasis by Enhancing Fatty Acid Oxidation

open access: yesAdvanced Science, EarlyView.
The FAK‐STAT3‐NNMT axis drives anoikis resistance in circulating tumor cells by reprogramming fatty acid oxidation. Targeting this metabolic vulnerability suppresses metastasis, untangling a key mechanism of breast cancer progression and revealing NNMT as a promising therapeutic target.
Qingchao Tong   +13 more
wiley   +1 more source

Response and Resistance to Paradox-Breaking BRAF Inhibitor in Melanomas [PDF]

open access: yes, 2018
FDA-approved BRAF inhibitors produce high response rates and improve overall survival in patients with BRAF V600E/K-mutant melanoma, but are linked to pathologies associated with paradoxical ERK1/2 activation in wild-type BRAF cells.
Aplin, Andrew E.   +10 more
core   +1 more source

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