Results 81 to 90 of about 105,962 (246)
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
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
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
Circulating microRNAs as biomarkers of cachexia and sex‐specific cancer in senior dogs. In 25 client‐owned dogs, four circulating miRNAs (miR‐15a, miR‐15b, miR‐16, miR‐140) were downregulated in cachexia, with miR‐16 the strongest individual biomarker (AUC = 0.899).
Soon‐Seok Park +6 more
wiley +1 more source
Translating whole‐genome doubling into precision medicine in cancer
Whole‐genome doubling creates a WGD‐positive tumor state characterized by persistent chromosomal instability, karyotypic diversification, and cellular stress. These same biological pressures drive aggressive tumor evolution while exposing therapeutic vulnerabilities, providing a rationale for WGD‐informed precision medicine. Whole‐genome doubling (WGD)
Sejung Lee, Junghyeok Lim, Jinhyuk Bhin
wiley +1 more source
This review summarizes the transcription factors, repressive chromatin‐modifying complexes, and epigenetic mechanisms that control fetal hemoglobin repression. Notably, many regulators of γ‐globin silencing also function in transcriptional and epigenetic networks that drive cancer, highlighting opportunities to translate advances in hemoglobinopathy ...
Meigen Yu +3 more
wiley +1 more source
Interferon type 1 (IFN‐1) production and signaling is associated with the acquisition of therapy resistance, following chronic DNA damage, via Interferon‐related DNA damage resistance signature (IRDS) gene expression. An alternative, DNA damage‐independent role of sustained IFN‐1 mediated resistance was identified and characterized by the emergence of ...
Ashlyn Conant +11 more
wiley +1 more source
Hereditary pseudocholinesterase deficiency in a 4-year-old girl: a case report
Background This report outlines a case of pseudocholinesterase deficiency in a pediatric patient, whose autosomal recessive condition is caused by two different pathologic variants of the butyrylcholinesterase gene, resulting in a rare case of functional
Julia Schulze-Berge +6 more
doaj +1 more source
Delayed emergence from anesthesia caused by an intraoperative cerebral embolism of a malignant peripheral nerve sheath tumor in a neurofibromatosis type 1 patient: a case report. [PDF]
Kawano K, Tani M, Morimatsu H.
europepmc +1 more source
PANoptosis in the pathogenesis of myelodysplastic syndromes
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla +4 more
wiley +1 more source

