TCF19 (Transcription Factor 19)

The three major PitNET lineages exhibited distinct immune cell frequencies, with the PIT1 lineage notably enriched in Treg and Tfh cells, as well as collagen-producing CAF3. Furthermore, a novel immunosuppressive interaction between Treg cells and macrophages, mediated by the CTLA4-CD86 pathway, was identified, suggesting its potential regulatory role within the TME.

Transcription factor expression was associated with distinct clinical features and short-term outcomes. The PIT1 and TPIT lineages were linked to shorter tumor-free survival. Enhanced postoperative surveillance is recommended for these subgroups. These findings underscore the clinical and prognostic heterogeneity of non-functioning PitNETs.

The predominance of GH∕PRL-secreting PitNETs in patients with prior systemic malignancies supports the hypothesis of endocrine and molecular crosstalk through the GH∕insulin-like growth factor-1 (IGF-1) axis. Although causality cannot be established, these findings underscore the need for oncological surveillance and endocrine monitoring in patients with PitNETs, especially in those with a previous malignancy.

WES revealed significantly mutated genes, most of which were associated with the physiological activation of lymphoma cells. This finding contributed to the identification of novel gene variants that might impact on the function of BM CD34+ cells in cHL patients.

All of the results listed above had explored the molecular mechanisms of hypoxic tumor proliferation, which undoubtedly provided TCF19 as a promising synergistic target to treat selenite-resistant hypoxic lung tumors.

These findings highlight common biological mechanisms rather than direct causal relationships, suggesting the limited benefits of additional PrCa screening in COVID-19 survivors. Furthermore, the identified genes represent promising targets for future mechanistic research and clinical interventions, warranting further validation.

We also found that Ras-related nuclear protein (RAN) might mediate the nuclear localization of TCF19, thereby affecting GDF15 expression and its pro-proliferative function. In summary, we demonstrated that GDF15 is positively regulated by TCF19, promoting the development of HCC.

Thus, ZNF191 directly upregulates SAC1 transcription, then inhibits Cdc42 activation and actin cytoskeletal assembly in ICC cells, eventually inhibiting metastasis. Collectively, ZNF191 may serve as a new prognostic biomarker and potential therapeutic target for ICC metastasis.

Transcription factor 19 (TCF19) stood out as an unprecedented epithelial gene upregulated in metastatic disease, with prognostic potential and negatively associated with the activity of the androgen receptor. By combining computational and empirical approaches, our data revealed that TCF19 is required for full metastatic capacity, and its depletion influences core cancer-related processes, such as tumor growth and vascular permeability, supporting the role of this gene in the dissemination of prostate tumor cells.

RNA-sequencing variant calling and single-cell transcriptome projections revealed associations between these four TCs and germline variants. These findings support the potential of the identified WB-based transcriptional patterns to complement tumor characteristics in predictive and prognostic models for improved patient stratification.

High TCF19 expression is closely linked to poorer outcomes, especially in breast cancer. These findings highlight TCF19 as a promising biomarker with broad potential applications in cancer diagnosis and prognosis.

TCF19 downregulation inhibited OS growth, metabolic reprogramming, and CDKN2A expression in OS mice. TCF19 is enriched in the CDKN2A promoter and enhances its expression, which in turn activates glycolysis and M2 polarization, ultimately promoting OS progression.