Tongue Carcinoma

P=N/A, N=392, Completed, Tata Memorial Hospital | Active, not recruiting --> Completed | Trial completion date: Sep 2026 --> Dec 2025 | Trial primary completion date: Aug 2026 --> Dec 2025

P2, N=69, Not yet recruiting, Shanghai Zhongshan Hospital

SCA potently inhibits TSCC progression in cell lines, xenografts, and patient-derived organoids. Its mechanism involves activation of p53 phosphorylation, shifting the BCL-2/BAX balance, and triggering caspase-dependent apoptosis. These findings position SCA as a promising therapeutic candidate and underscore the utility of organoid models in oncology drug development.

N4BP1 not only drives cancer cell evolution but also establishes an immune-suppressive microenvironment. N4BP1 is an endoribonuclease that specifically regulates a subset of mRNA targets (including CCL2 and GM-CSF) and plays an essential role in oral cancer.

The in vivo validation suggested that SIRT2 played a regulatory role in FZD1 expression and Wnt/β-catenin pathway, thereby hindering the growth and metastasis of the orthotopic tongue cancer xenograft model. SIRT2 inhibits the transcriptional expression of FZD1 through H3K27 deacetylation to block the Wnt/β-catenin pathway, consequently suppressing the growth and metastasis of tongue cancer.

Given the tumor's extent, she was treated with definitive chemoradiation using weekly cisplatin and 70 Gy in 35 fractions...This case highlights the importance of molecular diagnostics in distinguishing HCCC from other clear cell neoplasms and suggests a potential role for chemoradiation in unresectable cases, though treatment-related toxicity remains a significant concern. Further investigation into systemic and targeted therapies for HCCC is warranted.

RREB1::MRTFB fusion was confirmed in both cases. In summary, the two reported cases expand the anatomical spectrum and improve our understanding of this rare emerging entity.

Therefore, SAB, through its ability to reduce oxidative stress, fibrosis, and metabolic dysregulation, is a promising therapeutic candidate for mitigating arecoline-induced tumor progression. Our study offers novel insights into the role of SAB in protecting against the pathophysiology of oral cancer and highlights its potential as a natural compound for the prevention and treatment of this disease.

SNHG26 depletion reversed NK cell suppression and cisplatin resistance in vitro and in vivo. Thus, our study identifies exosomal SNHG26 as a key mediator of cisplatin resistance and NK cell dysfunction in TSCC, suggesting its potential as a promising therapeutic target.

The findings confirm MMP-14 overexpression in OSCC and its association with perineural invasion, underscoring its role in tumor progression. No significant correlations were found with lymph node metastasis, clinical stage, or histological grade. Limitations include MMP-14's ubiquitous expression, reducing biomarker specificity. Further research incorporating additional molecular markers is warranted to refine prognostic accuracy.

A multidisciplinary approach combining radical surgery and adjuvant RT is crucial; however, the rapid distant progression highlights the critical need for more effective systemic treatment options and the integration of genetic profiling to guide personalized therapies. Further comprehensive research is essential to optimize management strategies and improve the limited survival outcomes associated with this rare and challenging malignancy.

At the last follow-up in August 2025, the patient had a progression-free survival (PFS) of 29.8 months, with no evidence of recurrence in the lung lesions. This case demonstrates the efficacy of a multimodal induction chemoimmunotherapy in achieving complete response and preserving organ function, thereby providing a promising therapeutic option for patients with synchronous lung and base-of-tongue SCC.