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Burkitt Lymphoma (BL)

Given the limitations of existing therapies, there is a critical need for the development of more effective and less toxic targeted therapeutics for Burkitt lymphoma (BL). At Protheragen, we focus on developing novel therapeutics and building accurate animal models to accelerate preclinical studies of potential therapies for BL. Our expertise ensures that your research receives the most reliable and relevant support, accelerating your drug development journey.

Overview of Burkitt Lymphoma (BL)

Burkitt lymphoma (BL) is a type of aggressive B-cell non-Hodgkin lymphoma (NHL) noted for the brisk multiplication of the malignant B cells. The following table shows the three subtypes of Burkitt lymphoma.

Subtypes Causes Characteristics
Endemic BL MYC translocation; ID3/TCF3 mutations; Epstein-Barr virus (EBV) infection High EBV viral load
Sporadic BL MYC translocation; TP53 mutations; EBV infection Rapid nodal/extranodal spread
Immunodeficiency-associated BL MYC translocation; BCL6 aberrations; EBV infection Lymph node/extranodal involvement

Pathogenesis of Burkitt Lymphoma (BL)

Burkitt lymphoma (BL) is caused by chromosomal translocations of the MYC oncogene, which results in overexpression of MYC, leading to cell cycle dysregulation and excessive B-cell proliferation. In endemic BL, the infection of Epstein-Barr virus (EBV) works in conjunction with MYC by inducing genomic instability and interfering with programmed cell death via proteins such as EBNA1 and LMP1.

Two classic models of the pathogenesis of Burkitt lymphoma.Fig.1 Two classic models of the pathogenesis of Burkitt lymphoma (BL). (Molina, Ester, et al., 2023)

Therapy Development for Burkitt Lymphoma (BL)

The Burkitt lymphoma (BL) therapeutics market was assessed at 1.2 billion USD in 2024, with projections to attain 2.5 billion USD by 2033. This market is anticipated to grow at a compound annual growth rate (CAGR) of 8.9% from 2026 to 2033, driven by growing disease prevalence and awareness.

Drug Names Mechanism of Action Targets NCT Number Research Phase
Rituximab Induces antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis CD20 NCT00118209 Approved
Doxorubicin Hydrochloride Liposome Intercalates DNA, inhibits topoisomerase II, generates free radicals DNA/Topoisomerase II NCT00392990 Phase II
Filgrastim Stimulates neutrophil production G-CSF receptor NCT00039130 Phase II
CPI-613 Inhibits mitochondrial metabolism and disrupts cancer cell energy production Mitochondrial enzymes NCT03793140 Phase II

Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.

Our Services

Protheragen leads the development of diagnostic and therapeutic solutions for Burkitt lymphoma (BL) and other lymphoproliferative disorders (LPDs). Our therapeutic development services focus on developing novel therapies that intricately target BL's root mechanisms. We develop and validate these therapeutics with specialized disease models to ensure they withstand the meticulous testing.

Services We Offer

Animal Model Development

Protheragen specializes in the development of genetically engineered models and xenograft models tailored for Burkitt lymphoma (BL) research.

  • MYC Transgenic Model
  • Patient-Derived Xenograft (PDX) Model (Cell lines include BL717, BL719, BL720, BL725, BL740, etc.)

At Protheragen, we strive to enable the creation of new therapeutics by offering extensive preclinical research services such as pharmacodynamics (PD), pharmacokinetic (PK) and toxicology studies. Our bespoke approaches sharpen the focus of your investigations and work toward maximizing the market potential of your drug candidates. If you are interested in our services, please feel free to contact usfor more details and quotation information of related services.

Reference

  • Molina, Ester, et al. "MYC directly transactivates CR2/CD21, the receptor of the Epstein–Barr virus, enhancing the viral infection of Burkitt lymphoma cells." Oncogene 42.45 (2023): 3358-3370.