Adenoid Cystic Carcinoma

P1/2, N=242, Recruiting, VM Oncology, LLC | Phase classification: P1 --> P1/2 | N=82 --> 242 | Trial completion date: Jun 2027 --> Jun 2028 | Trial primary completion date: Dec 2026 --> Dec 2027

Adjuvant RT did not improve the OS and BCSS of the M0 ADCC patients with tumors ≤10 mm who had undergone BCT. Therefore, adjuvant RT may not be necessary for M0 ADCC patients with tumors ≤10 mm who have undergone BCT.

Emerging data support the use of immune checkpoint inhibitors in squamous BGC and targeted agents (e.g., mTOR/CDK4/6 inhibitors) in adenocarcinoma. We propose a practical molecular testing algorithm and highlight the urgent need for prospective, multinational collaboration to establish BGC-specific guidelines.

Additionally, the transcription factor myocyte enhancer factor 2 C (MEF2C) was found to bind to the promoters of PDGFA, PDGFB, ANGPT1, and ANGPT2, initiating their transcription. Knockdown of MEF2C inhibited the pro-angiogenic activity of MCAM+ myCAFs both in vitro and in vivo MCAM+ myCAFs promote the transcription of pro-angiogenic factors through MEF2C, thereby enhancing angiogenesis and promoting tumor growth in solid-type ACC.

In situ hybridization and RT-PCR confirmed the presence of HPV42 in digital papillary adenocarcinoma. Our study confirms the presence of mutations in TP53 and Jak1 and suggests that HPV42 does not contribute to malignant adnexal tumors of the head and neck.

Our findings indicate that soluble LOX secreted by CAFs promotes metastatic progression through the induction of pulmonary fibrosis. Targeting this LOX-mediated pathway may represent a promising therapeutic strategy for preventing lung metastasis in patients with SACC. Furthermore, given the complexity of metastasis, future studies should investigate how fibrosis influences key stages of metastatic colony formation, including the extravasation and dormancy of circulating tumour cells.

Recognition of LG-TNBCs is essential to prevent overtreatment and guide personalized patient management. Molecular characterization provides diagnostic confirmation and therapeutic opportunities, particularly for NTRK-fusion-positive tumors treatable with targeted inhibitors, highlighting the importance of precision medicine in rare breast tumors.

A 264-gene signature from HPVon HMSC cells correlated with worse prognosis in HPV + OPSCC (p < 0.003), suggesting an alternate role for HPV. Further validation of the HPV-MYB association and gene signature may improve therapeutic strategies in HPV-related malignancies.

In conclusion, we characterize the breadth of angiocentric glioma patterns in terms of demographics, anatomic location, and MYB fusion patterns. The updated molecular diagnosis of angiocentric glioma as of 2021 warrants continued exploration of the scope of MYB oncogene fusions as drivers of prognosis and targets for future therapies.

The presence of intraductal carcinoma or cribriform growth patterns was not associated with increased likelihood of mutations in homologous recombination repair genes. These findings support the use of clinical parameters such as age and Grade Group, rather than histologic subtype alone, in guiding decisions for genetic testing.

This study demonstrated that PSMA is commonly expressed in malignant SGTs, suggesting that PSMA could be effective for targeted imaging and therapeutics in these tumor types.