TBX1 (T-Box Transcription Factor 1)

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.

Here, we extended that study, by identifying genomically amplified and overexpressed MAPK1/ERK2 at 22q11 together with MCTS1 at Xq22. Using pharmacological inhibitors and siRNA-mediated knockdown assays, our data collectively revealed novel regulatory connections between TBX1, MAPK1 and MCTS1, which may play a role in drug resistance.

Loss of RIPPLY1 promotes cancer cell stemness via facilitating the TBX19 transcriptional activity in CTNNB1-mutated HCCs.

In conclusion, MGRN1 loss in HCC-SR cells blocked TBX19 degradation and strengthened TBX19-mediated AQP7 repression, leading to immune evasion. Targeting this signaling might offer a promising therapeutic strategy to overcome SR in HCC.

Therefore, OTX2 plays important roles in restraining the differentiation and promoting progression of gastric cancer cells in young adults. Moreover, OTX2/CEBPB signal axis is likely to be a key molecular event in regulating the differentiation of gastric cancer cells in young adults.

A clear classification system that can guide clinical and neurosurgical management of patients with GH- and PRL-secreting PitNETs is not currently available, but certain clinicopathological factors can be used to predict patient prognosis. In our study, somatostatin receptor expression, ki-67, and postoperative values of GH and IGF-1, as well as the maximal postoperative tumor diameter, were the strongest predictors of outcome.

The browning effect of CK was nullified by SIRT3 knockdown, suggesting that CK induces beige remodeling of WAT by regulating mitochondrial dynamics and SIRT3 expression. These findings suggest CK's potential as a therapeutic agent for obesity and metabolic disorders that promotes the transformation of WAT into a metabolically active beige phenotype.