Ask about this productRelated genes to: MDM2 antibody
- Gene:
- MDM2 NIH gene
- Name:
- MDM2 proto-oncogene
- Previous symbol:
- -
- Synonyms:
- HDM2, MGC5370
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-10
- Date modifiied:
- 2017-12-01
Related products to: MDM2 antibody
Related articles to: MDM2 antibody
- Primary mucoepidermoid carcinoma of the liver (MEC-L) is an exceptionally rare malignant tumor characterized by mucinous, epidermoid, and intermediate cells, resembling its salivary gland counterpart. To date, only 24 cases of MEC-L have been reported in the English literature. We present two additional MEC-L cases diagnosed at the Third Affiliated Hospital of Sun Yat-sen University from January 2023 to May 2025, along with a review of 24 published cases. Clinical data, laboratory results, pathological findings, and follow-up information were collected. Thirty-three cases of conventional cholangiocarcinoma (CCA) were included for comparison. Next-generation sequencing (NGS) was performed for all cases. The median age of MEC-L patients was 64 years (range: 35-81 years), with a male-to-female ratio of 16:10, and a median tumor size of 8 cm. MEC-L displayed non-specific clinical and radiological features, with pathology similar to MECs arising in other anatomical sites. Only 16.67% (1/6) of MEC-L cases showed MAML2 rearrangement. Mutations in TP53, CDKN2A and CDKN2B were identified in one case, and mutations in KRAS, PIK3CA, CDK4, MDM2 and MYC were found in another case. The clinicopathological features and mutational profiles of MEC-L closely resembled conventional CCA, but MEC-L had a significantly poorer overall survival (p < 0.05). Age and tumor type were independent prognostic factors for CCA, but no distinct clinicopathological factors were identified for MEC-L. In conclusion, MEC-L is a rare subtype of CCA, who shows similar clinicopathological features and mutational profiles with conventional CCA except for poor prognosis. - Source: PubMed
Publication date: 2026/09/05
Zhu YiliShao YitingGuo JinruiLin WeizhenDeng JunwenPan YuhangShi HezhanHe DanZhou JingDu YuChen Jianning - Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, with limited therapeutic options and poor survival. Resistance to standard temozolomide (TMZ) therapy remains a major challenge, necessitating novel agents. Tropolone derivatives, particularly the synthetic trichlorotropolone JO-122(2), have shown broad preclinical antitumor activity. This study aimed to determine whether JO-122(2), alone or combined with TMZ, can suppress GBM growth in vivo and to define the accompanying changes in the p53/MDM2/Bcl-2 apoptotic axis. - Source: PubMed
Publication date: 2026/06/24
Kit Oleg IMaksimov Aleksey YuGolovinov Igor VKuznetsova Natalia SKaplieva Irina VKhodakova Daria VSagakyants Alexander BGalina Anastasia VShulga Anna AGurova Sofya VBondarenko Elena SRostorguev Eduard ESayapin Yurii AGusakov Eugeny A - Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders characterized by dysregulated myeloid proliferation and hyperactive JAK-STAT signaling pathway. While JAK inhibitors have become standard therapies for the management of these conditions, significant challenges remain due to resistance to these medications and adverse effects such as cytopenias and infectious complications. This review explores novel therapeutic strategies that target pathways beyond JAK-STAT signaling. We discuss BET inhibitors (pelabresib), PIM kinase inhibitors (TP-3654), telomerase inhibition (imetelstat), nuclear export inhibition (selinexor), LSD1 inhibition (bomedemstat), MDM2 antagonism (navtemadlin), mutant CALR-directed immunotherapies, and activin receptor ligand traps (elritercept). Emerging data suggest that pairing JAK inhibitors with agents that target transcriptional regulation, clonal persistence, anemia, or fibrosis can demonstrate improved responses and enhance safety profiles. Strategies such as high-molecular-risk mutation profiling and variant allele frequency monitoring to assess disease progression and clonal burden will also be discussed. As the focus of MPN management shifts towards curative nontransplant options, a combination of improved access to clinical trials and accounting for patient-reported outcomes will be vital if we are to realize the promise of these next-generation therapies. - Source: PubMed
Publication date: 2026/07/30
Aluri AkshayKishtagari Ashwin - The PIDDosome multiprotein complex is formed by PIDD1 and RAIDD (alias CRADD) and serves as activation platform for caspase-2. One of the best characterized triggers for PIDDosome activation is the presence of extra centrosomes, which are frequently observed in cancer and in naturally polyploid tissues such as liver and heart. Depending on the cell type, activated caspase-2 can (1) cleave MDM2, thereby triggering a p53 response, or (2) cleave the BH3-only protein BID to induce apoptosis. Here, we describe our biochemical and cell biological tools to study the PIDDosome and caspase-2 activity. These include methods to experimentally induce PIDDosome formation in cells, as well as techniques to monitor pathway activity via protein and mRNA expression analysis, and flow cytometry. Moreover, we describe how to follow centrosome maturation for PIDDosome activation using immunofluorescence microscopy. - Source: PubMed
Publication date: 2026/06/03
Eichin FelixHirschberger RotraudVillunger AndreasSladky Valentina C - Pancreatic hepatoid carcinoma (PHC) is an extremely rare pancreatic malignancy characterized pathologically by hepatocellular-like differentiation. Some patients may present with elevated serum alpha-fetoprotein (AFP). Owing to the limited number of reported cases, the clinical features, molecular characteristics, and systemic treatment strategies for PHC remain poorly defined. BRAF V600E is an actionable alteration with established therapeutic value in several solid tumors; however, its clinical significance in PHC remains unclear. - Source: PubMed
Publication date: 2026/08/18
Li YingliXie ShengzhiSun XianchangWang FangweiGuo HanbingChen DiDang JianhuaYang XiaoliWang YufeiMa Xueping