Gastric Cancer

P2, N=0, Withdrawn, Institut Cancerologie de l'Ouest | N=49 --> 0 | Trial completion date: Jun 2034 --> Jan 2026 | Not yet recruiting --> Withdrawn | Trial primary completion date: Jun 2029 --> Jan 2026

P3, N=2000, Recruiting, Cancer Institute and Hospital, Chinese Academy of Medical Sciences | Trial completion date: Dec 2025 --> Dec 2030 | Trial primary completion date: Dec 2025 --> Dec 2030

P3, N=2000, Recruiting, Cancer Institute and Hospital, Chinese Academy of Medical Sciences | Trial completion date: Dec 2025 --> Dec 2030 | Trial primary completion date: Dec 2025 --> Dec 2030

We demonstrate that N-Exo exerts tumor-suppressive effects by delivering miR-101-3p, which dually targets and suppresses MCL1 expression. Moreover, rmIL-36γ treatment enhances both miR-101-3p abundance and anti-tumor efficacy in neutrophils. These findings highlight the N-Exo/miR-101-3p/MCL1 axis as a therapeutic target and support cytokine priming as a strategy to enhance neutrophil-based cancer therapy.

However, some studies, particularly in colorectal and gastric cancers, have reported that MSI-L correlates with distinct clinical and molecular features, including poorer prognosis, increased tumour mutational burden (TMB) following chemotherapy, and better response to platinum/5-fluorouracil-based neoadjuvant chemotherapy...Moreover, recent data provide initial evidence that MSI-L may be associated with subtle alterations of genes involved in DNA damage tolerance pathways. This review aims to clarify the current understanding of MSI-L by (a) comparing diagnostic methods and their influence on MSI-L classification, (b) summarizing clinical and molecular associations of MSI-L specifically in gastric and colorectal cancer, (c) highlighting new aspects regarding potential mechanisms underlying MSI-L, focusing on the particular unstable marker and a possible role of the DNA damage tolerance pathways, and (d) discussing whether MSI-L, particularly defined by dinucleotide repeat instability, may serve as a marker for therapeutic vulnerability.

In this review, we summarize advances in our understanding of Hh-mediated cell death in gastrointestinal cancers and the role and mechanisms, and highlight the underlying therapeutic opportunities. These new findings advance the rapidly expanding field of translational cancer research focused on the Hh signaling pathway.

P3, N=555, Recruiting, RemeGen Co., Ltd. | Not yet recruiting --> Recruiting

P=N/A, N=50000, Recruiting, National Taiwan University Hospital | Enrolling by invitation --> Recruiting | N=30000 --> 50000 | Trial completion date: Dec 2025 --> Dec 2030 | Trial primary completion date: Dec 2025 --> Dec 2030

Subsequent administration of the irreversible FGFR1-4 inhibitor futibatinib was associated with a declining trend in tumor biomarkers, indicating preliminary antitumor activity against the resistant clone. This case underscores the clinical activity of FGFR inhibition in FGFR2-altered SGC and exemplifies the emergence of kinase domain mutations as a principal resistance pathway. It further suggests that irreversible FGFR inhibitors may represent a rational therapeutic strategy upon progression on prior FGFR-directed therapy, warranting further clinical investigation in this molecularly defined patient subset.

Our findings highlight the pivotal role of DARS-AS1 in enhancing GC progression through the activation of angiogenesis via the Wnt signaling pathway. By elucidating the mechanism underlying DARS-AS1-mediated tumorigenesis, we posit that DARS-AS1 could serve as a prognostic biomarker and a potential therapeutic target for GC intervention, warranting further exploration in clinical settings.

While endoscopic resection is preferred for localized lesions, surgical intervention remains necessary in complex or obstructive cases. Understanding IFPs' molecular profile and cellular origin may refine future diagnostic and therapeutic approaches.

In addition, we also noticed an increased infiltration of neutrophils in TNB-High group (p-value=0.04). In summary, this study indicated that the prognosis of TNB-High patients was significantly better than their counterparts, which might be associated with impaired energy metabolism.