BIRC5 monoclonal antibody, clone 60.11
- Known as:
- BIRC5 mab (anti-), clonality 60.11
- Catalog number:
- MAB2366
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- BIRC5 monoclonal antibody clone 60.11
Related genes to: BIRC5 monoclonal antibody, clone 60.11
- Gene:
- BIRC5 NIH gene
- Name:
- baculoviral IAP repeat containing 5
- Previous symbol:
- API4
- Synonyms:
- EPR-1, survivin
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-04
Related products to: BIRC5 monoclonal antibody, clone 60.11
Related articles to: BIRC5 monoclonal antibody, clone 60.11
- Patients with advanced malignant adrenal tumors face poor prognoses with limited treatment options. Emerging data suggest that these rare tumors exhibit immunogenicity, potentially benefiting from intensified immunotherapy. - Source: PubMed
Publication date: 2026/07/06
Schultheiß ChristophBesemer BrendaWillscher EdithPaschold LisaMersceman TifannyTalpin AliceSerger ClaraZippelius AlfredBerruti AlfredoGrisanti SalvatoreMenke-van der Houven van Oordt Catharina WillemienBaudin EricLandwehr Laura-SophieCapdevila JaumeSubbiah VivekGranberg DanGedske Daugaard KirstenTriebig AlexandraGauduchon ThibaultDo Cao ChristineGarcia Marie-EveMagalhaes JoaoChêne LaurentBinder Mascha - Pulsed electromagnetic fields (PEMF) can be used to improve the efficacy of chemotherapeutic agents, such as doxorubicin (DOX). DOX induces mitotic slippage, leading to cell death in various cancers including breast cancer. Herein, we investigated whether PEMF exposure enhances DOX-induced mitotic slippage and subsequent cell death in breast cancer cells. - Source: PubMed
Woo Sung-HunLee Yong-HeumJung Byung ChulKim Yoon Suk - Adrenocortical carcinoma (ACC) is a rare but highly aggressive malignancy with limited treatment options. Anoikis plays a critical role in the progression of various cancers; however, its function in ACC remains unclear. - Source: PubMed
Publication date: 2026/06/11
Cao JuanXu MingZhou WenjunZhong ShuxiCao XiaoxuanXie HuipingShen Zhiming - Malignant rhabdoid tumor (MRT) is an aggressive pediatric cancer defined by biallelic loss of SMARCB1 and characterized by an unusually simple mutational landscape. Despite the absence of recurrent activating oncogenic mutations, MRT exhibits highly malignant behavior, creating a clinical paradox. Loss of SMARCB1 disrupts SWI/SNF-mediated chromatin organization, leading to enhancer redistribution and reorganization of transcriptional control. MRT therefore provides a defined model to examine how structural disruption of chromatin regulation sustains tumor maintenance in the absence of mutation-driven signaling activation. We propose that this epigenetic collapse reduces regulatory diversity and concentrates control of essential survival and cell-cycle programs within limited transcriptional nodes. We define this structural state as transcriptional bottleneck formation, in which tumor viability depends on concentrated transcriptional control rather than recurrent genetic alteration. Bottleneck nodes are characterized by enriched chromatin occupancy at survival and cell-cycle genes, limited compensatory regulation, and functional sensitivity to perturbation. In MRT, members of the RUNX family illustrate a representative concentrated transcriptional node linking chromatin reorganization to regulation of BIRC5 and related survival genes. This disease-focused perspective supports an architecture-centered therapeutic strategy aimed at disrupting concentrated transcriptional control. Identification of biomarkers reflecting this architectural state may facilitate selection of bottleneck-directed interventions in MRT. - Source: PubMed
Publication date: 2026/06/24
Masuda TatsuyaWatanabe TakayoshiOzaki ToshinoriKamikubo Yasuhiko - Despite significant progress achieved by combining VEGFR tyrosine-kinase inhibitors (TKIs) with immune checkpoint inhibitors (ICIs), complete responses remain rare in metastatic renal cell carcinoma (mRCC), highlighting the need for strategies that optimize therapeutic synergy. Here, we show that the efficacy of VEGFR blockade, vaccination, and PD-1 inhibition critically depends on treatment sequence. Using an orthotopic RENCA model, we show that short-term VEGFR inhibition with axitinib transiently remodels tumor vasculature, alleviates hypoxia, and limits suppressive myeloid subsets, thereby generating an immune-permissive window. Administering a survivin-based long-peptide vaccine (SVX) during this preconditioning phase elicits strong Th1-polarized CD4⁺ and cytotoxic CD8⁺ T-cell infiltration, which exhibit a polyfunctional cytokine and chemokine profile. When PD-1 blockade is introduced concomitantly with vaccination, after, rather than during, axitinib treatment, the triple regimen (axitinib + [SVX + anti-PD-1]) achieves durable tumor control with a high rate of complete responses, outperforming all other treatment schedules. Mechanistically, this sequence aligns vascular reprogramming, antigen-specific priming, and checkpoint release, converting an immune-excluded tumor into a T-cell-dominated, cytotoxic niche. Collectively, these findings identify temporal coordination as a critical determinant of therapeutic success and establish a mechanistically grounded framework for integrating vascular preconditionning, tumor-antigen vaccination, and PD-1 blockade as a curative immunotherapy strategy in renal carcinoma. - Source: PubMed
Publication date: 2026/06/24
Méjean FannyTran ThiMerabet MayaGey AlainMunoz AndyaraMorin BenjaminBal AliBourhis MorganeMabrouk NesrineTerme MagaliTartour EricTanchot Corinne