Ask about this productRelated genes to: NOTCH1 antibody
- Gene:
- NOTCH1 NIH gene
- Name:
- notch receptor 1
- Previous symbol:
- TAN1
- Synonyms:
- -
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-13
- Date modifiied:
- 2019-04-23
Related products to: NOTCH1 antibody
Related articles to: NOTCH1 antibody
- In adults with Philadelphia chromosome-negative (Ph-) acute lymphoblastic leukemia (ALL) genetic risk is usually combined with measurable residual disease (MRD) assignment to consolidation therapy. However, this combination is not uniform across trials and centralized assessment is not always performed. This study analyzed patients' outcomes using centrally assessed MRD and genetics. Patients with high genetic risk (HGR), those who required two induction cycles for complete remission (CR), and CR patients with end-of-induction (EOI) MRD ≥0.01% were assigned to allogeneic hematopoietic stem cell transplant (alloHSCT), while the remaining patients were assigned to delayed consolidation and maintenance. HGR for B-ALL included KMT2A rearrangements, low hypodiploidy and age >35 years, homozygous TP53 mutations/deletions, or concomitant IKZF1 and CDKN2A/B deletions. HGR in T-ALL included absence of NOTCH1/FBXW7 mutations and/or K/NRAS or PTEN alterations. Patients with early T-ALL (ETP) received a different induction regimen, and all were assigned to alloHSCT. Median (range) age of 436 patients was 39 (18-60) years, 332 with B-lineage ALL and 104 T-ALL. By intention to treat, 243 non-ETP patients (61%) were assigned to alloHSCT and 157 (39%) to CT. The 3-year overall survival (OS) probability (95% CI) was 64% (58%-69%). For patients with CR and EOI MRD<0.01% without HGR (n=109), the OS probability was 81% (70%-89%), compared with 50% (34%-63%) for MRD-negative patients with HGR (n=64). In patients with ETP-ALL the probability of 3-year OS was 61% (37%-79%). The combination of genetics and MRD allows accurate identification of adult Ph- ALL patients candidates to alloHSCT or chemotherapy. The trial was registered at www.ClinicalTrials.gov: NCT04179929. - Source: PubMed
Publication date: 2026/05/04
Ribera Josep-MariaTorrent AnnaMorgades MireiaBarrena SusanaRibera JordiGenesca EulaliaGonzález-Campos JoséMartínez-Cibrian NuriaMontesinos PauHernández Sánchez AlbertoBarba PereZapico EdgarSánchez RicardoNovo AndrésSitges MartaMaluquer Artigal ClaraSuch EsperanzaBotella CarmenQueipo de Llano Maria PazCabrero MonicaVicent AnaLopez de Ugarriza PaulaTormo MarGonzález-González Bernardo-JavierGarcia-Cadenas IreneRodríguez-Medina CarlosMartinez Sanchez PilarBermúdez AranchaGómez-Centurión IgnacioHerrero-Garcia MariaCiudad JuanaNavas-Acosta JosgreyHermosín LourdesSerrano JosefinaRaposo-Puglia José-ÁngelSolan LauraRoldán-Galiacho Verónicade Laiglesia AlmudenaGómez-Pérez LucíaSolé-Rodríguez MaríaCasado María-SoledadLlorente Gonzalez LauraBarrios Decoud DanielVall-Llovera FerránAlgarra Jesús-LorenzoAmador LourdesGarcía-Boyero RaimundoCladera AntòniaBergua Burgues Juan MiguelCalasanz Maria J JoséGranada IsabelFeliu EvaristHernández-Rivas Jesús-MaríaOrfao Alberto - Aberrant activation of Notch1 signalling in Cervical Cancer Stem Cells (CCSCs) plays a key role in the disease development, progression, metastasis, recurrence, and chemoresistance. Thus, targeting Notch1 is crucial for CCSC eradication. SF1, a standardised fraction from , has shown potent cytotoxic effects against cervical cancer cells, including CCSCs. However, its mechanism is uncertain. This study aimed to elucidate whether SF1 can inhibit Notch1 signalling in CCSCs. - Source: PubMed
Publication date: 2025/10/31
Ismail FaridahZakaria YusmazuraMd Isa Muhammad LokmanNik Hassan Nik FakhuruddinTan Suat Cheng - Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by immune dysregulation that leads to widespread inflammation and damage across multiple organs. B lymphocytes play a vital role in SLE, with abnormal development and activation leading to autoreactive antibody production and immune complex formation, which damages tissues. The PPARα agonist WY14643 has anti-inflammatory effects in various inflammatory conditions, including CNS diseases. We investigated whether WY14643 decreases inflammatory mediator production in CD45R cells in the MRL/lpr mouse model of SLE. Flow cytometry was used to evaluate WY14643's impact on the expression of IFN-γ, IL-6, iNOS, MCP-1, IL-1α, IL-2, Notch-1, Notch-3, GITR, and NF-κB p65 in splenic CD45R B cells. Additionally, we assessed the effect of WY14643 on the mRNA levels of these markers in the kidney using RT-PCR. WY14643 decreased inflammatory markers such as CD45RIFN-γ, CD45RIL-6, CD45RiNOS, CD45RMCP-1, CD45RIL-1α, CD45RIL-2, CD45RNotch1, CD45RNotch3, CD45RGITR, and CD45RNF-κB p65 in splenic cells from MRL/lpr mice. Furthermore, WY14643 also lowered mRNA expression of IFN-γ, IL-6, iNOS, MCP-1, IL-2, IL-1α, Notch-1, Notch-3, GITR, and NF-κB p65 in the kidney. This study shows that WY14643 inhibits the production of inflammatory mediators and significantly reduces autoimmune features, including kidney inflammation, in MRL/lpr mice. Our results indicate that WY14643, a PPAR-α agonist, could be a potential therapy for lupus nephritis. - Source: PubMed
Publication date: 2026/04/18
Al-Mazroua Haneen AAlhamami Hussain NAnsari Mushtaq ANadeem AhmedAttia Sabry MBakheet Saleh AAlsaad Abdulaziz M SAlomar Hatun AAlanteet Alaa AAhmad Sheikh F - Atypical fibroxanthoma (AFX) and pleomorphic dermal sarcoma (PDS) are rare cutaneous mesenchymal tumours sharing clinical and histopathological features. Compared to AFX, PDS has an increased risk of local recurrence and metastasis. A precise diagnosis is critical to ensure proper clinical management and follow-up. AFX and PDS show a similar genetic background, but also a heterogeneous pattern of different molecular abnormalities still poorly investigated due to the rarity of these tumours. Multiple data from different institutions and geographical areas, facilitate the identification of molecular alteration/s of valuable diagnostic and/or sub-classification power. We investigated the DNA profile of 32 AFX and PDS samples using a custom targeted Next-Generation Sequencing panel including 228 cancer genes. We confirm a common pattern of gene mutations affecting TP53, CDKN2A and NOTCH1. Differences appeared in less frequently detected genes (e.g. TSC2) and in NF2 harbouring novel genetic alterations. Integrating our results with published datasets of AFX and PDS mutation profiles we observed a divergent distribution of alterations in genes signalling through angiogenic pathway (KDR, PDGFRB), DNA damage response (ATR), cellular migration/metastasis (DDR2, CDH1). These differences do not reach statistical significance, and histopathological evaluation remains the diagnostic gold standard, however, they offer valuable insights into the pathogenesis of these tumours. - Source: PubMed
Publication date: 2026/05/03
Caprini ElisabettaScaglione Giovanni LucaScarponi ClaudiaMorelli MartinaMadonna StefaniaMarani CarlaSebastiani ValeriaScala EnricoAlbanesi CristinaRahimi Siavash - The progressive skeletal muscle degeneration observed in Duchenne Muscular Dystrophy (DMD) patients requires multiple cycles of satellite cells (SCs) activation to promote tissue regeneration. Dystrophic SCs present intrinsic defects, and the disrupting fibrotic niche hinders appropriate muscle recovery. Traditional 2D culture systems face challenges in modeling the DMD muscle niche and SCs behavior. Our aim was to validate a 3D culture of skeletal muscle spheroids (iSMS) for DMD modeling, as compared to the traditional 2D culture, while investigating the pathophysiological mechanisms of dystrophin deficiency in vitro. - Source: PubMed
Publication date: 2026/05/02
Esposito Joycede Souza Leite FelipeBarbosa Igor Nevesda Mata Martins Thaís Mariade Oliveira Olberg Giovanna GonçalvesAl Tanoury ZiadTelles-Silva Kayque Alvesda Silva Pardo Mayana CristinaJazedje TatianaBortolin Raul HernandesHirata Mario HiroyukiPourquié OlivierZatz Mayana