Endocrine Cancer

Collectively, METTL3-modulated m6A modification of TACSTD2 exerts an indispensable tumor-suppressive function in PTC progression. The METTL3/TACSTD2/YTHDC2 axis may serve as a molecular target for PTC therapy.

Importantly, inactivation of the necroptosis executioner MLKL reverses pre-tumoral inflammation, decreases metastasis as well as neuronal-like reprogramming. Taken together, our findings suggest that pre-tumoral inflammatory cell death contributes to neuronal progenitor mimicry, immunosuppression and increased metastasis in SCLC.

P2, N=32, Recruiting, Washington University School of Medicine | Not yet recruiting --> Recruiting

PRNETs, though rare, should be considered in the differential diagnosis of renal masses, particularly in patients with congenital renal abnormalities such as horseshoe kidney. Nephron-sparing surgery may be a feasible option in selected cases, with favorable short-term outcomes. Long-term follow-up is essential due to the potential for delayed metastasis. Immunohistochemical profiling plays a critical role in diagnosis and therapeutic planning, especially regarding the potential use of somatostatin analogs.

We showed that this peptide variant binds with a stronger affinity to its target proteins than the wild-type peptide and inhibits CBP/p300 acetylase activity. This peptide variant also modulates interactomes and CBP/p300-mediated gene transcription and exhibits effective antiproliferative activity in cell-based assays.

Long-term cardiac prognosis is determined by right ventricular function and presence of residual tumor after resection. Management requires individualized and multidisciplinary surgical planning, balancing tumor resection with timely cardiac intervention.

This study has established the circ-0000258/miR-146b/p53 regulatory axis as a crucial mechanism underlying tumor suppression in PTC. It has also demonstrated the translational potential of hUCMSC-EVs as a safe and efficient delivery vehicle. By integrating the functional role of circ-0000258 with the targeted delivery advantages of engineered EVs, this research not only provides a novel strategy for the targeted treatment of thyroid cancer but also offers a theoretical basis and technical paradigm for the development of novel anti-tumor biological agents. It is anticipated to advance the field of precision oncology to a new level.

P1/2, N=208, Recruiting, IDEAYA Biosciences | N=90 --> 208

P2, N=48, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Nov 2025 --> Apr 2026 | Trial primary completion date: Nov 2025 --> Apr 2026

Among skin carcinomas, RB1 inactivation is the hallmark of primary cutaneous neuroendocrine carcinoma commonly known as Merkel cell carcinoma (MCC), but it has also been described in other tumours including a subset of squamous cell carcinomas, sebaceous carcinomas and the recently described Wnt/beta-catenin-activated non-pilomatrical carcinomas. In this context, we provide a brief overview of the contribution of RB1 inactivation to oncogenesis and tumour cell phenotypes in general and summarise current knowledge regarding RB1-deficient cutaneous carcinomas, highlighting the potential uses of RB1 pathway characterisation for diagnosis, prognosis and therapeutic purposes.

Our case and related literature review suggest that the multiplex genetic mutation-detection assay should be considered for patients with LCNEC. Furthermore, it also suggests that biomarkers which enable us to distinguish patients who are likely to harbor driver gene alterations are required in near future.

Androgen deprivation therapy (ADT) and next-generation AR blockade (e.g., enzalutamide) are initially effective, but virtually all patients develop castration-resistant prostate cancer (CRPC), which frequently transitions to treatment-emergent neuroendocrine PCa (tNEPC) following AR suppression...Thus, we uncover a single stress-induced node (PSMA2) that both maintains AR-dependent survival under ADT and fuels the neuroendocrine transition. PSMA2 marks an AR-hypersensitized transitional state and is itself a therapeutically actionable driver of tNEPC evolution, revealing an opportunity for rational interception of the lethal ADT-CRPC-tNEPC trajectory.