GOAT ANTI MOUSE IgM Alk. Phos.(HUMAN ADSORBED)

Price:
374 EUR
448 USD
310 GBP
known as: GOAT ANTI MOUSE IgM Alk. Phos.(HUMAN ADSORBED)
Catalog number: genta-ABS0026
Product Quantity: 0.8 mg
Category:
Supplier: AbD

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Gene target: alk phos adsorbed

Related genes to: GOAT ANTI MOUSE IgM Alk. Phos.(HUMAN ADSORBED)

Symbol : Alk NIH gene
chromosome : Un
description : anaplastic lymphoma receptor tyrosine kinase
type of gene : protein-coding
Other designations : ALK tyrosine kinase receptor
Modification date : 2016-02-20
Symbol : IGM NIH gene
description : IgM constant region
type of gene : other
Modification date : 2016-04-02
Symbol : phoS NIH gene
LocusTag : YE4201
Synonyms : pstS
description : phosphate ABC transporter substrate-binding protein
type of gene : protein-coding
Modification date : 2015-06-26

Related Pathways to: GOAT ANTI MOUSE IgM Alk. Phos.(HUMAN ADSORBED)

Gene about :ALK
Pathway :Hs Differentiation Pathway
ALK
Gene about :IgM
Pathway :Rn Inflammatory Response Pathway
IgM

Related product to: GOAT ANTI MOUSE IgM Alk. Phos.(HUMAN ADSORBED)

Related Articles about: GOAT ANTI MOUSE IgM Alk. Phos.(HUMAN ADSORBED)

Real-world first-line treatment and overall survival in non-small cell lung cancer without known EGFR mutations or ALK rearrangements in US community oncology setting.

To establish a baseline for care and overall survival (OS) based upon contemporary first-line treatments prescribed in the era before the introduction of immune checkpoint inhibitors, for people with metastatic non-small cell lung cancer (NSCLC) without common actionable mutations. - Source :PubMed

Specific IgM and Regulation of Antibody Responses.

Specific IgM, administered together with the antigen it recognizes, enhances primary antibody responses, formation of germinal centers, and priming for secondary antibody responses. The response to all epitopes on the antigen to which IgM binds is usually enhanced. IgM preferentially enhances responses to large antigens such as erythrocytes, malaria parasites, and keyhole limpet hemocyanine. In order for an effect to be seen, antigens must be administered in suboptimal concentrations and in close temporal relationship to the IgM. Enhancement is dependent on the ability of IgM to activate complement, but the lytic pathway is not required. Enhancement does not take place in mice lacking complement receptors 1 and 2 (CR1/2) suggesting that the role of IgM is to generate C3 split products, i.e., the ligands for CR1/2. In mice, these receptors are expressed on follicular dendritic cells (FDCs) and B cells. Optimal IgM-mediated enhancement requires that both cell types express CR1/2, but intermediate enhancement is seen when only FDCs express the receptors and low enhancement when only B cells express them. These observations imply that IgM-mediated enhancement works through several, non-mutually exclusive, pathways. Marginal zone B cells can transport IgM-antigen-complement complexes, bound to CR1/2, from the marginal zone and deposit them onto FDCs. In addition, co-crosslinking of the BCR and the CR2/CD19/CD81 co-receptor complex may enhance signaling to specific B cells, a mechanism likely to be involved in induction of early extrafollicular antibody responses. - Source :PubMed

ALK Fusion Detection in Circulating Free DNA: Finding an Important Needle in the Haystack.

- Source :PubMed

Clinicopathological characteristics of ROS1- and RET-rearranged NSCLC in caucasian patients. Data from a cohort of 713 non-squamous NSCLC lacking KRAS/EGFR/HER2/BRAF/PIK3CA/ALK alterations.

Targeted therapies have substantially changed the management of non-small cell lung cancer (NSCLC) patients with driver oncogenes. Given the high frequency, EGFR and ALK aberrations were the first to be detected and paved the way for tyrosine kinase inhibitor (TKI) treatments. Other kinases such as ROS1 and more recently RET have emerged as promising targets, and ROS1 and RET TKIs are already available for precision medicine.We screened a large cohort of 713 Caucasian non-squamous NSCLC patients lacking EGFR/KRAS/BRAF/HER2/PI3KCA/ALK aberrations for ROS1 and RET rearrangements using fluorescence in situ hybridization to determine the frequency and clinicopathological characteristics of ROS1- and RET-positive patients.Frequencies of ROS1 and RET rearrangements were 2.1% and 2.52%, respectively. Contrary to common belief, both ROS1 and RET rearrangements were detected in patients with a history of smoking, and the RET-positive patients were not younger than the negative patients. Moreover, RET but not ROS1 rearrangement was associated with the female gender. Nearly half of the ROS1-rearranged patients were successfully treated with ROS1 TKIs. In contrast, only 5/18 RET-positive patients received off-label RET TKIs. Two patients had stable disease, and three experienced disease progression. In addition to the 18 RET-positive cases, 10 showed isolated 5' signals. The clinical relevance is unknown but if the frequency is confirmed by other groups, the question whether these patients are eligible to TKIs will arise. More potent RET TKIs are under development and may improve the response rate in RET-positive patients. Therefore, we recommend the routine implementation of RET testing in non-squamous NSCLC patients, including those with a history of smoking. - Source :PubMed

Meta-analysis of incidence and risk of severe adverse events and fatal adverse events with crizotinib monotherapy in patients with ALK-positive NSCLC.

Numerous clinical trials show crizotinib has promising efficacy for anaplastic lymphoma kinase (ALK) positive non-small cell lung cancer (NSCLC) patients which trigger the substitution of traditional chemotherapy to be the current standard first-line treatment for these patients. Conversely, few reports systematically analyze toxicity of crizotinib. Hence, we performed a first meta-analysis to determine the risk of crizotinib-related severe adverse events (SAEs) and fatal adverse events (FAEs) in ALK positive NSCLC patients. - Source :PubMed

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