SESN1 (Sestrin 1)

He commenced first-line systemic therapy with methotrexate, but had no response. He was switched to brentuximab vedotin and has received eight cycles with partial response...Approach to mycosis fungoides in children: consensus-based recommendations. J Am Acad Dermatol 2024; 91: 1078-85).

Our results and published data show that MAFF levels in pancreatic cancer tissues markedly exceeds that of normal tissues and have a bad effect on prognosis. The study identifies a prognostic gene signature for PAAD, revealing its potential in personalized medicine and immunotherapy, and highlights the role of immunosenescence in cancer treatment.

TFH could promote HIF-2α protein degradation by activating the Sesn1/Keap1/Nrf2 signaling pathway to scavenge ROS, thereby inhibiting erythropoietin (Epo) production.

This review examines the molecular mechanisms underlying these dual functions, with a particular focus on mTOR signalling and oxidative stress. We also discuss Sestrin expression patterns and functional outcomes in various cancer types, including lung, liver, colon, skin, prostate, and follicular lymphomas, highlighting their potential as diagnostic markers and therapeutic targets.

Surgery/anesthesia had little effect on CD4+ and CD8+ T cells, and continued to affect the functional changes of Treg. It had more impact on monocytes, which may cause them to promote tumor development to a certain extent.

We demonstrate that SESN1&2 inactivation stimulates STAT3 by downregulating the PTPRD phosphatase, a protein responsible for STAT3 dephosphorylation. Our study demonstrates that SESN1&2 deficiency may cause STAT3 activation and facilitate carcinogenesis and drug resistance, making SESN1&2 reactivation a potential cancer treatment strategy.

The key genes involved in oxidative stress could predict the prognosis of DLBCL and potentially become therapeutic targets.

Furthermore, some of these genes were central to PCa occurrence, with BBC3 also influencing progression and prognosis. Importantly, BBC3 expression was upregulated in clinical PCa samples and affected PCa cells sensitive to olaparib, suggesting its potential as a predictive marker for PCa development and olaparib resistance.

SESN1 functions as a new tumor suppressor gene via TLR signaling pathway in NB.

However, the GE pattern of other genes differed between saliva and blood. In summary, the current human in vivo study, (I) reveals significant radiation-induced GE associations of five transcriptional biomarkers in salivary samples, (II) suggests genes predicting diverse clinical outcomes such as acute and late radiotoxicity as well as ARS severity, and (III) supports the view that blood-based GE response can be reflected in saliva samples, indicating that saliva is a "mirror of the body" for certain but not all genes and, thus, studies for each gene of interest in blood are required for saliva.

To reveal the mechanism of drug resistance, the molecular networks of anti-cancer drugs such as cisplatin, carboplatin, oxaliplatin, and arsenic trioxide were analyzed in several types of cancers...The upstream regulators of the molecular networks of cisplatin-treated lung adenocarcinoma included the anti-cancer drug trichostatin A (TSA), a histone deacetylase inhibitor...Analysis of oxaliplatin, a platinum drug, revealed that the SPINK1 pancreatic cancer pathway is inactivated in ischemic cardiomyopathy. The study showed the importance of the molecular networks of anti-cancer drugs and tumor microenvironment in the treatment of cancer resistant to anti-cancer drugs.

In conclusion, based on this research results, metformin enhanced the radio sensitivity of breast cancer cells via modulating  the expression of miR-21-5p and SESN1.