TBX1 (T-Box Transcription Factor 1)

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.

This study established a novel radiosensitivity-related prognostic model, offering insights into NPC prognosis and radiotherapy resistance mechanisms.

In addition, vitamin B12 treatment rescued a behavioural anomaly in Tbx1 +/- mice. Further studies will be required to establish whether the specific metabolites affected by Tbx1 haploinsufficiency are potential biomarkers of brain disease status in 22q11.2DS patients.

This research provides comprehensive evidence that chimeric SFT2D2-TBX19 promotes prostate cancer progression by encoding the TBX19-202 protein and stabilizing mitochondrial ATP synthase via ATP5F1A phosphorylation. These findings highlight SFT2D2-TBX19 as a potential therapeutic target for prostate cancer.

A panel combining PJ-MDMs and plasma CA19-9 discriminates PDAC from both healthy and disease control groups with high accuracy. This provides support for combining pancreatic juice and blood-based biomarkers for enhancing diagnostic sensitivity and successful early PDAC detection.