B-cell non-Hodgkin lymphomas (B-NHLs) represent a heterogeneous group of hematological malignancies, and the World Health Organization (WHO) classification of lymphoid malignancies has identified approximately 50 different clinical, pathological and Malignant lymphoproliferative disorders of B cell origin and genetic features. The most common of these are diffuse large B-cell lymphoma (DLBCL), follicular lymphoma, mucosa-associated lymphoid tissue lymphoma (MALT), small lymphocytic lymphoma/chronic lymphocytic leukemia (CLL), and mantle cell lymphoma (MCL) etc. At present, the first-line treatment regimen for B-NHLs is still the classic standard R-CHOP regimen.

Although the survival rate of B-NHLs patients after mature first-line standard treatment has increased compared with that before treatment, some patients still have disease progression or disease progression due to drug resistance.

Relapse leads to a poor prognosis. In recent years, with the continuous development of medical technology, targeted therapy drugs have shown more and more prominent effects. However, the development of excellent targeted drugs needs to be based on the profound molecular mechanism of B-NHLs.

Therefore, we provide an in vivo transfection system for B-NHLs-related genes for in-depth study of the molecular mechanism of B-NHLs.

Target Genes Delivered In Vivo in Non-hodgkin lymphoma B cell

Figure 1. Origin of Non Hodgkin B cell lymphomas and mechanisms related to their development. (Carlos Panizo, et al.; 2012)

BTK

BTK, a member of the Tec kinase family, is an essential enzyme in the regulation of downstream signaling pathways for the survival and proliferation of malignant B lymphocytes, and its activation plays an important role in many cellular processes. Therefore, inhibition of BTK activity will weaken the proliferation of malignant B lymphocytes, decrease the survival rate of tumor cells, and destroy the adhesion and migration of tumor cells to the microenvironment conducive to growth. Therefore, BTK is an important part of the mechanism of B-NHLs, and it is also worthy of further research.

PI3K / AKT / mTOR

The phosphatidylinositol 3-kinase (PI3K) family consists of serine/threonine and lipid kinases, which, along with downstream AKT (also known as protein kinase B) and mammalian target of rapamycin (mTOR), are in It plays an important role in various key processes such as cell growth, differentiation, metabolism, survival and cell proliferation, and has become one of the important targets of current cancer targeted therapy research. B cell receptor (BCR) is an important signaling pathway for B cell survival and one of the mechanisms for the activation of the physiological PI3K pathway. Relevant studies have shown that the abnormal activation of PI3K pathway has a competitive growth and survival advantage in the occurrence and development of B-cell lymphoma, and increases the metastasis ability and resistance of tumor cells to conventional therapy. Clinical trials of the efficacy of novel inhibitors of the drug in lymphoma patients are ongoing.

CD20

CD20 antigen is a phosphorylated protein molecule, which is expressed on the surface of all B lymphocytes except plasma cells and stem cells, and plays an important role in cell proliferation, differentiation, and ion transmembrane transport. Studies have found that CD20 antigen has the characteristics of non-internalization after targeted binding, not easy to fall off, and no free in serum, which is considered to be a research hotspot in the treatment of R/RB-NHL.

Bcl-2

Members of the Bcl-2 family of proteins regulate intrinsic apoptosis mainly through complex interactions between proteins and are critical for the survival of diffuse large B-cell lymphoma (DLBCL) cells. Therefore, Bcl-2 has also been used as a target for the treatment of R/R B-NHL.

In addition to the above genes, there are interesting non-hodgkin lymphoma B cell-related genes that need to be explored and studied. Therefore, there is a need for an in vivo transfection system that can precisely target non-hodgkin lymphoma B cell tissue and be taken up by tumor cells to function in vivo. The system can help researchers overcome various challenges encountered during in vivo transfection:

• Relevant molecular function studies can only be carried out in vitro, lacking important in vivo data
• Using in vitro transfection system for in vivo transfection, the transfection efficiency is very low;
• The in vivo transfection system used is not specific to non-hodgkin lymphoma B cell tissues and cells, and is toxic to the body;
• The in vivo transfection system used cannot penetrate the non-hodgkin lymphoma B cell tissue into the tumor tissue;
• The nucleic acid load of the in vivo transfection system is low, and it is difficult to achieve the expected effect;
• Etc…

Our Advantage:

• We can provide an in vivo transfection system for non-hodgkin lymphoma B cell tissues and cells to achieve efficient transfection
• Our system can target multiple targets at the same time, improving targeting accuracy
• The in vivo transfection system has low toxicity to the body and is safe to use
• In vivo transfection system vectors can protect nucleic acids from degradation during in vivo delivery
• Persistent knockout effect in experimental animals after a single injection
• The system load is high, and the transfection needs of different doses can be completed
• Professional design and service team to provide you with reliable service and technical support
• Timely feedback of technical reports

CD BioSciences specializes in developing transfection systems and customizing transfection reagents for gene transfection using our core technologies. With our high-quality products and services, your transfection results can be greatly improved. If you can't find a perfect in vivo transfection system, you can contact us. We can provide one-to-one personal customization service.

References

1. Nogai H, et al.; Pathogenesis of non-Hodgkin's lymphoma. J Clin Oncol. 2011, 29(14):1803-11.
2. Pal Singh S, et al.; Role of Bruton's tyrosine kinase in B cells and malignancies. Mol Cancer. 2018, 17(1):57.
3. Pongas G, Cheson BD. PI3K signaling pathway in normal B cells and indolent B-cell malignancies. Semin Oncol. 2016, 43(6):647-654.
4. Tomita A. Advances in antibody therapy for B cell lymphoma. Rinsho Ketsueki. 2020;61(8):901-911.
5. Warren CFA, et al.; BCL-2 family isoforms in apoptosis and cancer. Cell Death Dis. 2019, 10(3):177.
6. Carlos Panizo, et al.; Lymphoproliferative Disorders in Patients with Systemic Lupus Erythematosus. Systemic Lupus Erythematosus. 2012, SN: 978-953-51-0266-3.

* For research use only. Not for use in clinical diagnosis or treatment of humans or animals.