MCID: BRK010
MIFTS: 63

Burkitt Lymphoma malady

Genetic diseases, Rare diseases, Cancer diseases, Blood diseases, Immune diseases categories

Aliases & Classifications for Burkitt Lymphoma

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Sources:
46OMIM, 30LifeMap Discovery®, 8Disease Ontology, 9diseasecard, 42NIH Rare Diseases, 10DISEASES, 44Novoseek, 48Orphanet, 22GTR, 32MedlinePlus, 61UMLS, 39NCIt, 33MeSH, 56SNOMED-CT, 27ICD9CM, 26ICD10 via Orphanet, 62UMLS via Orphanet, 34MESH via Orphanet, 25ICD10
See all sources

Aliases & Descriptions for Burkitt Lymphoma:

Name: Burkitt Lymphoma 46 8 9 42 44 48 30 61
Lymphoma 8 10 44 32 61
Burkitt's Lymphoma 30 8 42
Small Non-Cleaved Cell Lymphoma 42 48
Lymphoid Neoplasm 44 61
Burkitts Lymphoma 10 22
Small Non-Cleaved Cell Lymphoma, Burkitt's Type 8
 
Malignant Lymphoma, Burkitt's Type 8
Lymphoma, Small Noncleaved-Cell 61
Burkitt Lymphoma/leukaemia 8
Lymphoid Cancer 8
Burkitt's Tumor 8
Bl 42


Classifications:



Characteristics (Orphanet epidemiological data):

48
burkitt lymphoma:
Inheritance: Not applicable; Prevalence: 1-9/1000000 (Europe),1-5/10000 (Africa),1-9/1000000 (United States); Age of onset: All ages; Age of death: any age


External Ids:

OMIM46 113970
Disease Ontology8 DOID:8584, DOID:0060058
ICD9CM27 200.2
Orphanet48 543
ICD10 via Orphanet26 C83.7
UMLS via Orphanet62 C0006413, C0079770
MESH via Orphanet34 D002051, D008228
ICD1025 C83.7

Summaries for Burkitt Lymphoma

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MedlinePlus:32 Lymphoma is a cancer of a part of the immune system called the lymph system. there are many types of lymphoma. one type is hodgkin disease. the rest are called non-hodgkin lymphomas. non-hodgkin lymphomas begin when a type of white blood cell, called a t cell or b cell, becomes abnormal. the cell divides again and again, making more and more abnormal cells. these abnormal cells can spread to almost any other part of the body. most of the time, doctors don't know why a person gets non-hodgkin lymphoma. you are at increased risk if you have a weakened immune system or have certain types of infections. non-hodgkin lymphoma can cause many symptoms, such as swollen, painless lymph nodes in the neck, armpits or groin unexplained weight loss fever soaking night sweats coughing, trouble breathing or chest pain weakness and tiredness that don't go away pain, swelling or a feeling of fullness in the abdomen your doctor will diagnose lymphoma with a physical exam, blood tests, a chest x-ray, and a biopsy. treatments include chemotherapy, radiation therapy, targeted therapy, biological therapy, or therapy to remove proteins from the blood. targeted therapy uses substances that attack cancer cells without harming normal cells. biologic therapy boosts your body's own ability to fight cancer. if you don't have symptoms, you may not need treatment right away. this is called watchful waiting. nih: national cancer institute

MalaCards based summary: Burkitt Lymphoma, also known as lymphoma, is related to central nervous system lymphoma and intraocular lymphoma, and has symptoms including lymphoma An important gene associated with Burkitt Lymphoma is MYC (v-myc avian myelocytomatosis viral oncogene homolog), and among its related pathways are FoxO family signaling and Lymphocyte Signaling. The drugs cyclophosphamide and mitoxantrone and the compounds suberoylanilide hydroxamic acid and depsipeptide have been mentioned in the context of this disorder. Affiliated tissues include b cells, t cells and lymph node, and related mouse phenotypes are no phenotypic analysis and homeostasis/metabolism.

Disease Ontology:8 A mature b-cell neoplasm of b-cells found in the germinal center.

NIH Rare Diseases:42 Burkitt lymphoma (bl) is a rare, aggressive form of b-cell non-hodgkin's lymphoma, a type of cancer that affects the organs of the immune system. it is more common in males than females. three forms exist: one endemic to africa that is linked to the epstein barr virus (ebv); a sporadic form that develops mainly in the abdomen; and an immunodeficiency-associated form that occurs most commonly in individuals with hiv infection. bl can also develop in the ear, nose, throat and more rarely in other locations. signs and symptoms may differ depending on the form of bl and the organs or body systems affected. the exact cause of the condition is not known. treatment typically includes a few months of intensive chemotherapy; the current cure rate is estimated to be about 80-90%. last updated: 6/26/2012

OMIM:46 Burkitt lymphoma is a rare, aggressive B-cell lymphoma that accounts for 30 to 50% of lymphomas in children but only 1... (113970) more...

Related Diseases for Burkitt Lymphoma

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Diseases related to Burkitt Lymphoma via text searches within MalaCards or GeneCards Suite gene sharing:

(show top 50)    (show all 1207)
idRelated DiseaseScoreTop Affiliating Genes
1central nervous system lymphoma32.1BCL6
2intraocular lymphoma31.9CXCR5
3malt lymphoma31.8IGHM, CXCR5, BCL6
4primary effusion lymphoma31.7BCL6, TCL1A, MYC
5peripheral t-cell lymphoma31.6TCL1A, BCL6
6follicular lymphoma31.2AICDA, IGHM, MYC, TCL1A, CXCR5, BCL6
7chronic lymphocytic leukemia31.0AICDA, IGHM, TCL1A, BCL6
8hodgkin lymphoma30.9AICDA, IGHM, SH2D1A, MPP1, TCL1A, IL13RA2
9prolymphocytic leukemia30.7TCL1A, MYC
10b-cell lymphomas30.6AICDA, IGHM, MYC, TCL1A, CXCR5, BCL6
11central nervous system lymphoma, primary30.6BCL6, CXCR5, IGHM
12precursor b-cell acute lymphoblastic leukemia30.5CXCR5, MYC
13plasmacytoma30.4AICDA, MYC, CXCR5, BCL6
14agammaglobulinemia30.2SH2D1A, IGHM
15common variable immunodeficiency30.0SH2D1A, AICDA
16leukemia29.9AICDA, SH2D1A, MYC, TCL1A, CXCR5, BCL6
17lymphoma, non-hodgkin29.9AICDA, SH2D1A, MYC, TCL1A, CXCR5, BCL6
18hiv-129.8AICDA, IGHM, TCL1A, BCL6
19myeloma29.7IGHM, MYC, TCL1A, CXCR5, BCL6, BCL2L11
20ipex syndrome28.7AICDA, IGHM, SH2D1A, MPP1, CXCR5, BCL6
21mantle cell lymphoma11.2
22anaplastic large cell lymphoma11.2
23cutaneous t cell lymphoma11.1
24marginal zone b-cell lymphoma11.0
25gastric lymphoma11.0
26adult t-cell leukemia11.0
27angioimmunoblastic t-cell lymphoma10.9
28thyroiditis10.9
29mediastinitis10.9
30primary malignant lymphoma10.9
31intravascular large b-cell lymphoma10.8
32thyroid lymphoma10.8
33panniculitis10.8
34sarcoma10.8
35subcutaneous panniculitis-like t-cell lymphoma10.8
36cerebritis10.8
37breast lymphoma10.7
38enteropathy-associated t-cell lymphoma10.7
39nodular lymphocyte predominant hodgkin lymphoma10.7
40gastrointestinal lymphoma10.7
41primary mediastinal large b-cell lymphoma10.7
42mycosis fungoides10.7
43cerebral lymphoma10.7
44composite lymphoma10.7
45diffuse large b-cell lymphoma10.7
46alk-positive anaplastic large cell lymphoma10.7
47lymphomatoid papulosis10.7
48testicular lymphoma10.7
49hepatosplenic t-cell lymphoma10.7
50bone lymphoma10.6

Graphical network of the top 20 diseases related to Burkitt Lymphoma:



Diseases related to burkitt lymphoma

Symptoms for Burkitt Lymphoma

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Symptoms by clinical synopsis from OMIM:

113970

Clinical features from OMIM:

113970

HPO human phenotypes related to Burkitt Lymphoma:

id Description Frequency HPO Source Accession
1 lymphoma HP:0002665

Drugs & Therapeutics for Burkitt Lymphoma

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FDA approved drugs:

(show all 22)
id Drug Name Active Ingredient(s)13 Pharmaceutical Company Approval Date
1
Adcetris13 38 BRENTUXIMAB VEDOTIN Seattle Genetics Approved August 2011
FDA Label: Adcetris
Malady that Drug Treats: Hodgkin lymphoma and anaplastic large cell lymphoma
Indications and Usage:13 ADCETRIS is a CD30-directed antibody-drug conjugate indicated for; treatment of patients with:; Hodgkin lymphoma after failure of autologous stem cell transplant; (ASCT) or after failure of at least two prior multi-agent chemotherapy; regimens in patients who are not ASCT candidates (1.1).; Systemic anaplastic large cell lymphoma after failure of at least one; prior multi-agent chemotherapy regimen (1.2).; Accelerated approval was granted for the above indications based on; overall response rate. An improvement in patient-reported outcomes or; survival has not been established. Continued approval for these indications; may be contingent upon verification and description of clinical benefit in; confirmatory trials.
DrugBank Targets:11 Tumor necrosis factor receptor superfamily member 8
Mechanism of Action:13 
Target: microtubule
Action: disruptor
FDA: Brentuximab vedotin is an ADC. The antibody is a chimeric IgG1 directed against CD30. The; small molecule, MMAE, is a microtubule disrupting agent. MMAE is covalently attached to the; antibody via a linker. Nonclinical data suggest that the anticancer activity of ADCETRIS is due; to the binding of the ADC to CD30-expressing cells, followed by internalization of the; ADC-CD30 complex, and the release of MMAE via proteolytic cleavage. Binding of MMAE to; tubulin disrupts the microtubule network within the cell, subsequently inducing cell cycle arrest; and apoptotic death of the cells.
2
Arranon13 38 NELARABINE GlaxoSmithKline Approved October 2005
FDA Label: Arranon
Malady that Drug Treats: Lymphoblastic Leukemia
Indications and Usage:13 ARRANON is a nucleoside metabolic inhibitor indicated for the treatment of; patients with T-cell acute lymphoblastic leukemia and T-cell lymphoblastic; lymphoma whose disease has not responded to or has relapsed following; treatment with at least two chemotherapy regimens. This use is based on the; induction of complete responses. Randomized trials demonstrating increased; survival or other clinical benefit have not been conducted. (1)
DrugBank Targets:11 DNA
Mechanism of Action:13 
Target: DNA synthesis
Action: disruptor --> apoptosis
FDA: Nelarabine is a pro-drug of the deoxyguanosine analogue 9-²-D-arabinofuranosylguanine; 266 (ara-G), a nucleoside metabolic inhibitor. Nelarabine is demethylated by adenosine deaminase; 267 (ADA) to ara-G, mono-phosphorylated by deoxyguanosine kinase and deoxycytidine kinase, and; 268 subsequently converted to the active 5 -triphosphate, ara-GTP. Accumulation of ara-GTP in; 269 leukemic blasts allows for incorporation into deoxyribonucleic acid (DNA), leading to inhibition; 270 of DNA synthesis and cell death. Other mechanisms may contribute to the cytotoxic and; 271 systemic toxicity of nelarabine.
3
Beleodaq13 38 BELINOSTAT Spectrum Pharmaceuticals Approved July 2014
FDA Label: Beleodaq
Malady that Drug Treats: relapsed or refractory peripheral T-cell lymphoma
Indications and Usage:13 Beleodaq is a histone deacetylase inhibitor indicated for the treatment of; patients with relapsed or refractory peripheral T-cell lymphoma (PTCL). This; indication is approved under accelerated approval based on tumor response; rate and duration of response. An improvement in survival or disease-related; symptoms has not been established. Continued approval for this indication; may be contingent upon verification and description of clinical benefit in the; confirmatory trial. (1)
DrugBank Targets: no targets
Mechanism of Action:13 
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: Beleodaq is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from the; lysine residues of histones and some non-histone proteins. In vitro, belinostat caused the accumulation of; acetylated histones and other proteins, inducing cell cycle arrest and/or apoptosis of some transformed cells.; Belinostat shows preferential cytotoxicity towards tumor cells compared to normal cells. Belinostat inhibited; the enzymatic activity of histone deacetylases at nanomolar concentrations (<250 nM).
4
Bexxar13 38 TOSITUMOMAB; IODINE I 131 TOSITUMOMAB Corixa Approved June 2003
FDA Label: Bexxar
Malady that Drug Treats: Non-Hodgkin's Lymphoma
Indications and Usage:13 BEXXAR (tositumomab and Iodine I 131 tositumomab) is a CD20-directed; radiotherapeutic antibody indicated for the treatment of patients with CD20-; positive, relapsed or refractory, low-grade, follicular, or transformed nonHodgkin's; lymphoma who have progressed during or after rituximab therapy,; including patients with rituximab-refractory non-Hodgkin's lymphoma. (1.1); Determination of the effectiveness of the BEXXAR therapeutic regimen is; based on overall response rates in patients whose disease is refractory to; chemotherapy and rituximab. The effects of the BEXXAR therapeutic; regimen on survival are not known. (1.1); Important Limitation of Use BEXXAR therapeutic regimen is only indicated for a single course of; treatment and is not indicated for a first-line treatment. (1.2)
DrugBank Targets:11 1. B-lymphocyte antigen CD20; 2. Low affinity immunoglobulin gamma Fc region receptor III-B; 3. Complement C1r subcomponent; 4. Complement C1q subcomponent subunit A; 5. Complement C1q subcomponent subunit B; 6. Complement C1q subcomponent subunit C; 7. Low affinity immunoglobulin gamma Fc region receptor III-A; 8. High affinity immunoglobulin gamma Fc receptor I; 9. Low affinity immunoglobulin gamma Fc region receptor II-a; 10.Low affinity immunoglobulin gamma Fc region receptor II-b; 11. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:13 
Target: CD20
Action: cytotoxic antibody
FDA: Tositumomab binds specifically to an epitope within the extracellular domain of the; 586 CD20 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B lymphocytes; 587 to mature B lymphocytes) and on B-cell non-Hodgkin's lymphomas. The CD20 molecule is not; 588 shed from the cell surface and is not internalized following antibody binding. The BEXXAR; 589 therapeutic regimen induces cell death by emitting ionizing radiation to CD20-expressing; 590 lymphocytes or neighboring cells. In addition to cell death mediated by the radioisotope, other; 591 possible mechanisms of action include antibody-dependent cellular cytotoxicity, complement-; 592 dependent cytotoxicity, and CD20-mediated apoptosis.
5
Elitek13 38 RASBURICASE sanofi-aventis Approved October 2009
FDA Label: Elitek
Malady that Drug Treats: management of plasma uric acid levels in adults with malignancies
Indications and Usage:13 Elitek is a recombinant urate-oxidase indicated for initial management of; plasma uric acid levels in pediatric and adult patients with leukemia,; lymphoma, and solid tumor malignancies who are receiving anti-cancer; therapy expected to result in tumor lysis and subsequent elevation of plasma; uric acid (1).; Limitation of use: Elitek is indicated only for a single course of treatment (1).
DrugBank Targets:11 1. Uric acid
Mechanism of Action:13 
Target: uric acid
Action: converter to alantoin
FDA: In humans, uric acid is the final step in the catabolic pathway of purines. Rasburicase catalyzes; enzymatic oxidation of poorly soluble uric acid into an inactive and more soluble metabolite; (allantoin).
6
Elliotts B Solution13 CALCIUM CHLORIDE; DEXTROSE; MAGNESIUM SULFATE; POTASSIUM CHLORIDE; SODIUM BICARBONATE; SODIUM CHLORIDE; SODIUM PHOSPHATE, DIBAS Orphan Medical Approved October 1996
FDA Label: -
Malady that Drug Treats: meningeal leukemia or lymphocytic lymphoma
Indications and Usage:13 -
DrugBank Targets: -
Mechanism of Action:13 
Target: cerebrospinal fluid
Action: comparable in pH, electrolyte composition, glucose content, and osmolarity
FDA: -
7
Folotyn13 38 PRALATREXATE Allos Therapeutics Approved September 2009
FDA Label: Folotyn
Malady that Drug Treats: peripheral T-cell lymphoma
Indications and Usage:13 FOLOTYN is a folate analog metabolic inhibitor indicated for the treatment of; patients with relapsed or refractory peripheral T-cell lymphoma (PTCL). This; indication is based on overall response rate. Clinical benefit such as; improvement in progression-free survival or overall survival has not been; demonstrated. (1)
DrugBank Targets:11 1. Dihydrofolate reductase; 2. Thymidylate synthase
Mechanism of Action:13 
Target: dihydrofolate reductase
Action: inhibitor
FDA: Pralatrexate is a folate analog metabolic inhibitor that competitively inhibits dihydrofolate reductase. It is also a; competitive inhibitor for polyglutamylation by the enzyme folylpolyglutamyl synthetase. This inhibition results; in the depletion of thymidine and other biological molecules the synthesis of which depends on single carbon; transfer. ;
8
Imbruvica13 38 IBRUTINIB Pharmacyclics Approved November of 2013/Approved February 2014
FDA Label: Imbruvica
Malady that Drug Treats: mantle cell lymphoma/chronic lymphocytic leukemia
Indications and Usage:13 IMBRUVICA is a kinase inhibitor indicated for the treatment of patients with:; Mantle cell lymphoma (MCL) who have received at least one prior; therapy (1.1).; ; Accelerated approval was granted for this indication based on overall; ; response rate. Continued approval for this indication may be contingent; ; upon verification of clinical benefit in confirmatory trials.; ; Chronic lymphocytic leukemia (CLL) who have received at least one; prior therapy (1.2).; Chronic lymphocytic leukemia with 17p deletion (1.3).; Waldenström s macroglobulinemia (WM) (1.4).
DrugBank Targets:11 1. Tyrosine-protein kinase BTK
Mechanism of Action:13 
Target: Bruton's tyrosine kinase (Btk)
Action: selective inhibitor
FDA: Ibrutinib is a small-molecule inhibitor of BTK. Ibrutinib forms a covalent bond with a cysteine; residue in the BTK active site, leading to inhibition of BTK enzymatic activity. BTK is a; signaling molecule of the B-cell antigen receptor (BCR) and cytokine receptor pathways. BTK s; role in signaling through the B-cell surface receptors results in activation of pathways necessary; for B-cell trafficking, chemotaxis, and adhesion. Nonclinical studies show that ibrutinib inhibits; malignant B-cell proliferation and survival in vivo as well as cell migration and substrate; adhesion in vitro.
9
Intron A13 38 INTERFERON ALFA-2B Schering-Plough Approved December 1997/ Approved December 1995/ Approved March 1997
FDA Label: Intron A
Malady that Drug Treats: non-Hodgkin's lymphoma/ malignant melanoma / Hepatitis C
Indications and Usage:13 Hairy Cell Leukemia INTRON® A is indicated for the treatment of patients 18 years of; age or older with hairy cell leukemia.; Malignant Melanoma INTRON A is indicated as adjuvant to surgical treatment in; patients 18 years of age or older with malignant melanoma who are free of disease but; at high risk for systemic recurrence, within 56 days of surgery.; Follicular Lymphoma INTRON A is indicated for the initial treatment of clinically; aggressive (see Clinical Pharmacology) follicular Non-Hodgkin s Lymphoma in; conjunction with anthracycline-containing combination chemotherapy in patients 18; years of age or older. Efficacy of INTRON A therapy in patients with low-grade, lowtumor; burden follicular Non-Hodgkin s Lymphoma has not been demonstrated.; Condylomata Acuminata INTRON A is indicated for intralesional treatment of selected; patients 18 years of age or older with condylomata acuminata involving external; surfaces of the genital and perianal areas (see DOSAGE AND ADMINISTRATION).; The use of this product in adolescents has not been studied.; AIDS-Related Kaposi's Sarcoma INTRON A is indicated for the treatment of selected; patients 18 years of age or older with AIDS-Related Kaposi's Sarcoma. The likelihood; of response to INTRON A therapy is greater in patients who are without systemic symptoms, who have limited lymphadenopathy and who have a relatively intact immune; system as indicated by total CD4 count.; Chronic Hepatitis C INTRON A is indicated for the treatment of chronic hepatitis C in; patients 18 years of age or older with compensated liver disease who have a history of; blood or blood-product exposure and/or are HCV antibody positive. Studies in these; patients demonstrated that INTRON A therapy can produce clinically meaningful effects; on this disease, manifested by normalization of serum alanine aminotransferase (ALT); and reduction in liver necrosis and degeneration.; A liver biopsy should be performed to establish the diagnosis of chronic hepatitis.; Patients should be tested for the presence of antibody to HCV. Patients with other; causes of chronic hepatitis, including autoimmune hepatitis, should be excluded. Prior; to initiation of INTRON A therapy, the physician should establish that the patient has; compensated liver disease. The following patient entrance criteria for compensated liver; disease were used in the clinical studies and should be considered before INTRON A; treatment of patients with chronic hepatitis C:; No history of hepatic encephalopathy, variceal bleeding, ascites, or other; clinical signs of decompensation; Bilirubin Less than or equal to 2 mg/dL; Albumin Stable and within normal limits; Prothrombin Time Less than 3 seconds prolonged; WBC Greater than or equal to 3000/mm3; Platelets Greater than or equal to 70,000/mm3; Serum creatinine should be normal or near normal.; Prior to initiation of INTRON A therapy, CBC and platelet counts should be; evaluated in order to establish baselines for monitoring potential toxicity. These tests; should be repeated at Weeks 1 and 2 following initiation of INTRON A therapy, and; monthly thereafter. Serum ALT should be evaluated at approximately 3-month intervals; to assess response to treatment (see DOSAGE AND ADMINISTRATION).; Patients with preexisting thyroid abnormalities may be treated if thyroidstimulating; hormone (TSH) levels can be maintained in the normal range by medication.; TSH levels must be within normal limits upon initiation of INTRON A treatment and TSH; testing should be repeated at 3 and 6 months (see PRECAUTIONS, Laboratory; Tests).; INTRON A in combination with REBETOL® is indicated for the treatment of; chronic hepatitis C in patients 3 years of age and older with compensated liver disease; previously untreated with alpha interferon therapy and in patients 18 years of age and; older who have relapsed following alpha interferon therapy. See REBETOL prescribing; information for additional information. Chronic Hepatitis B INTRON A is indicated for the treatment of chronic hepatitis B in; patients 1 year of age or older with compensated liver disease. Patients who have been; serum HBsAg positive for at least 6 months and have evidence of HBV replication; (serum HBeAg positive) with elevated serum ALT are candidates for treatment. Studies; in these patients demonstrated that INTRON A therapy can produce virologic remission; of this disease (loss of serum HBeAg) and normalization of serum aminotransferases.; INTRON A therapy resulted in the loss of serum HBsAg in some responding patients.; Prior to initiation of INTRON A therapy, it is recommended that a liver biopsy be; performed to establish the presence of chronic hepatitis and the extent of liver damage.; The physician should establish that the patient has compensated liver disease. The; following patient entrance criteria for compensated liver disease were used in the; clinical studies and should be considered before INTRON A treatment of patients with; chronic hepatitis B:; No history of hepatic encephalopathy, variceal bleeding, ascites, or other; signs of clinical decompensation; Bilirubin Normal; Albumin Stable and within normal limits; Prothrombin Time Adults less than 3 seconds prolonged; Pediatrics less than or equal to 2 seconds prolonged; WBC Greater than or equal to 4000/mm3; Platelets Adults greater than or equal to 100,000/mm3; Pediatrics greater than or equal to 150,000/mm3; Patients with causes of chronic hepatitis other than chronic hepatitis B or chronic; hepatitis C should not be treated with INTRON A. CBC and platelet counts should be; evaluated prior to initiation of INTRON A therapy in order to establish baselines for; monitoring potential toxicity. These tests should be repeated at treatment Weeks 1, 2,; 4, 8, 12, and 16. Liver function tests, including serum ALT, albumin, and bilirubin,; should be evaluated at treatment Weeks 1, 2, 4, 8, 12, and 16. HBeAg, HBsAg, and; ALT should be evaluated at the end of therapy, as well as 3- and 6-months posttherapy,; since patients may become virologic responders during the 6-month period; following the end of treatment. In clinical studies in adults, 39% (15/38) of responding; patients lost HBeAg 1 to 6 months following the end of INTRON A therapy. Of; responding patients who lost HBsAg, 58% (7/12) did so 1 to 6 months post-treatment.; A transient increase in ALT greater than or equal to 2 times baseline value (flare); can occur during INTRON A therapy for chronic hepatitis B. In clinical trials in adults; and pediatrics, this flare generally occurred 8 to 12 weeks after initiation of therapy and; was more frequent in responders (adults 63%, 24/38; pediatrics 59%, 10/17) than in; nonresponders (adults 27%, 13/48; pediatrics 35%, 19/55). However, in adults and; pediatrics, elevations in bilirubin greater than or equal to 3 mg/dL (greater than or equal; to 2 times ULN) occurred infrequently (adults 2%, 2/86; pediatrics 3%, 2/72) during; therapy. When ALT flare occurs, in general, INTRON A therapy should be continued unless signs and symptoms of liver failure are observed. During ALT flare, clinical; symptomatology and liver function tests including ALT, prothrombin time, alkaline; phosphatase, albumin, and bilirubin, should be monitored at approximately 2-week; intervals (see WARNINGS).
DrugBank Targets:11 1. Interferon alpha/beta receptor 2; 2. Interferon alpha/beta receptor 1
Mechanism of Action:13 
Target: intracellular oncogene expression, natural killer and cytotoxic T-cells, microphage, cytokine production
Action: stimulation, induction (unspecified effects on oncogene expression)
FDA: -
10
Istodax13 38 ROMIDEPSIN Gloucester Pharmaceuticals Approved November 2009
FDA Label: Istodax
Malady that Drug Treats: cutaneous T-cell lymphoma
Indications and Usage:13 ISTODAX is a histone deacetylase (HDAC) inhibitor indicated for:; Treatment of cutaneous T-cell lymphoma (CTCL) in patients who have; received at least one prior systemic therapy (1).; Treatment of peripheral T-cell lymphoma (PTCL) in patients who have; received at least one prior therapy (1).; These indications are based on response rate. Clinical benefit such as; improvement in overall survival has not been demonstrated (1).
DrugBank Targets:11 -
Mechanism of Action:13 
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: Romidepsin is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from acetylated lysine residues in histones, resulting in the; modulation of gene expression. HDACs also deacetylate non-histone proteins, such as transcription factors. In vitro, romidepsin causes the accumulation of acetylated; histones, and induces cell cycle arrest and apoptosis of some cancer cell lines with IC50 values in the nanomolar range. The mechanism of the antineoplastic effect of; romidepsin observed in nonclinical and clinical studies has not been fully characterized.
11
Mozobil13 38 PLERIXAFOR Genzyme Approved December 2008
FDA Label: Mozobil
Malady that Drug Treats: non-Hodgkin s lymphoma and multiple myeloma
Indications and Usage:13 Mozobil, a hematopoietic stem cell mobilizer, is indicated in combination; with granulocyte-colony stimulating factor (G-CSF) to mobilize; hematopoietic stem cells (HSCs) to the peripheral blood for collection and; subsequent autologous transplantation in patients with non-Hodgkin s; lymphoma and multiple myeloma. (1)
DrugBank Targets:11 1. C-X-C chemokine receptor type 4
Mechanism of Action:13 
Target: hematopoietic stem cell/ CXCR4 chemokine receptor
Action: monilizer/ inhibitor
FDA: Plerixafor is an inhibitor of the CXCR4 chemokine receptor and blocks binding of its cognate; ligand, stromal cell-derived factor-1± (SDF-1±). SDF-1± and CXCR4 are recognized to play a; role in the trafficking and homing of human hematopoietic stem cells (HSCs) to the marrow; compartment. Once in the marrow, stem cell CXCR4 can act to help anchor these cells to the; marrow matrix, either directly via SDF-1± or through the induction of other adhesion molecules.; Treatment with plerixafor resulted in leukocytosis and elevations in circulating hematopoietic; progenitor cells in mice, dogs and humans. CD34+ cells mobilized by plerixafor were capable of; engraftment with long-term repopulating capacity up to one year in canine transplantation; models.
12
Revlimid13 38 LENALIDOMIDE Celgene Approved June 2013
FDA Label: Revlimid
Malady that Drug Treats: mantle cell lymphoma
Indications and Usage:13 REVLIMID is a thalidomide analogue indicated for the treatment of patients; with:; Multiple myeloma (MM), in combination with dexamethasone (1.1).; Transfusion-dependent anemia due to low- or intermediate-1-risk; myelodysplastic syndromes (MDS) associated with a deletion 5q; abnormality with or without additional cytogenetic abnormalities (1.2).; Mantle cell lymphoma (MCL) whose disease has relapsed or progressed; after two prior therapies, one of which included bortezomib (1.3).; Limitations of Use:; REVLIMID is not indicated and is not recommended for the treatment; of patients with chronic lymphocytic leukemia (CLL) outside of; controlled clinical trials (1.4).
DrugBank Targets:11 1. Protein cereblon; 2. Tumor necrosis factor ligand superfamily member 11; 3. Cadherin-5; 4. Prostaglandin G/H synthase 2
Mechanism of Action:13 
Target: T cells and natural killer cells/ pro-inflammatory cytokines by monocytes
Action: activator/inhibitor
FDA: Lenalidomide is an analogue of thalidomide with immunomodulatory, antiangiogenic, and antineoplastic properties. Lenalidomide inhibits; proliferation and induces apoptosis of certain hematopoietic tumor cells including multiple myeloma, mantle cell lymphoma, and del (5q); myelodysplastic syndromes in vitro. Lenalidomide causes a delay in tumor growth in some in vivo nonclinical hematopoietic tumor models; including multiple myeloma. Immunomodulatory properties of lenalidomide include activation of T cells and natural killer (NK) cells, increased; numbers of NKT cells, and inhibition of pro-inflammatory cytokines (e.g., TNF-± and IL-6) by monocytes. In multiple myeloma cells, the; combination of lenalidomide and dexamethasone synergizes the inhibition of cell proliferation and the induction of apoptosis.
13
Rituxan13 38 RITUXIMAB Biogen IDEC, Genentech Approved November 1997
FDA Label: Rituxan
Malady that Drug Treats: non-hodgkin's lymphoma
Indications and Usage:13 Rituxan® (rituximab) is a CD20-directed cytolytic antibody indicated for the; treatment of patients with:; Non-Hodgkin s Lymphoma (NHL) (1.1); Chronic Lymphocytic Leukemia (CLL) (1.2); Rheumatoid Arthritis (RA) in combination with methotrexate in adult; patients with moderately-to severely-active RA who have inadequate; response to one or more TNF antagonist therapies (1.3); Granulomatosis with Polyangiitis (GPA) (Wegener s Granulomatosis) and; Microscopic Polyangiitis (MPA) in adult patients in combination with; glucocorticoids (1.4); Limitations of Use: Rituxan is not recommended for use in patients with; severe, active infections (1.5).
DrugBank Targets:11 1. Low affinity immunoglobulin gamma Fc region receptor III-B; 2. Complement C1r subcomponent; 3. Complement C1q subcomponent subunit A; 4. Complement C1q subcomponent subunit B; 5. Complement C1q subcomponent subunit C; 6. Low affinity immunoglobulin gamma Fc region receptor III-A; 7. Complement C1s subcomponent; 8. High affinity immunoglobulin gamma Fc receptor I; 9. Low affinity immunoglobulin gamma Fc region receptor II-a; 10. Low affinity immunoglobulin gamma Fc region receptor II-b; 11. Low affinity immunoglobulin gamma Fc region receptor II-c; 12. B-lymphocyte antigen CD20
Mechanism of Action:13 
Target: CD20 antigen expressed on the surface of; pre-B and mature B-lymphocytes
Action: mediator of B-cell lysis through different possible types of cytotoxicity
FDA: Rituximab is a monoclonal antibody that targets the CD20 antigen expressed on the surface of; pre-B and mature B-lymphocytes. Upon binding to CD20, rituximab mediates B-cell lysis. Possible; mechanisms of cell lysis include complement dependent cytotoxicity (CDC) and antibody dependent; cell mediated cytotoxicity (ADCC). The antibody induced apoptosis in the DHL 4 human B cell; lymphoma cell line.; B cells are believed to play a role in the pathogenesis of rheumatoid arthritis (RA) and associated; chronic synovitis. In this setting, B cells may be acting at multiple sites in the; autoimmune/inflammatory process, including through production of rheumatoid factor (RF) and; other autoantibodies, antigen presentation, T-cell activation, and/or proinflammatory cytokine; production.
14
Targretin13 38 bexarotene VALEANT LUXEMBOURG 12/29/1999
FDA Label: Targretin
Malady that Drug Treats: cutaneous T-cell lymphoma
Indications and Usage:13 TARGRETIN (bexarotene) is a retinoid indicated for the treatment of; cutaneous manifestations of cutaneous T-cell lymphoma in patients who are; refractory to at least one prior systemic therapy. (1)
DrugBank Targets:11 1. Retinoic acid receptor RXR-alpha; 2. Retinoic acid receptor RXR-beta; 3. Retinoic acid receptor RXR-gamma
Mechanism of Action:13 
Target: retinoid X receptor subtypes (RXRalpha, RXRbeta, RXRgama)
Action: activator
FDA: Bexarotene selectively binds and activates retinoid X receptor subtypes (RXRað, RXRbð, RXRgð).; RXRs can form heterodimers with various receptor partners such as retinoic acid receptors (RARs),; vitamin D receptor, thyroid receptor, and peroxisome proliferator activator receptors (PPARs). Once; activated, these receptors function as transcription factors that regulate the expression of genes that; control cellular differentiation and proliferation. Bexarotene inhibits the growth in vitro of some; tumor cell lines of hematopoietic and squamous cell origin. It also induces tumor regression in vivo; in some animal models. The exact mechanism of action of bexarotene in the treatment of cutaneous; T-cell lymphoma (CTCL) is unknown.
15
Treanda13 38 BENDAMUSTINE HYDROCHLORIDE Cephalon Approved October 2008
FDA Label: Treanda
Malady that Drug Treats: Chronic lymphocytic leukemia and B-cell non-Hodgkin s lymphoma
Indications and Usage:13 TREANDA is an alkylating drug indicated for treatment of patients with:; Chronic lymphocytic leukemia (CLL). Efficacy relative to first line; therapies other than chlorambucil has not been established. (1.1); Indolent B-cell non-Hodgkin lymphoma (NHL) that has progressed during; or within six months of treatment with rituximab or a rituximab-containing; regimen. (1.2)
DrugBank Targets: -
Mechanism of Action:13 
Target: -
Action: -
FDA: Bendamustine is a bifunctional mechlorethamine derivative containing a purine-like benzimidazole ring.; Mechlorethamine and its derivatives form electrophilic alkyl groups. These groups form covalent bonds with electronrich; nucleophilic moieties, resulting in interstrand DNA crosslinks. The bifunctional covalent linkage can lead to cell; death via several pathways. Bendamustine is active against both quiescent and dividing cells. The exact mechanism of; action of bendamustine remains unknown.
16
UVADEX13 METHOXSALEN Therakos Approved February 1999
FDA Label: UVADEX
Malady that Drug Treats: skin manifestations of cutaneous T-cell lymphoma (CTCL)
Indications and Usage:13 UVADEX"! (methoxsalen) Sterile Solution is indicated for extracorporeal administration with; the UVAR"! XTS"! or THERAKOS"! CELLEX"! Photopheresis System in the palliative; treatment of the skin manifestations of Cutaneous T-Cell Lymphoma (CTCL) that is; unresponsive to other forms of treatment. ;
DrugBank Targets:11 1. DNA
Mechanism of Action:13 
Target: DNA
Action: inhibitor of DNA synthesis, cell division, and epidermal turnover
FDA: The exact mechanism of action of methoxsalen is not known. The best-known biochemical; reaction of methoxsalen is with DNA. Methoxsalen, upon photoactivation, conjugates and forms; covalent bonds with DNA which leads to the formation of both monofunctional (addition to a; single strand of DNA) and bifunctional adducts (crosslinking of psoralen to both strands of; DNA). Reactions with proteins have also been described. The formation of photoadducts results; in inhibition of DNA synthesis, cell division and epidermal turnover.; For the palliative treatment of Cutaneous T-Cell Lymphoma, Photopheresis consists of removing; a portion of the patient's blood and separating the red blood cells from the white cell layer (buffy; coat) by centrifugation. The red cells are returned to the patient and the UVADEX"! Sterile; Solution is then injected into the instrument and mixed with the buffy coat. The instrument then; irradiates this drug-cell mixture with ultraviolet light (UVA light, 320-400 nm) and returns the; treated cells to the patient. See the appropriate Operator's Manual for details of this process.; Although extracorporeal phototherapy exposes less than 10% of the total body burden of; malignant cells to methoxsalen plus light, some patients achieve a complete response. Animal; studies suggest that the photopheresis may activate an immune-mediated response against the; malignant T-cells.; Use of the UVAR"! and UVAR"! XTS"! Systems after oral administration of methoxsalen; were previously approved for the treatment of Cutaneous T-Cell Lymphoma. Interpatient; variability in peak plasma concentration after an oral dose of methoxsalen ranges from 6 to 15; fold. UVADEX"! is injected directly into the separated buffy coat in the instrument in an; attempt to diminish this interpatient variability and to improve the exposure of the cells to the; drug.; Methoxsalen is reversibly bound to serum albumin and is also preferentially taken up by; epidermal cells. Methoxsalen is rapidly metabolized in humans, with approximately 95% of the; drug excreted as metabolites in the urine within 24 hours.; Systemic administration of methoxsalen followed by UVA exposure leads to cell injury. The; most obvious manifestation of this injury after skin exposure is delayed erythema, which may; not begin for several hours and peaks at 48-72 hours. The inflammation is followed over several; days to weeks, by repair which is manifested by increased melanization of the epidermis and; thickening of the stratum corneum.; The total dose of methoxsalen delivered in UVADEX"! is substantially lower (approximately; 200 times) than that used with oral administration. More than 80% of blood samples collected; 30 minutes after reinfusion of the photoactivated buffy coat had methoxsalen levels below; detection limits of the assay (<10 ng/ml), and the mean plasma methoxsalen concentration was; approximately 25 ng/ml.
17
Valchlor13 MECHLORETHAMINE HYDROCHLORIDE Ceptaris Therapeutics Approved August 2013
FDA Label: Valchlor
Malady that Drug Treats: Stage IA/IB mycosisfungoides-type cutaneous T-cell lymphoma
Indications and Usage:13 VALCHLOR is an alkylating drug indicated for the topical treatment; of Stage IA and IB mycosis fungoides type cutaneous T cell; lymphoma in patients who have received prior skin directed therapy; (1).  
DrugBank Targets:11 1. DNA
Mechanism of Action:13 
Target: rapidly-proliferating cells
Action: inhibitor
FDA: Mechlorethamine, also known as nitrogen mustard, is an alkylating agent which inhibits rapidly proliferating cells.
18
Velcade13 38 BORTEZOMIB Millennium Pharmaceuticals Approved May 2003
FDA Label: Velcade
Malady that Drug Treats: Multiple Myeloma
Indications and Usage:13 VELCADE is a proteasome inhibitor indicated for:; treatment of patients with multiple myeloma (1.1); treatment of patients with mantle cell lymphoma (1.2)
DrugBank Targets:11 1. 26S proteasome non-ATPase regulatory subunit 2; 2. 26S proteasome non-ATPase regulatory subunit 1; 3. Proteasome subunit beta type-1; 4. Proteasome subunit beta type-5; 5. Proteasome subunit beta type-2
Mechanism of Action:13 
Target: 26S proteasome
Action: reversible inhibitor of chymotrypsin-like activity
FDA: Bortezomib is a reversible inhibitor of the chymotrypsin-like activity of the 26S proteasome in mammalian; cells. The 26S proteasome is a large protein complex that degrades ubiquitinated proteins. The ubiquitinproteasome; pathway plays an essential role in regulating the intracellular concentration of specific proteins,; thereby maintaining homeostasis within cells. Inhibition of the 26S proteasome prevents this targeted; proteolysis, which can affect multiple signaling cascades within the cell. This disruption of normal homeostatic; mechanisms can lead to cell death. Experiments have demonstrated that bortezomib is cytotoxic to a variety of; cancer cell types in vitro. Bortezomib causes a delay in tumor growth in vivo in nonclinical tumor models,; including multiple myeloma.
19
Xalkori13 38 CRIZOTINIB Pfizer Approved August of 2011
FDA Label: Xalkori
Malady that Drug Treats: ALK+ non-small cell lung cancer
Indications and Usage:13 XALKORI is a kinase inhibitor indicated for the treatment of patients with ; metastatic non-small cell lung cancer (NSCLC) whose tumors are anaplastic; lymphoma kinase (ALK)-positive as detected by an FDA-approved test. (1)
DrugBank Targets:11 1. ALK tyrosine kinase receptor; 2. Hepatocyte growth factor receptor
Mechanism of Action:13 
Target: receptor tyrosine kinases
Action: inhibitor
FDA: Crizotinib is an inhibitor of receptor tyrosine kinases including ALK, Hepatocyte Growth Factor Receptor; (HGFR, c-Met), ROS1 (c-ros), and Recepteur d Origine Nantais (RON). Translocations can affect the ALK; gene resulting in the expression of oncogenic fusion proteins. The formation of ALK fusion proteins results in; activation and dysregulation of the gene s expression and signaling which can contribute to increased cell; proliferation and survival in tumors expressing these proteins. Crizotinib demonstrated concentration-dependent; inhibition of ALK, ROS1, and c-Met phosphorylation in cell-based assays using tumor cell lines and; demonstrated antitumor activity in mice bearing tumor xenografts that expressed EML4- or NPM-ALK fusion; proteins or c-Met.
20
Zevalin13 38 IBRITUMOMAB TIUXETAN Biogen IDEC Approved February 2002
FDA Label: Zevalin
Malady that Drug Treats: Non-Hodgkin's lymphoma
Indications and Usage:13 Zevalin is a CD20-directed radiotherapeutic antibody administered as part of; the Zevalin therapeutic regimen indicated for the treatment of patients with:; relapsed or refractory, low-grade or follicular B-cell non-Hodgkin's; lymphoma (NHL) (1.1).; previously untreated follicular NHL who achieve a partial or complete; response to first-line chemotherapy (1.2). ;
DrugBank Targets:11 1. B-lymphocyte antigen CD20; 2. Low affinity immunoglobulin gamma Fc region receptor III-B; 3. Complement C1r subcomponent; 4. Complement C1q subcomponent subunit A; 5. Complement C1q subcomponent subunit B; 6. Complement C1q subcomponent subunit C; 7. Low affinity immunoglobulin gamma Fc region receptor III-A; 8. Complement C1s subcomponent; 9. High affinity immunoglobulin gamma Fc receptor I; 10. Low affinity immunoglobulin gamma Fc region receptor II-a; 11. Low affinity immunoglobulin gamma Fc region receptor II-b; 12. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:13 
Target: CD20 antigen --> Y-90
Action: beta emission causes damage
FDA: Ibritumomab tiuxetan binds specifically to the CD20 antigen (human B-lymphocyte-restricted differentiation antigen,; Bp35). The apparent affinity (KD) of ibritumomab tiuxetan for the CD20 antigen ranges between approximately 14 to; 18 nM. The CD20 antigen is expressed on pre-B and mature B lymphocytes and on > 90% of B-cell non-Hodgkin s; lymphomas (NHL). The CD20 antigen is not shed from the cell surface and does not internalize upon antibody binding.; The chelate tiuxetan, which tightly binds Y-90, is covalently linked to ibritumomab. The beta emission from Y-90; induces cellular damage by the formation of free radicals in the target and neighboring cells.; Ibritumomab tiuxetan binding was observed in vitro on lymphoid cells of the bone marrow, lymph node, thymus, red and; white pulp of the spleen, and lymphoid follicles of the tonsil, as well as lymphoid nodules of other organs such as the; large and small intestines.
21
Zydelig13 38 IDELALISIB Gilead Approved July 2014
FDA Label: Zydelig
Malady that Drug Treats: relapsed CLL, follicular B-cell NHL and small lymphocytic lymphoma
Indications and Usage:13 Zydelig is a kinase inhibitor indicated for the treatment of patients with:; Relapsed chronic lymphocytic leukemia (CLL), in combination with; rituximab, in patients for whom rituximab alone would be considered; appropriate therapy due to other co-morbidities. (1.1); Relapsed follicular B-cell non-Hodgkin lymphoma (FL) in patients; who have received at least two prior systemic therapies. (1.2); Relapsed small lymphocytic lymphoma (SLL) in patients who have; received at least two prior systemic therapies. (1.3); Accelerated approval was granted for FL and SLL based on overall; response rate. Improvement in patient survival or disease related; symptoms has not been established. Continued approval for these; indications may be contingent upon verification of clinical benefit in; confirmatory trials.
DrugBank Targets:11 1. Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta isoform (P110´)
Mechanism of Action:13 
Target: PI3K´ kinase
Action: inhibitor
FDA: Idelalisib is an inhibitor of PI3K´ kinase, which is expressed in normal and malignant Bcells.; Idelalisib induced apoptosis and inhibited proliferation in cell lines derived from; malignant B-cells and in primary tumor cells. Idelalisib inhibits several cell signaling; pathways, including B-cell receptor (BCR) signaling and the CXCR4 and CXCR5; signaling, which are involved in trafficking and homing of B-cells to the lymph nodes and; bone marrow. Treatment of lymphoma cells with idelalisib resulted in inhibition of; chemotaxis and adhesion, and reduced cell viability.
22
Zykadia13 38 CERITINIB Novartis Approved April 2014
FDA Label: Zykadia
Malady that Drug Treats: ALK+ metastatic non-small cell lung cancer
Indications and Usage:13 ZYKADIA is a kinase inhibitor indicated for the treatment of patients with; anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung; cancer (NSCLC) who have progressed on or are intolerant to crizotinib. This; indication is approved under accelerated approval based on tumor response; rate and duration of response. An improvement in survival or disease-related; symptoms has not been established. Continued approval for this indication; may be contingent upon verification and description of clinical benefit in; confirmatory trials. (1)
DrugBank Targets:11 1. ALK tyrosine kinase receptor
Mechanism of Action:13 
Target: ALK, insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1
Action: kinase inhibitor
FDA: Ceritinib is a kinase inhibitor. Targets of ceritinib inhibition identified in either biochemical or cellular assays at clinically; relevant concentrations include ALK, insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1.; Among these, ceritinib is most active against ALK. Ceritinib inhibited autophosphorylation of ALK, ALK-mediated; phosphorylation of the downstream signaling protein STAT3, and proliferation of ALK-dependent cancer cells in in vitro; and in vivo assays.; Ceritinib inhibited the in vitro proliferation of cell lines expressing EML4-ALK and NPM-ALK fusion proteins and; demonstrated dose-dependent inhibition of EML4-ALK-positive NSCLC xenograft growth in mice and rats. Ceritinib; exhibited dose-dependent anti-tumor activity in mice bearing EML4-ALK-positive NSCLC xenografts with demonstrated; resistance to crizotinib, at concentrations within a clinically relevant range.

Drug clinical trials:

Search ClinicalTrials for Burkitt Lymphoma

Search NIH Clinical Center for Burkitt Lymphoma

Inferred drug relations via UMLS61/NDF-RT40:

Cell-based therapeutics:


LifeMap Discovery
Data from LifeMap, the Embryonic Development and Stem Cells Database
Read about Burkitt Lymphoma cell therapies at LifeMap Discovery.

Genetic Tests for Burkitt Lymphoma

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Genetic tests related to Burkitt Lymphoma:

id Genetic test Affiliating Genes
1 Burkitt Lymphoma22

Anatomical Context for Burkitt Lymphoma

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MalaCards organs/tissues related to Burkitt Lymphoma:

31
B cells, T cells, Lymph node, Testes, Bone, Bone marrow, Lung, Liver, Ovary

LifeMap Discovery
Data from LifeMap, the Embryonic Development and Stem Cells Database

Cells/anatomical compartments in embryo or adult related to Burkitt Lymphoma:
id TissueAnatomical CompartmentCell Relevance
1 BloodHematopoietic Bone MarrowHematopoietic Stem Cells Potential therapeutic candidate
2 BloodPeripheral BloodMature B-Cells Potential therapeutic candidate, affected by disease

Animal Models for Burkitt Lymphoma or affiliated genes

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MGI Mouse Phenotypes related to Burkitt Lymphoma:

35
idDescriptionMGI Source AccessionScoreTop Affiliating Genes
1MP:00030128.6AICDA, IGHM, MYC, BCL6, BCL2L11
2MP:00053768.0GALK1, BCL2L11, BCL6, IL13RA2, MYC, SH2D1A
3MP:00053847.7AICDA, IGHM, MPP1, MYC, CXCR5, BCL6
4MP:00053977.0BCL2L11, AICDA, IGHM, SH2D1A, MPP1, MYC
5MP:00053876.9AICDA, IGHM, SH2D1A, MPP1, MYC, CXCR5

Publications for Burkitt Lymphoma

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Articles related to Burkitt Lymphoma:

(show top 50)    (show all 163)
idTitleAuthorsYear
1
Survival of AIDS-related diffuse large B-cell lymphoma, Burkitt lymphoma, and plasmablastic lymphoma in the German HIV Lymphoma Cohort. (25403997)
2014
2
Endemic Burkitt lymphoma is associated with strength and diversity of Plasmodium falciparum malaria stage-specific antigen antibody response. (23645841)
2013
3
Ileocolic intussusception due to Burkitt lymphoma: a case report. (23599821)
2013
4
Decitabine represses translocated MYC oncogene in Burkitt lymphoma. (23341364)
2013
5
Re-expression of microRNA-150 induces EBV-positive Burkitt lymphoma differentiation by modulating c-Myb in vitro. (23521217)
2013
6
Biologic characterization of adult MYC-translocation positive mature B-cell lymphomas other than molecular Burkitt lymphoma. (24179151)
2013
7
Patterns of genomic aberrations suggest that Burkitt lymphomas with complex karyotype are distinct from other aggressive B-cell lymphomas with MYC rearrangement. (23012230)
2013
8
Triple-hit B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma associated with a novel complex karyotype including t(2;3)(q21;q27), t(8;14)(q24;q32) and t(14;18)(q32;q21). (23205706)
2013
9
B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and burkitt lymphoma: study of 39 cases. (23600716)
2013
10
Intussusception as a presenting feature of Burkitt lymphoma: implications for management and outcome. (21969235)
2012
11
E2F4 plays a key role in Burkitt lymphoma tumorigenesis. (22475873)
2012
12
Relationship of Epstein-Barr virus and interleukin 10 promoter polymorphisms with the risk and clinical outcome of childhood Burkitt lymphoma. (23029361)
2012
13
Prognostic value of MYC rearrangement in cases of B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma. (21882178)
2012
14
PTLD Burkitt Lymphoma in a Patient with Remote Lymphomatoid Granulomatosis. (22312369)
2012
15
Angioedema associated with dihydropyridine calcium-channel blockers in a child with Burkitt lymphoma. (21330681)
2011
16
A novel flow cytometric antibody panel for distinguishing Burkitt lymphoma from CD10+ diffuse large B-cell lymphoma. (20395518)
2010
17
Simple karyotype and bcl-6 expression predict a diagnosis of Burkitt lymphoma and better survival in IG-MYC rearranged high-grade B-cell lymphomas. (20348878)
2010
18
Burkitt lymphoma versus diffuse large B-cell lymphoma: a practical approach. (19844983)
2010
19
Primary hepatic burkitt lymphoma presenting with acute liver failure. (20405241)
2010
20
Expression profiling of transcription factors in B- or T-acute lymphoblastic leukemia/lymphoma and burkitt lymphoma: usefulness of PAX5 immunostaining as pan-Pre-B-cell marker. (20023257)
2010
21
Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma. (20428981)
2010
22
Burkitt lymphoma in the setting of common variable immunodeficiency. (19252909)
2009
23
Silencing of genes required for glycosylphosphatidylinositol anchor biosynthesis in Burkitt lymphoma. (19302917)
2009
24
Frequent expression of multiple myeloma 1/interferon regulatory factor 4 in Burkitt lymphoma. (19144381)
2009
25
pRb2/p130 protein expression and RBL2 mutation analysis in Burkitt lymphoma from Uganda. (19691827)
2009
26
A requirement for calcium in the caspase-independent killing of Burkitt lymphoma cell lines by Rituximab. (18544085)
2008
27
CD40L-mediated inhibition of NF-kappaB in CA46 Burkitt lymphoma cells promotes apoptosis. (18661398)
2008
28
Multicentric reticulohistiocytosis associated with Burkitt lymphoma and adenocarcinoma. (18792542)
2008
29
Methemoglobinemia and hemolytic anemia caused by rasburicase administration in a newly diagnosed child with Burkitt lymphoma/leukemia. (17387701)
2008
30
Tiling resolution array comparative genomic hybridization, expression and methylation analyses of dup(1q) in Burkitt lymphomas and pediatric high hyperdiploid acute lymphoblastic leukemias reveal clustered near-centromeric breakpoints and overexpression of genes in 1q22-32.3. (17613536)
2007
31
Successful management of bleeding with recombinant factor VIIa (NovoSeven) in a patient with Burkitt lymphoma and thrombosis of the left femoral and left common iliac veins. (16514611)
2007
32
Gene-expression analysis identifies novel RBL2/p130 target genes in endemic Burkitt lymphoma cell lines and primary tumors. (17485552)
2007
33
IL-10 can induce the expression of EBV-encoded latent membrane protein-1 (LMP-1) in the absence of EBNA-2 in B lymphocytes and in Burkitt lymphoma- and NK lymphoma-derived cell lines. (16332968)
2006
34
Burkitt lymphoma-induced ileocolic intussusception in Wiskott-Aldrich syndrome. (16394894)
2006
35
Burkitt lymphoma in a child with Joubert syndrome. (15562502)
2005
36
Burkitt lymphoma and Williams syndrome: a model for children with a multisystem disorder and malignancy. (15701989)
2005
37
The human Burkitt lymphoma cell line Namalwa represents a homogenous cell system characterized by high levels of Toll-like receptor 9 and activation by CpG oligonucleotides. (15894327)
2005
38
Selective serotonin reuptake inhibitors directly signal for apoptosis in biopsy-like Burkitt lymphoma cells. (12515726)
2003
39
Zinc-mediated regulation of caspases activity: dose-dependent inhibition or activation of caspase-3 in the human Burkitt lymphoma B cells (Ramos). (11313717)
2001
40
Regulation of CD45-induced signaling by galectin-1 in Burkitt lymphoma B cells. (10764829)
2000
41
Preparative high-resolution two-dimensional electrophoresis enables the identification of RNA polymerase B transcription factor 3 as an apoptosis-associated protein in the human BL60-2 Burkitt lymphoma cell line. (10333297)
1999
42
Inhibition of CPP32 blocks surface IgM-mediated apoptosis and D4-GDI cleavage in human BL60 Burkitt lymphoma cells. (9485209)
1998
43
CD40-triggered protein tyrosine phosphorylation on Vav and on phosphatidylinositol 3-kinase correlates with survival of the Ramos-Burkitt lymphoma B cell line. (9178638)
1997
44
Wild-type p53-induced apoptosis in a Burkitt lymphoma cell line is inhibited by interferon gamma. (8690509)
1996
45
Second-messenger pathways involved in the regulation of survival in germinal-centre B cells and in Burkitt lymphoma lines. (1459737)
1992
46
The effect of cytokines and mitogens on the induction of C epsilon germline transcripts in a human Burkitt lymphoma B cell line. (1498085)
1992
47
Disseminated strongyloidiasis with central nervous system involvement diagnosed antemortem in a patient with acquired immunodeficiency syndrome and Burkitts lymphoma. (2245399)
1990
48
Recurrent mutation of immunoglobulin and c-myc genes and differential expression of cell surface antigens occur in variant cell lines derived from a Burkitt lymphoma. (2298494)
1990
49
Identification of a human transcription unit affected by the variant chromosomal translocations 2;8 and 8;22 of Burkitt lymphoma. (2470097)
1989
50
Rearrangement of immunoglobulin kappa gene in a variant-type Burkitt lymphoma cell line, KOBK101, carrying a translocation between chromosomes 2 and 8. (3082812)
1986

Variations for Burkitt Lymphoma

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Clinvar genetic disease variations for Burkitt Lymphoma:

5
id Gene Variation Type Significance SNP ID Assembly Location
1MYCNM_002467.4(MYC): c.214C> T (p.Pro72Ser)single nucleotide variantPathogenicrs28933407GRCh37Chr 8, 128750677: 128750677
2MYCNM_002467.4(MYC): c.302A> C (p.Asn101Thr)single nucleotide variantPathogenicrs121918683GRCh37Chr 8, 128750765: 128750765
3MYCNM_002467.4(MYC): c.162G> C (p.Glu54Asp)single nucleotide variantPathogenicrs121918684GRCh37Chr 8, 128750625: 128750625
4MYCNM_002467.4(MYC): c.220C> G (p.Pro74Ala)single nucleotide variantPathogenicrs121918685GRCh37Chr 8, 128750683: 128750683

Cosmic variations for Burkitt Lymphoma:

6
id Cosmic Mut ID Gene Symbol COSMIC Disease Classification
(Primary site, Site subtype, Primary histology, Histology subtype)
Conf
144571TP53haematopoietic and lymphoid tissue,lymph node,lymphoid neoplasm,Hodgkin lymphoma1

Expression for genes affiliated with Burkitt Lymphoma

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Search GEO for disease gene expression data for Burkitt Lymphoma.

Pathways for genes affiliated with Burkitt Lymphoma

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Pathways related to Burkitt Lymphoma according to GeneCards Suite gene sharing:

idSuper pathways (with members indented)ScoreTop Affiliating Genes
19.7BCL2L11, BCL6
29.4BCL6, SH2D1A, AICDA
3
Show member pathways
DNA damage response (only ATM dependent)36
Wnt Signaling Pathway and Pluripotency36
9.4BCL2L11, BCL6, MYC
49.4IGHM, BCL6, BCL2L11
59.1BCL6, IL13RA2, AICDA

Compounds for genes affiliated with Burkitt Lymphoma

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Sources:
44Novoseek, 24HMDB, 11DrugBank, 50PharmGKB
See all sources

Compounds related to Burkitt Lymphoma according to GeneCards Suite gene sharing:

idCompoundScoreTop Affiliating Genes
1suberoylanilide hydroxamic acid449.9BCL2L11, MYC
2depsipeptide449.8BCL2L11, MYC
3cytidine44 24 1111.6BCL6, MYC, AICDA
4imatinib44 50 1111.5BCL2L11, BCL6, MYC
5cycloheximide449.2AICDA, MYC, BCL6, BCL2L11
6threonine448.9SH2D1A, MYC, TCL1A, GALK1

GO Terms for genes affiliated with Burkitt Lymphoma

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Biological processes related to Burkitt Lymphoma according to GeneCards Suite gene sharing:

idNameGO IDScoreTop Affiliating Genes
1positive regulation of cysteine-type endopeptidase activity involved in apoptotic processGO:00432809.9BCL2L11, MYC

Sources for Burkitt Lymphoma

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2CDC
12ExPASy
13FDA
14FMA
22GTR
23HGMD
24HMDB
25ICD10
26ICD10 via Orphanet
27ICD9CM
28IUPHAR
29KEGG
33MeSH
34MESH via Orphanet
35MGI
38NCI
39NCIt
40NDF-RT
43NINDS
44Novoseek
46OMIM
47OMIM via Orphanet
51PubMed
52QIAGEN
57SNOMED-CT via Orphanet
61UMLS
62UMLS via Orphanet