CALR antibody - C-terminal region (ARP30114_P050)
- Known as:
- CALR (anti-) - C-terminal region (ARP30114_P050)
- Catalog number:
- arp30114_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CALR antibody - C-terminal region (ARP30114_P050)
Related genes to: CALR antibody - C-terminal region (ARP30114_P050)
- Gene:
- CALR NIH gene
- Name:
- calreticulin
- Previous symbol:
- -
- Synonyms:
- RO, SSA, cC1qR, CRT, FLJ26680
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
Related products to: CALR antibody - C-terminal region (ARP30114_P050)
Related articles to: CALR antibody - C-terminal region (ARP30114_P050)
- Philadelphia-negative myeloproliferative neoplasms (MPNs) can progress to blast phase (MPN-BP), a biologically distinct and highly lethal entity with a median survival typically under six months. Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the only potentially curative approach, yet relapse and non-relapse mortality limit durable benefit. We retrospectively analyzed post-transplant outcomes in 51 consecutive adults undergoing 53 allo-HSCTs for MPN-BP. Median age was 62 years; most cases evolved from myelofibrosis, and JAK2 was the predominant driver mutation. Neutrophil engraftment occurred in all but two patients (median 12 days). At 1-year, cumulative incidences were 35.8% for grade II-IV acute GVHD, 7.5% for moderate-severe chronic GVHD, 44.3% for relapse, and 25.8% for non-relapse mortality. One-year overall survival (OS) and disease-free survival were 43.4% and 37.7%, respectively; relapse was the leading cause of death. In multivariable analysis, TP53 mutations and higher peripheral blast burden adversely affected OS, while CALR mutations appeared to be associated with improved OS, peripheral blasts also independently predicted relapse. These data underscore the cure rate of approximately one-third of MPN-BP and highlight peripheral blasts and TP53 as actionable risk markers for transplant strategies. - Source: PubMed
Publication date: 2026/04/16
Barbullushi KordeliaGagelmann NicoRathje KristinBadbaran AnitaRichter JohannaSchäfersküpper MathiasMarquard Franziska EMassoud RadwanKlyuchnikov EvgenySteiner NormannReichard MirjamRudolph InaHeidenreich SilkeNiederwieser ChristianLück CatherinaJanson DietlindeWolschke ChristineAyuk FrancisKröger Nicolaus - Deer antlers have the potential to contribute to a range of novel biomedical models. Although androgen is undoubtedly an undisputed prerequisite for pedicle initiation (initial stage of antler formation), the molecular mechanisms underlying androgen stimulation remain unclear. - Source: PubMed
Publication date: 2026/03/31
Liu ZhenLi XiongzhiGuo QianqianLi GuangyuSun HongmeiZou JiangbinXing BaoruiAkhtar Rana WaseemGuo YingyanZhao Haiping - Triple-negative breast cancer (TNBC) with bone metastasis is challenging to treat due to an immunosuppressive microenvironment and the limited, transient immune activation from conventional external beam radiotherapy. Inducing immunogenic cell death (ICD) offers a strategy to remodel this environment, but its systemic effects remain to be validated. Here, we investigate iodine-125 (I) brachytherapy as a method to induce sustained ICD and activate systemic antitumor immunity in TNBC bone metastasis using transcriptomic analysis, a dual-tumor model, and CALR-targeted molecular imaging. - Source: PubMed
Publication date: 2026/03/31
Li MinCui ZhenzhenYang JiaxinSun QiyuHu YanboShen JuanLi ZhihaoHan XiaoyangWang YixuanTang JiagengYu HengsongMa XiaowenWang Jing - Splanchnic vein thrombosis (SVT) is a rare, life-threatening condition that is often associated with cirrhosis, pancreatic malignancy and thrombophilia. Myeloproliferative neoplasms are under-recognised causes, posing diagnostic challenges. In this case, we present a male in his late 20s with a history of unprovoked pulmonary embolism and portal/splenic vein thrombosis, on indefinite anticoagulation therapy presenting 3 years later due to abdominal pain. Imaging revealed cirrhosis, cavernous transformation of the main portal vein and splenomegaly. These findings and a prior negative hypercoagulability workup prompted haematology consultation. Bone marrow biopsy confirmed primary myelofibrosis (PMF), demonstrating 90% cellularity, megakaryocytic hyperplasia, MF-3 fibrosis and calreticulin (CALR) mutation. This case underscores PMF as a treatable cause of SVT in young patients with recurrent thrombosis and highlights the consequences of diagnostic inertia, as marked thrombocytosis at initial presentation was overlooked. When Janus Kinase 2 (JAK2) is negative, CALR testing should be pursued to enable early diagnosis and targeted therapy. - Source: PubMed
Publication date: 2026/04/14
Abboud BrianTaha IsraShah ZiniyaShildt AllisonRischall ArielWheeler Joseph - Molecular monitoring of Philadelphia-negative myeloproliferative neoplasms (MPN) relies on genomic DNA (gDNA) from peripheral blood (PB). As variant allele frequency (VAF) reduction correlates with clinical outcomes, optimizing monitoring strategies has become important. However, whether gDNA accurately reflects bone marrow (BM) clonal dynamics and whether cell-free DNA (cfDNA) provides complementary information remains undefined. - Source: PubMed
Publication date: 2026/03/27
Ma XiaotongYang CanDuan YusiZhang HuixuanTang XuemeiZhang QingyunQin WenjiaoZhang WenhaoTang GushengGuan MingWu Zhiyuan