Esophageal Cancer

P2/3, N=840, Recruiting, Pfizer | Not yet recruiting --> Recruiting

P2, N=25, Recruiting, University Medical Center Groningen | Not yet recruiting --> Recruiting | Trial completion date: Dec 2024 --> Dec 2026 | Trial primary completion date: Dec 2024 --> May 2026

P1, N=13, Terminated, Zhejiang Doer Biologics Co., Ltd. | N=94 --> 13 | Trial completion date: Jun 2025 --> Mar 2026 | Recruiting --> Terminated | Trial primary completion date: Jun 2025 --> Dec 2025; This trial was terminated voluntarily by the Sponsor for reasons related to its corporate strategic development, with no safety concerns or efficacy signals related to the investigational product identified.

P1, N=21, Completed, University Medical Center Groningen | Recruiting --> Completed | N=31 --> 21

P1, N=383, Recruiting, Iambic Therapeutics, Inc | N=243 --> 383 | Trial completion date: Mar 2028 --> Dec 2028 | Trial primary completion date: Mar 2027 --> Dec 2027

P1, N=158, Active, not recruiting, Janssen Research & Development, LLC | Trial completion date: Dec 2026 --> Apr 2027

P2, N=64, Not yet recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2028 --> Feb 2030 | Trial primary completion date: Jan 2028 --> Feb 2030

This study identified survival-associated AS signatures, potentially improving the prediction of survival outcomes in ESCA patients. Moreover, the splicing factor SF3A3 was shown to promote tumor progression by regulating AS of LGALS9, suggesting it as a promising therapeutic target.

Most importantly, miR-663a-induced aggressive phenotype in esophageal cancer cells relied on the repression of FKBP8 expression. The miR-663a/FKBP8 axis regulated by ARID1A plays a critical role in esophageal cancer cell proliferation and migration and represents a potential therapeutic target for this malignancy.

This case illustrates an exceptionally rare MiNEN of the EGJ with enteroblastic differentiation and morphologic-immunophenotypic discordance. Despite the presence of aggressive histologic features, long-term disease-free survival was achieved with surgical resection alone. This report highlights the importance of thorough histopathological and immunohistochemical evaluation for accurate diagnosis and suggests that curative surgery alone may provide durable disease control in carefully selected patients with localized disease.

Importantly, restoring YTHDF2 SUMOylation via Senp1 knockdown reversed SLC7A11 overexpression and resensitized resistant cells to cisplatin both in vitro and in vivo. These findings reveal a SUMOylation-dependent switch in m6A reader function as a novel mechanism underlying chemoresistance, reconciling previously conflicting reports on the role of METTL3 in SLC7A11 regulation, and identify the METTL3-YTHDF1/2-SLC7A11 axis, particularly the Senp1-YTHDF2 node, as a potential target warranting further investigation for overcoming cisplatin resistance in ESCC.

These findings demonstrate that DEX enhances CDDP efficacy by activating pyroptosis through suppression of the SREBF1/miR-185-5p axis and upregulation of Caspase-1. Collectively, our study identifies a novel regulatory pathway through which DEX enhances CDDP chemosensitivity in EC cells.