TP53 overexpression

LACTB repressed EC cell proliferation and metastasis, and reprogramed lipid metabolism via attenuating the MDM2-mediated ubiquitination and degradation of p53.

Wild-type p53 might promote Caspase-dependent apoptosis of human breast cancer cells through PP1 activation.

Overexpression of aromatase and p53 overexpression has clinical relevance in mCMT, and an intratumoral ERα expression is positively associated with HER-2 expression and aromatase production by stromal components.

Using a cut-off set at 30% expression of neoplastic cells, we noted an overexpression of p53 in T-MF and T-SS compared with nontransformed forms (47% vs. 12%, respectively, P < 0.01) and in MF compared with SS (23% vs. 7%, respectively, P < 0.01). Overexpression of p53 with a cut-off at 30% therefore seems to be a discriminating tool in the differential diagnosis of MF/SS versus their transformed forms as well as the differential diagnosis between MF and SS.

EC imaging phenotypes identified through MRI radiomics features were associated with pathologic, molecular characteristics, and DFS, suggesting potential for preoperative risk stratification.

To conclude, breast cancer in carriers of TP53 PGVs has some unique clinicopathological features that suggest differential mechanisms of tumor formation. p53 immunohistochemistry cannot be used as a surrogate marker to identify germline TP53-mutated breast cancers.

Conversely, knockout of p21, a major target gene of p53, increased TMEM206-mediated currents, suggesting expression control of TMEM206 by p21 downstream signaling. Our results show that in colorectal cancer cells, TMEM206 expression is elevated, contributes to cancer hallmark functions, and its regulation is dependent on p53 through a p21-dependent mechanism.

Conclusion Considering that elevated p53 protein expression is linked to aggressive tumor behavior, a more intensive treatment strategy is recommended for patients with non-muscle-invasive bladder cancer (NMIBC) who show high p53 protein scores. On the other hand, the downregulation or absence of E-cadherin expression has been recognized as a strong indicator of advanced grade and higher clinical stages.

Therefore, melanoma tumor development was prevented by the overexpression of cell cycle inhibitors p16, p21, p27, and p53 due to UM + LunLip treatments. Since the topical application was effective, less invasive, and more practical for the user, this application will be recommended for future steps in in vivo studies.

Molecular characterization of glioma is an important step in modern glioma diagnostics and immunohistochemistry can play an important role. IDH-1 mutation is commonly observed in adults, frontal lobe location, patients presenting with seizures, and WHO grade 2 tumors with the highest frequencies in oligodendrogliomas. ATRX and p53 can be used as surrogate markers for tumors of astrocytic lineage.

Overexpression of miR-205 in HN12-SK2 cells decreased tumor formation capacity and NOK-SK2 cells abrogated the tumor growth in mice. Our results indicate crosstalk between SK2 and p53 in regulating miR-205 and miR-296, which could be potential targets for HNSCC therapy.

P2, N=29, Active, not recruiting, City of Hope Medical Center | Trial completion date: Aug 2024 --> Dec 2024