Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

Leica Biosystems 1ml NCL-L-MUM1

Supplier:  Leica Biosystems MUM1LCE

Encompass

Antigen Background The MUM-1 (multiple myeloma oncogene 1) gene was originally identified because of its involvement in the t(6:14) translocation observed in multiple myeloma, which causes the juxtaposition of the MUM-1 gene to the Ig heavy chain locus. MUM-1 is expressed in late plasma cell directed stages of B cell differentiation and in activated T cells, suggesting that MUM-1 may serve as a marker for lympho-hemopoietic neoplasms derived from these cells. The morphologic spectrum of MUM-1 expressing cells has been found to range from that of a centrocyte to that of a plasmablast/plasma cell. Consequently the histogenic value of MUM-1 may be to provide a marker to aid in the identification of the transition from BCL-6 positive (germinal center B cells) to CD138 positive (immunoblasts and plasma cells). Disclaimer Multiple Myeloma Oncogene 1 (MUM-1) is recommended for the detection of specific antigens of interest in normal and neoplastic tissues, as an adjunct to conventional hist

Catalog No. 50-255-2202


May include imposed supplier surcharges.
Only null left
Add to Cart
This item is not returnable. View return policy

Product Content Correction

The Fisher Scientific Encompass Program offers items which are not part of our distribution portfolio. These products typically do not have pictures or detailed descriptions. However, we are committed to improving your shopping experience. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Your feedback has been submitted: Thank you for helping us improve our website.