Tongue Carcinoma

Both P65 knockdown and miR-302 overexpression dramatically slowed tumor growth in vivo. Our results demonstrate the therapeutic potential of a novel miR-302/P65 axis that limited the progression of TSCC by regulating apoptosis and oncogenic transcription.

Such combined treatment showed promising synergistic interaction via several molecular pathways, which is well tolerated and readily applicable strategy to improve the therapeutic outcome of PDT in cancer cell treatment.

SCC9 and SCC9-CisR cells were treated with Rha alone or in combination with 2-deoxy-D-glucose (2-DG) or sodium lactate (LacNa). Mechanistically, Rha inhibited HIF-1α, thereby attenuating glycolytic flux and decreasing lactate-driven H3K18la. Rha inhibits TSCC progression and enhances cisplatin sensitivity by targeting HIF-1α and repressing the glycolysis/lactate/H3K18la axis, suggesting that Rha is a promising candidate for disrupting metabolic/epigenetic crosstalk in TSCC.

P=N/A, N=33, Recruiting, Centre Hospitalier Universitaire, Amiens | N=14 --> 33 | Trial completion date: Oct 2023 --> Oct 2026 | Trial primary completion date: Oct 2023 --> Oct 2026

RhoBTB1 is lowly expressed in TSCC and may inhibit its malignant phenotype by negatively regulating the ROCK1/PTEN/AKT pathway, suggesting its potential as an oncogene and therapeutic target.

In vivo analysis confirmed target engagement (NUDT21-down) and functional restoration (PTEN-, WEE1-, TGF-β-up). This work validates a "post-transcriptional re-engineering" strategy, executed by a logically designed nanoplatform, as a powerful and safe modality for precision gene therapy.

Current evidence does not support Bcl-xL as a general prognostic marker in head and neck squamous cell carcinoma. Nevertheless, Bcl-xL may have prognostic relevance in oral tongue cancer if further studies confirm the original finding.

Molecular findings suggest distinct patterns of TP53 alterations and chromosomal instability in younger patients. The growing burden of OTSCC in young women underscores the need for improved early detection and multi-institutional molecular studies to clarify mechanisms and inform tailored prevention and treatment strategies.

P2, N=24, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027

Delayed diagnosis is common due to low suspicion in "low-risk" individuals. This review underscores NSND OSCC as a unique entity requiring expanded risk assessment, heightened clinical vigilance for persistent oral lesions regardless of habit history, and targeted research into novel prevention and therapeutic strategies.

Mechanistically, DNPEP directly bound to the RACK1 protein, activating the ERK signaling pathway. DNPEP plays a critical role in TSCC progression and cisplatin resistance by interacting with RACK1 and activating ERK signaling, highlighting its potential as a therapeutic target to inhibit TSCC and overcome chemotherapy resistance.

 EpCAM overexpression was detected in approximately 28.6% of OSCC cases in this Northeast Indian cohort. The observed trends suggest increased EpCAM overexpression in males, those with alcohol consumption, and tongue carcinomas, while a significant association was observed with higher histological grade. This pilot study is limited by a small sample size and a lack of TNM staging and survival data, restricting prognostic interpretation. These findings should be considered preliminary and exploratory in nature. Larger prospective multi-centre studies are needed to validate these observations and determine the prognostic and therapeutic relevance of EpCAM in OSCC.