🚨 ⭐ Mark your calenders and register for an event around #ESMO26 Meeting, Madrid, Spain @myESMO 📌 I’m looking forward to joining the International Alliance for Personalised Medicine Alliance @united4cancer event on 23 October 2026 in Madrid. 👉 The event will bring together experts and stakeholders to discuss the challenges and opportunities in personalised medicine, fostering dialogue on how to translate innovation into meaningful benefits for patients. 👉 Looking forward to the discussions and to connecting with colleagues in Madrid! #128467;️ October 23rd, 2026 Venue;IFEMA Congress Centre, Room A4.2, Mezzanine Level, Madrid @OncoAlert @oncodaily Register here free event link: docs.google.com/forms/d/e/1F…

🚨⭐️👉Mark your calenders for RAPID ORAL TALKS @myESMO 👉Delighted to be presenting our updated Tumor agnostic RET inhibitor- Pralsetinib data across all RET+ solid tumors. 👉Knew this drug would make it right from the first patient enrolled. We need this drug approved on a tumor-agnostic basis so RET + patients can have more options + access it. 👉1005RO - Efficacy and safety of pralsetinib in RET fusion-positive solid tumors: Pooled analysis of the ARROW and TAPISTRY trials 👉Rapid oral: Developmental therapeutic Room Cordoba Auditorium - Hall 4 Date Sun, 25.10.2026 Time 08:30 - 10:00 Lecture Time 09:02 - 09:07 Abstract Background Pralsetinib is an oral tyrosine kinase inhibitor that selectively and potently targets oncogenic RET fusion and mutation proteins. We report pooled results from the global, open-label, multicohort phase 2 studies ARROW (NCT03037385) and TAPISTRY (NCT04589845) evaluating efficacy and safety of pralsetinib in patients with RET fusion-positive solid tumors. Methods Eligible patients age ≥18 y with advanced RET fusion-positive solid tumors from ARROW, and aged ≥12 y with unresectable, locally advanced or metastatic RET fusion-positive solid tumors from TAPISTRY received pralsetinib 400 mg/d until disease progression or unacceptable toxicity. Patients with non-small cell lung cancer or thyroid tumors were excluded. The primary end point in both studies was overall response rate (ORR). Safety was a co-primary end point in ARROW. Key secondary end points included duration of response (DOR), progression-free survival (PFS), and overall survival (OS). Results The pooled response-evaluable population (n=49) represented a range of tumor types: colorectal (24%); pancreatic (16%); hepatobiliary (14%); sarcoma, neuroendocrine and adrenal, and head and neck (10% each); unknown primary and small cell lung (4% each); and ovarian, thymic, and gastric (2% each). ORR was 53% (95% CI: 38.3, 67.5; table), with 7 (14%) complete and 19 (39%) partial responses. All patients in the safety population (n=57) had ≥1 adverse event, most commonly increased aspartate aminotransferase (26; 46%), anemia (24; 42%), constipation (24; 42%), and increased alanine aminotransferase (23; 40%). Hypertension occurred in 17 (30%) patients. Conclusions Pralsetinib demonstrated robust and durable activity against RET fusion-positive solid tumors, with an ORR of 53% in this pooled cohort from the ARROW and TAPISTRY studies. These data support the potential use of pralsetinib in a tumor-agnostic approach for RET fusion-positive solid tumors @OncoAlert @oncodaily @Dr_R_Kurzrock

⭐️⭐️⭐️🚨Looking forward to presenting this #Tumor agnostic landscape project @myESMO MADRID. Please come by poster and say 👋 ⭐️4294P - The tumor-agnostic (TA) therapy biomarker landscape: Established and emerging markers across 385,420 solid tumors Presentation Number #4294P Date Fri, 23.10.2026 Time 15:15 - 16:00 Abstract Background TA approvals have increasingly been granted by the FDA for molecularly-guided cancer therapies. With a growing number of therapies under investigation in pan-tumor trials, we assessed the real-world landscape of currently approved (cTA) and emerging (eTA) biomarkers in a cohort of patients (pts) tested with comprehensive genomic profiling (CGP). Methods The prevalence of biomarkers associated with current and potential future TA indications was assessed across 385,420 solid tumor samples from unique pts profiled with FoundationOne®CDx. Across 196 active Ph1 or 2 pan-solid tumor trials evaluating 213 unique therapies, 105 enrollment biomarkers were assessed for TA potential. eTA biomarkers included those associated with a multi-tumor ORR ≥ 20% with responses in ≥4 tumor types: ALK rearrangements, ERBB2 mutations [muts]/amplifications [amps], FGFR2 alterations, MET amps/fusions, NRG1 fusions, KRAS/HRAS muts, TP53 Y220C, and MTAP loss. HER2 IHC status was not available for this cohort. Results 18.7% of solid tumor pts had a cTA (1.8% BRAF V600E, 0.2% RET fusion, 0.1% NTRK fusion, 13.8% TMB-high, 0.1% MSI-high, 2.8% multiple) and an additional 31.7% of cTA-negative pts were eTA-positive (14.0% KRAS, 5.5% MTAP, 4.2% ERBB2, 2.9% others, 5.1% multiple), for a potential future TA biomarker prevalence of 50.4%. The largest potential increase in TA biomarker prevalence was in pancreatic (86.6%; 6.7% with biomarkers currently approved in-tumor type [ITT] or cTA to 93.3% with ITT, cTA, or eTA), small intestine (63.5%, 13.9% to 77.3%), and gallbladder (49.4%, 5.9% to 55.3%). CRC (96.5%), pancreatic (93.3%), melanoma (83.5%), and NSCLC (77.5%) had the highest resulting combined prevalence. eTA biomarkers with greatest impact on prevalence were KRAS in CRC (91.7% of ITT/cTA-negative samples), pancreatic (88.3%), and small intestine (56.6%); and MTAP in GBM (46.6%) and pancreatic (34.6%). Conclusions The expansion of approved TA indications, coupled with accelerating druggability of once-intractable targets, stands to fundamentally reshape treatment for cancers currently lacking targeted options. The breadth and cross-tumor prevalence of eTA biomarkers underscore CGP as an essential tool for clinical decision making @JiaJennyLiu @JulianaRBeal @niamhjcoleman @FoundationATCG @BenWestphalen @curijoey @chadinabhan @OncoAlert @oncodaily

🚨⭐️⭐️⭐️📍📌 Mark your calendars 📅 @myESMO MADRID 📍Saturday, Oct 24 · 14:45–15:45 · Santander Auditorium, Hall 10 👉Delighted to be delivering a lecture: “Drugging the Undruggables: The Next Wave of Targeted Therapies #PrecisionOncology.” 🧬🎯beyond KRAS, P53, MYC & much much more @Annals_Oncology #ESMOAmbassadors 👉Session: “YO Lecture: What to expect from precision medicine in the next decade” #ESMO26 #PrecisionOncology #TargetedTherapy 👉I’ll be presenting the latest+ greatest in the field, and looking for what comes next. 👉👉👉PLEASE ATTEND + Come with questions @OncoAlert @Aiims1742 @BalazsHalmosMD @oncologiaroma @PTarantinoMD @curijoey @FAndreMD @CharlesSwanton Session LINK: cslide.ctimeetingtech.com/es…

⭐️👉🏼Amazing to work on this review in @CellPressNews @CellCellPress @MedCellPress 👉🏼It started with a clinical question. One of my patients' glioblastoma transformed into gliosarcoma after treatment with BRAF & MEK inhibitor. Another patient's NSCLC adenocarcinoma became small cell lung cancer after RET inhibitor. A third patient's papillary thyroid cancer turned into anaplastic thyroid cancer again after BRAF inhibitor. @mgoudaMD & I started something from a clinical point of view. But we wanted more answers. 👉🏼Over coffee at an @AACR meeting, I asked the guru of EMT biology @SenduraiMani to look at this from the basic science/ translational point of view. From that conversation, a comprehensive search and this review were born. Wonderful to work with his team on this one. It took around 2 years to get this done but learned a lot on this. ⭐️⭐️⭐️If we want the next generation of cancer therapies to last, we have to treat cancer as an evolving system, not a static target. cell.com/med/abstract/S2666-…