Ask about this productRelated genes to: Reck antibody
- Gene:
- RECK NIH gene
- Name:
- reversion inducing cysteine rich protein with kazal motifs
- Previous symbol:
- ST15
- Synonyms:
- hRECK
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-30
- Date modifiied:
- 2016-01-28
Related products to: Reck antibody
Related articles to: Reck antibody
- - Source: PubMed
Publication date: 2026/09/16
Barlesi FabriceYao WenxiuDuruisseaux MichaëlDoucet LudovicAzkárate Martínez AitorGregorc VanesaJuan-Vidal OscarLu ShunDe Bondt Charlottede Marinis FilippoLinardou HelenaKim Young-ChulJotte RobertFelip EnriquetaLo Russo GiuseppeReck MartinMichenzIe Mary FYang WenjingMeade Julie NKorytowsky BeataMok Tony S K - Despite a decade in, immunotherapy (IO) treatment selection in non-small cell lung cancer (NSCLC) remains largely guided by subgroup analyses and imperfect programmed death ligand 1 (PD-L1) and clinical scores. To our knowledge, ILUNG ( NCT05537922 ) is currently the largest international, real-world, multimodal, artificial intelligence (AI)-based study, enrolling 2,396 patients. We integrated real-world clinical and blood (CB) data, computed tomography (CT) images, digital pathology (DP), and genomics into machine learning early fusion (MLEF) and deep learning intermediate fusion (DLIF) models. Machine learning (ML) and deep learning (DL) CB-only models achieved consistent performance across outcomes with area under the curve (AUC) up to 0.77 in the test (TEST) set. Performance drop in external validation (EXVAL) likely reflects population differences (AUC range: 0.55-0.72). AI models significantly surpassed PD-L1, Eastern Cooperative Oncology Group performance status (ECOG PS), neutrophil-to-lymphocyte ratio (NLR), lactate dehydrogenase (LDH) and Lung Immune Prognostic Index (LIPI) score in the independent TEST set. The clinical usability study showed that lung expert and nonexpert physicians improved their prediction with the explainable AI (XAI) ML CB-only based tool. Although multimodal integration with MLEF (CB+CT+DP) was associated with higher performance, its incremental benefit remains uncertain, not translated in TEST and EXVAL. The ILUNG project is a pioneering framework showing the clinical usefulness of AI tools. A prospective validation of the decision support system (both CB and multimodal) is currently undergoing in more than 2,000 patients. - Source: PubMed
Publication date: 2026/09/13
Prelaj ArselaMiskovic VanjaSacco MatteoFerrarin AlbertoLicciardello Cristina MariaProvenzano LeonardoFavali MargheritaLerma LudovicaZec AleksandraSpagnoletti AndreaGanzinelli MonicaLorenzini DanieleGuirges BeshoyInvernizzi LucaSilvestri CeciliaMazzeo LauraPrina Marco MeazzaCorrao GiuliaRuggirello MargheritaDumitrascu Andra DianaDi Mauro Rosa MariaMonzani DarioPravettoni GabriellaZanitti MicheleMacocchi DavideMarino Moreno BrunoCavalli ChiaraRomanò RebeccaGiani ClaudiaArmato Samuel GEsposito AlessandraBestvina Christine MSpector MariaNaama Bogot RBasheer RehamHafzadi Adi LahianiRoisman LailaWatermann IrisSzewczyk MarlenOlchers TillRichter HeinzBlanke-Roeser ConstantinSiniscalchi CostanzaDi Lello AnnaArangoa TeresaBartolomeo ValentinaSpathas NikolaosSarris EvangelosFountzilas ElenaRoca Aina ArbusàCaro-Consuegra RocioIranzo PatriciaFernández-Pinto MelissaRodríguez-Morató JoseAgnelli LucaOcchipinti MarioBrambilla MartaBeninato TeresaProto ClaudiaKosta SokolDi Palma Michele PioRulli ElianaSteurer StefanSimon RonaldWillis MichaelPruneri GiancarloDe Braud FilippoRestelli MarcelloFelip EnriquetaPeled NirPearson Alexander TLinardou HelenaReck MartinRusso Giuseppe LoTrovò FrancescoPedrocchi Alessandra Laura GiuliaGarassino Marina Chiara - Tyrosine kinase inhibitors (TKIs) have significantly changed the treatment of non-small cell lung cancer (NSCLC) harbouring epidermal growth factor receptor (EGFR) mutations, and osimertinib is now established as first-line therapy for NSCLCs. Combination therapies (e.g., osimertininb plus chemotherapy; lazertinib plus amivantamab) have been shown to improve median progression-free survival (mPFS) and median overall survival (mOS) relative to monotherapy. However, due to several resistance mechanisms, patients experience disease progression following EGFR TKI treatment. On-target resistance mechanisms include additional mutations (e.g., C797S/G/N, L718Q, L844V, G724X). Within the heterogeneous group of off-target resistance mechanisms, human epidermal growth factor receptor 2 (HER2) amplifications, mesenchymal-epithelial transition factor (MET) alterations, oncogenic fusions (e.g., BRAF, FGFR, RET), histological changes, epithelial-mesenchymal transitions, and alterations of the RAS/MEK/ERK and the PI3K/AKT/mTOR signal transduction pathways are critical and can confer resistance to EGFR TKIs. Several drugs have been identified to inhibit these pathways, with some of them already approved for clinical use. Most fourth-generation EGFR TKIs are orally bioavailable and are mainly allosteric thiazole amide-based reversible inhibitors. Their activity results from selective binding to an allosteric site, which can alter the EGFR protein conformation, allowing them to bypass C797X. A recommendation for the optimal treatment strategy and sequence for NSCLC patients with acquired EGFR TKI-resistant tumours still cannot be given. An improved understanding of the underlying resistance mechanisms will help to pave the way for the development of innovative and highly specific drugs for the therapy of osimertinib-resistant NSCLCs. The putative clinical relevance of fourth-generation EGFR TKIs for NSCLC patients needs to be defined, and many development hurdles need to be cleared before victory can be declared. - Source: PubMed
Publication date: 2026/09/03
Dempke Wolfram C MFenchel KlausSullivan LorettaReck Martin - Precision oncology has changed the management of advanced non-small-cell lung cancer (NSCLC). Biomarker-matched therapies now improve outcomes in an increasing number of molecularly defined subgroups. In this second paper in a Series on therapeutics in lung cancer, we summarise recent advances in NSCLC with established alterations, including EGFR, ALK, ROS1, KRAS, BRAF, RET, HER2, MET, and NTRK, and discuss emerging targets, such as NRG1 fusions, MTAP loss, and SMARCA4 deficiency. Newer generations of tyrosine kinase inhibitors, the introduction of bispecific antibodies, and antibody-drug conjugates have improved response durability, intracranial disease control, and in some settings, overall survival. However, durable benefit can remain limited by acquired resistance, tumour heterogeneity, lineage plasticity, and off-target escape, supporting repeat tissue biopsy and circulating-tumour DNA profiling to guide subsequent treatment. With several options available such as monotherapy and combination approaches, individualised treatment selection is becoming increasingly complex. We discuss these choices, including the management of CNS disease and oligoprogression, and long-term tolerability. As drug development extends beyond canonical drivers to rarer alterations and adverse co-mutations, the range of targetable disease is increasing. Further progress will depend on more effective and adaptive treatment strategies together with equitable access to comprehensive molecular profiling, timely biomarker testing, and next-generation targeted therapies. - Source: PubMed
Publication date: 2026/09/06
Hendriks Lizza E LLin Jessica JTan Daniel S WAcker FabianOgliari Francesca RMeyer May-LuciePlanchard DavidReck Martin - To assess outcomes with perioperative durvalumab by type of surgery in patients with resectable non-small cell lung cancer (NSCLC) from the AEGEAN study. - Source: PubMed
Publication date: 2026/09/03
Harpole DavidHeymach John VReck MartinTaube JanisGao ShugengLi GaofengYou JianVan Luong DinhSaeteng SomcharoenDoake RuthFouad Tamer MMitsudomi Tetsuya