MDM2 (phospho-Ser260) Antibody
- Known as:
- MDM2 (phosphorilated-Ser260) Antibody
- Catalog number:
- abx000147
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- MDM2 (phospho-Ser260) Antibody
Related genes to: MDM2 (phospho-Ser260) 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 (phospho-Ser260) Antibody
Related articles to: MDM2 (phospho-Ser260) Antibody
- Characterization of molecular features of cholangiocarcinoma (CCA) has questioned the traditional, anatomy-based classification scheme and has alternatively suggested biology-based classifications. Intrahepatic CCA has been classified into small-duct and large-duct types, and the latter is histologically and molecularly almost identical to perihilar CCA. Although distal and perihilar CCA have been classified together, they have different molecular abnormalities, with MDM2 amplification observed in 15% of perihilar CCA cases but in none of the distal CCA cases. FGFR2 and IDH1 are two main drug targets in small-duct intrahepatic CCA, and mismatch repair (MMR) deficiency is most common in small-duct intrahepatic CCA. In contrast, HER2 is a promising target for extrahepatic CCA and gallbladder cancer, as HER2 overexpression is seen in 17%-30% of cases. Classification of intrahepatic CCA is often challenging on biopsy specimens; however, recognition of pitfalls (e.g., hybrid morphology) will help avoid misclassification. Staining for ancillary markers, including CRP, albumin-ISH, and S100P, is also useful. Accurate distinction between distal CCA and pancreatic head cancer has become increasingly important, particularly in unresectable or borderline resectable cases, as systemic treatment strategies differ between these entities. Although these two neoplasms share many morphological and immunohistochemical features, the presence of clear or foamy cancer cells in biopsy specimens is uncommon in dCCA and may favour pancreatic ductal carcinoma. - Source: PubMed
Publication date: 2026/04/16
Zen Yoh - The transcription factor p53, often called the "guardian of the genome," is critical for preserving genomic integrity. Mutations in the TP53 gene are found in approximately half of all human malignancies, including breast, colon, lung, liver, prostate, bladder, and skin cancers. p53 is activated by a wide range of cellular stress signals and orchestrates specific cellular responses based on the context and nature of the stress. As a tumor suppressor, p53 controls cancer initiation and progression by regulating cell cycle arrest, apoptosis, senescence, and DNA repair. Beyond its classical role in genome surveillance, p53 is now recognized as a dynamic signaling hub whose functions can be therapeutically modulated in cancer. Natural products derived from medicinal plants represent a rich source for discovering and developing novel therapeutic and preventive agents against cancer. Several natural compounds have been reported to target mutant p53 in cancer cells, offering a potentially effective strategy for modulating the p53 signaling pathway. This review highlights recent advances in identifying and developing anticancer natural products that modulate the expression or activity of the p53 tumor suppressor gene for cancer treatment and prevention. - Source: PubMed
Publication date: 2026/04/16
Nandi SudeshnaNaskar ArghyaKhatua SomanjanaAcharya KrishnenduBüsselberg DietrichHerrera-Bravo JesúsArancibia-Diaz AlejandraSetzer William NRotariu Lia SandaDragunescu Anca AnetaButnariu MonicaSharifi-Rad Javad - MDM2 is an E3 ubiquitin ligase that promotes p53 tumor suppressor degradation and has emerged as a therapeutic target in the treatment of wild-type (wt) TP53 tumors. In acute myeloid leukemia (AML), TP53 mutations are infrequent (15-20%), but wt-p53 is often inactivated through overexpression of MDM2. Thus, MDM2 inhibitors are currently in clinical trials for AML. However, p53 stabilization with inhibitors upregulates MDM2, which limits their clinical efficacy. Proteolysis-targeting chimeric (PROTAC) molecules that degrade MDM2 may overcome this feedback. MD-265 is a PROTAC that recruits CRBN, degrades MDM2, restores p53 and induces apoptosis. We tested MD-265 in ex vivo cultures of 105 primary leukemic stem cells (LSCs). The median cytotoxic IC for MD-265 was 16 nM, median IC for MI-1061 was 150-fold higher. LSCs with IC > 1 µM were classified as MD-265 resistant and harbored mutations in TP53. Normal hematopoietic stem cells showed 100-fold higher IC (818 nM) than LSCs. AML patient-derived xenograft (PDX) models in NSG-SGM3 mice were treated with MD-265 or an oral MDM2 inhibitor. In PDX models, MD-265 was not toxic and prolonged survival. MD-265 is a potent and specific MDM2 degrader with broad pre-clinical activity and a promising drug candidate for the treatment of leukemias. - Source: PubMed
Publication date: 2026/04/15
Kandarpa MalathiPeterson Luke FPotu HarishRamappan MeghaLiu YihongPolk AveryWang ShaomengTalpaz Moshe - MDM4 (Murine Double Minute 4), also known as MDMX, is a crucial negative regulator of the tumor suppressor p53. MDM4 heterodimerizes with MDM2 to enhance MDM2-mediated ubiquitination and degradation of p53, thereby promoting tumorigenesis. Beyond its canonical role in inhibiting p53 activity, recent studies have revealed diverse p53-independent functions. MDM4 interacts with various proteins, including p73, E2F1, casein kinase 1α, PPARα, and TRIM21 to regulate cell cycle progression, β-catenin-mediated pre-leukemic progression, and ferroptosis independent of p53. In addition, MDM4 functions independently of both p53 and MDM2 by interacting with proteins, such as SMAD family members 3/4, retinoblastoma protein (pRB), p21, Nbs1 (also known as Nibrin), mTOR complex 1 (mTORC1), and the Polycomb Repressive Complexes (PRCs) complex, to control cell proliferation and survival, as well as protein degradation, double-strand break (DSB) repair, and replication fork progression. Intriguingly, multiple studies suggest that MDM4 exhibits oncogenic activity independent of p53; however, other reports highlight a potential tumor-suppressive role for MDM4 in the absence of p53. Thus, MDM4's functions extend well beyond the canonical p53-MDM2 axis. A deeper understanding of MDM4 biology may facilitate the development of novel targeted therapies for various cancers. - Source: PubMed
Publication date: 2026/03/25
Thapa DipeshSt John AllisonParrales AlejandroRanjan AtulIwakuma Tomoo - Targeted therapies are reshaping oncology by enabling treatment selection based on actionable molecular alterations, improving precision, and reducing unnecessary toxicity. This review provides an up-to-date overview of current targeted treatment modalities and the medicinal chemistry principles that support their discovery and optimization. We synthesize evidence on small-molecule and biologic strategies spanning receptor and non-receptor kinases and their major signaling axes (PI3K-AKT-mTOR and RAS-RAF-MEK-ERK), apoptosis regulation (BCL-2 family), DNA repair via poly(ADP-ribose) polymerase (PARP) inhibition, and epigenetic or metabolic targets including histone deacetylases (HDACs), bromodomain and extra-terminal proteins (BET), and mutant isocitrate dehydrogenases (IDH1/2). Across these areas, we summarize recurrent resistance mechanisms and the rationale for combination or sequential approaches. Biologic targeted therapy is discussed in parallel, including immune checkpoint blockade, antibody-drug conjugates, bispecific antibodies (BsAb), and cell therapies such as chimeric antigen receptor T cells, with emphasis on biomarker-guided patient stratification. Finally, we outline emerging directions beyond canonical nodes, including modulation of the p53-MDM2/MDM4 axis, ferroptosis control through AIFM2/FSP1, and innate immune pathways such as CD47-SIRPa and the stimulator of interferon genes (STING). Overall, the field is shifting from single-target inhibition toward integrated strategies that combine precise molecular targeting with an understanding of signaling network dynamics, resistance evolution, and therapeutic vulnerabilities. - Source: PubMed
Publication date: 2026/04/03
Giercuszkiewicz-Haśnik KlaudiaMorak-Młodawska BeataJeleń Małgorzata