TUBB1 (Tubulin Beta 1 Class VI)

The RT-qPCR results of zebrafish verified that Pitavastatin inhibited the expression of HMGCR, while Cabazitaxel inhibited the expression of TUBB1. Our study suggested that Pitavastatin has therapeutic effects on OA, while Cabazitaxel increases the risk of OA.

The expression of signature-related genes were validated in patients with BC. This study successfully constructed molecular subtypes and a prognostic signature based on ARGs in BC, and developed a nomogram.

Also, compared to the low-risk patients, the high-risk patients had higher expression of immune checkpoint molecules and showed a lower IC50 value to the chemotherapy agents. Our findings provided a myeloid cell differentiation-related gene signature that could effectively predict prognosis and guide treatment strategies for LUAD patients.

Conclusion  High proportion of CD34 + CD61 + MKs was a poor prognostic factor in MDS patients with MK mutation. CD62P, CXCL10, and S100A9 may be the potential targets to evaluate the molecular link between gene defects and platelet function.

The combined treatment of Phy and Bis exerts a synergistic inhibitory effect on NSCLC cell growth, mediated through the interplay of apoptosis and autophagy. The differential protein expression observed, along with the identified proteins and enriched pathways, provides valuable insights into the underlying molecular mechanisms. These findings offer a foundation for further exploration of the therapeutic potential of Phy and Bis in the management of NSCLC.

 This study demonstrated the high potential of WES in identifying rare molecular defects causing IBD in pediatric patients, improving their management, prognosis, and treatment, particularly for patients at risk of malignancy and/or bleeding due to invasive procedures.

Four hub genes (namely, cathepsin B [CCNB1], four-and-a-half LIM domains 2 (FHL2), major histocompatibility complex, class II, DP alpha 1 (HLA-DPA1) and tubulin beta 1 class VI (TUBB1)) were obtained via taking interaction of different analysis results. On the whole, the findings of this investigation enhance our understanding of the potential molecular mechanisms of PDAC and provide potential targets for further investigation.

Our findings suggest that HCC may result from a unique synergistic combination of 5mC-epigenetic mechanism mixed with mA-epitranscriptomic mechanism, and their crosstalk defines therapeutic response and pharmacogenomic landscape.

The PP2A activator FTY720 reduced levels of phosphorylated stathmin. Eribulin-resistant leiomyosarcoma cell lines had enhanced expression of the class Ⅰ β-tubulin TUBB1, multi-drug resistance 1 protein MDR1 and breast cancer-resistance protein BCRP, and decreased expression of stathmin. Taken together, these results suggest that stathmin expression modulates the pharmacological efficacy of eribulin in uterine leiomyosarcoma cells.

Genetic variants in mCRPC patients could explain different outcomes with cabazitaxel. Nonetheless, the small sample size and the high number of SNPs analyzed mean that the results are only hypothesis-generating and require further validation.

FGFR3 CNV was associated with erdafitnib sensitivity, TUBB1 CNV with docetaxel sensitivity, and MAP4 SNV with paclitaxel resistance. Conclusion We set up a protocol highly efficient on generating BLCa PDO that cover a wide range of disease stages and maintain the PT histopathological and molecular heterogeneity in terms of tumor content, deleterious SNVs and cell subpopulations. We showed the clinical relevance and feasibility of a PDO-based drug assay on stratifying patients according to drug sensitivity that can be used to improve their