Results 131 to 140 of about 52,240,321 (193)
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 +3 more
wiley +1 more source
, 2019 [[abstract]]Erlotinib inhibits the ATP-binding site of the tyrosine kinase associated with the epidermal growth factor receptor. We have recently demonstrated that gefitinib, a structurally similar receptor tyrosine kinase inhibitor, inhibited functions ...
Yang, CH;Yang, CS;Huang, CJ;Cheng, AL;Whang-Peng, J;Yang, PC
core
Molecular Oncology, EarlyView.We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober +16 more
wiley +1 more source
Cancer Research UK Cancer Awareness Measure Plus, 2024
copyright UK Data Service and data collection copyright owner.The Cancer Awareness Measure (CAM) was developed in 2007-8 to address the absence of a validated measure of general public awareness of cancer (Stubbings, S., Robb, K., Waller, J., Ramirez, A.,
Cancer Research UK
core
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
Molecular Oncology, EarlyView.Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder +10 more
wiley +1 more source
MITF maintains genome stability in nonmelanocyte lineages
Molecular Oncology, EarlyView.MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Molecular Oncology, EarlyView.The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka +9 more
wiley +1 more source
Cancer Trends: Cervical cancer
, 2017 In the period 2013-2015, invasive cancer of the cervix uteri (ICD10: C53) accounted for just over 1% of all invasive cancers (excluding non-melanoma skin cancer) in Ireland, with an average of 262 cases diagnosed per year.
National Cancer Registry Ireland (NCRI)
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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 +13 more
wiley +1 more source
copyright UK Data Service and data collection copyright owner.The Cancer Awareness Measure (CAM) was developed in 2007-8 to address the absence of a validated measure of general public awareness of cancer (Stubbings, S., Robb, K., Waller, J., Ramirez, A.,
Cancer Research UK
core +1 more source