Top 5 Papers
#1
Source: Lancet | Authors: Walter, Capdevila, et al. (incl. Strosberg, Moffitt Cancer Center); 49 centres, 14 countries | Published: July 2, 2026
Score: 17/20 — Base: Lancet (9) + Phase III RCT (+3) + PFS survival benefit (+2) + Colleague Engagement: surfaced by 3 curated KOLs on X (@DrRishabhOnco, @DaisukeKotani, @DraMartinezLago, +3) = 17
COMPETE randomized 309 patients (2:1) with advanced, progressive, somatostatin-receptor-positive grade 1-2 gastroenteropancreatic neuroendocrine tumours to peptide receptor radionuclide therapy ([177Lu]Lu-edotreotide, up to four cycles) versus everolimus 10 mg/day. Median PFS by blinded central review was significantly longer with PRRT: 23.9 vs 14.1 months (stratified HR 0.67, 95% CI 0.48-0.95; p=0.022). PRRT was also better tolerated — grade 3-4 treatment-related adverse events occurred in 18% vs 40%, with no treatment-related deaths in either arm. The trial adds a second randomized dataset (after NETTER-2) supporting PRRT in earlier lines and directly informs how we sequence radioligand versus targeted therapy in GEP-NETs.
Post angle: Phase 3 win for PRRT over everolimus in GEP-NETs — nearly 10 months of extra PFS AND half the grade 3-4 toxicity. The sequencing conversation in NETs keeps moving earlier. #NETs #PRRT #GIOnc #PrecisionMedicine
#2
Source: Journal of Clinical Oncology | Authors: Cleary, Schram, et al. (Dana-Farber, MSK, Gustave Roussy, multicenter) | Published: July 1, 2026
Score: 11/20 — Base: JCO (8) + Phase II (+2) + biomarker-guided/precision, first targeted therapy in an NRG1-fusion GI subtype (+1) = 11
The single-arm Phase 2 eNRGy basket reported the cholangiocarcinoma cohort: 22 previously treated patients with NRG1 fusion-positive advanced disease (all intrahepatic where subtype was known) received the HER2xHER3 bispecific antibody zenocutuzumab 750 mg IV every 2 weeks. Among 19 efficacy-evaluable patients, ORR was 36.8% (95% CI 16.3-61.6), clinical benefit rate 57.9%, median duration of response 7.4 months and median PFS 9.2 months. Toxicity was mostly grade 1-2 (diarrhea, fatigue, nausea) with a single grade 3 event and no AE discontinuations. NRG1 fusions are rare (well under 1% of biliary cancers), but this is the first credible targeted signal in the subtype and a concrete argument for RNA-based fusion testing across advanced cholangiocarcinoma.
Post angle: NRG1 fusions are vanishingly rare in biliary cancer — but eNRGy shows zenocutuzumab actually works there (ORR 37%, mPFS 9.2 mo). Another reason to run fusion testing on every advanced cholangiocarcinoma. #Cholangiocarcinoma #PrecisionMedicine #GIOnc
#3
Source: JAMA Oncology | Authors: Kataoka, Oki, et al. (CIRCULATE-Japan GALAXY) | Published: July 3, 2026
Score: 10/20 — Base: JAMA Oncology (7) + retrospective/prospective-cohort prognostic study (+1) + biomarker-guided/precision (+1) + Colleague Engagement (@DaisukeKotani surfaced on X, +1) = 10
This analysis of the prospective CIRCULATE-Japan GALAXY cohort (n=298) tested whether circulating tumor DNA measurable residual disease (MRD) should steer adjuvant chemotherapy after curative-intent resection of colorectal liver metastases. In the upfront-surgery group, postsurgical MRD positivity was strongly prognostic — worse disease-free survival (HR 4.14) and overall survival (HR 9.13). Crucially, the benefit of adjuvant chemotherapy was confined to MRD-positive patients (DFS HR 0.07; OS HR 0.27, p=0.03), while MRD-negative patients derived no measurable benefit. The data support ctDNA as a decision tool to escalate therapy in MRD-positive patients and potentially spare MRD-negative patients the toxicity of adjuvant chemo — the exact escalation/de-escalation question faced in the resected-CRLM clinic.
Post angle: After liver-met resection, ctDNA doesn't just prognosticate — GALAXY shows adjuvant chemo benefit is concentrated in MRD+ patients (DFS HR 0.07), while MRD- patients may be spared. This is the de-escalation question we actually face. #CRC #ctDNA #GIOnc
#4
Source: Journal of Gastrointestinal Cancer | Authors: Mannan, Shahzad, et al. (incl. Moffitt Cancer Center) | Published: July 3, 2026
Score: 7/20 — Base: J Gastrointest Cancer (5, Other tier) + meta-analysis (+2) = 7. Moffitt co-authored.
This Moffitt-involved systematic review and meta-analysis pooled 12 studies (n=404) evaluating anti-EGFR antibodies (cetuximab, panitumumab) in locally advanced and metastatic anal squamous-cell carcinoma. Pooled objective response rate was 52% (95% CI 36-68) with a complete-response rate of 37%; median overall survival was 11.9 months and median PFS 4.5 months. Grade >=3 adverse events occurred in 56%. The evidence base is retrospective and heterogeneous, so the numbers should be read as hypothesis-generating rather than practice-defining — but in a rare cancer with limited options and no approved targeted agents, a pooled ORR above 50% is a real signal that argues for prospective, biomarker-driven anal-cancer trials.
Post angle: Anal SCC has few options and no approved targeted therapy. This Moffitt-led meta-analysis (12 studies, n=404) shows anti-EGFR antibodies hit a pooled ORR of 52% — retrospective, but a strong case for prospective trials. #AnalCancer #GIOnc
Additional Papers of Interest
-
Lancet Oncology — First standardized SSTR-PET response criteria for neuroendocrine tumours (34 experts; partial response = >=40% target-lesion volume reduction), co-authored by Moffitt's Jonathan Strosberg; a pragmatic step toward outcome-validated PET response in NET trials and practice
-
Gut — Emulated trial across 36 Chinese hospitals (n=1249); postoperative GLP-1RA initiation associated with longer recurrence-free survival (HR 0.80, p=0.016) and overall survival (HR 0.58, p<0.001) vs DPP-4i, adding to the incretin-in-cancer signal but needing prospective confirmation
-
Gut — Tumor-cell SMPD1 sustains KRAS membrane localization in PDAC; the acid-sphingomyelinase inhibitor ARC39 synergizes with the KRAS-G12D inhibitor MRTX1133 in preclinical models — a candidate combination to deepen KRAS-inhibitor responses
-
Gut — USP20 links KRAS-driven cholesterol/autophagy adaptation to T-cell exhaustion; triple therapy (USP20 inhibitor GSK2643943A + MRTX1133 + anti-PD-1) drove tumor regression in preclinical PDAC, another route to unlock KRAS inhibitors
Back to all digests