Results 41 to 50 of about 8,187 (229)
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
Avaliação dos potenciais mecanismos moleculares associados à variante genética S836S do proto-oncogene RET na patogênese do Carcinoma Medular de Tireoide [PDF]
Carcinoma medular da tiroide (CMT), tumor maligno originário de células C ou parafoliculares tireoidianas, representa cerca de 4% de todos os tumores malignos dessa glândula.
Ceolin, Lucieli, Lucieli Ceolin
core
Mas signaling: resolved and unresolved issues
The Mas oncogene encodes for a seven-transmembrane G protein-coupled receptor (GPCR), Mas, which has a ubiquitous distribution. Mas is abundantly expressed in the brain and testes but is also found in the heart, kidneys, lungs, vasculature, adipose ...
Rhian M. Touyz +5 more
core +1 more source
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
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 +19 more
wiley +1 more source
ZRF1 controls oncogene-induced senescence through the INK4-ARF locus
The reactivation of the INK4-ARF locus, which is epigenetically repressed by Polycomb proteins in healthy cells, is a hallmark of senescence. One mechanism of reactivating Polycomb-silenced genes is mediated by the epigenetic factor ZRF1, which ...
Gutierrez, A +9 more
core +1 more source
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
MITF maintains genome stability in nonmelanocyte lineages
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
C-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis [PDF]
Understanding the regulation of the apoptotic program in neurons by intracellular pathways is currently a subject of great interest. Recent results suggest that c-Jun N-terminal kinases (JNK), mitogen-activated protein kinases and the transcription ...
Brugg, B. +4 more
core +1 more source
Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
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

