Other names
Types
Common symptoms and signs
Diagnostic tests
Non-pharmacological treatments
Drug treatments
Dietary molecular supplements
Drugs for immunity booster / regenerative / stem-cell” contexts
5) Surgeries (procedures & why they’re done)
Preventions
When to see doctors (or the ER) urgently
What to eat / what to avoid
FAQs

Burkitt lymphoma is a very fast-growing cancer of B lymphocytes, a type of white blood cell that normally helps your body fight infections. In this disease, a genetic change turns the MYC gene “on” too strongly. That change makes the cells divide extremely quickly. Because the cells grow so fast, the tumor can get large in days to weeks, not months. Burkitt lymphoma is a form of non-Hodgkin lymphoma and is most common in children and young adults, but it can occur at any age. Doctors consider it a medical urgency because treatment needs to start quickly, and when it does, many people—especially children—can be cured. NCBI+2dceg.cancer.gov+2

Burkitt lymphoma is a very fast-growing (high-grade) cancer of B-lymphocytes driven by MYC dysregulation. It needs urgent, intensive combination chemotherapy, CNS prophylaxis (medicine into the spinal fluid or high-dose methotrexate), and meticulous supportive care (e.g., tumor lysis prevention). Outcomes are good when treated quickly at expert centers. NCBI+2nssg.oxford-haematology.org.uk+2

Other names

Burkitt lymphoma is also called Burkitt’s lymphoma, Burkitt’s tumor, or malignant lymphoma, Burkitt type. These are older or alternate terms that mean the same condition. Wikipedia

Types

Doctors describe three main clinical patterns. All three share the same core biology (MYC gene rearrangement) but differ in where and in whom they most often occur.

1) Endemic Burkitt lymphoma (eBL).
This type happens mainly in equatorial Africa and Papua New Guinea. It is strongly linked to Epstein–Barr virus (EBV) infection and areas where malaria is common. Tumors often start in the jaw or facial bones and can grow very fast. PubMed

2) Sporadic Burkitt lymphoma (sBL).
This type occurs worldwide, including North America and Europe. It commonly begins in the abdomen, especially near the ileocecal region (where the small and large intestines meet). EBV is found much less often in this type. Mayo Clinic+1

3) Immunodeficiency-associated Burkitt lymphoma (iBL).
This type occurs in people with weakened immune systems, such as those with HIV infection or people taking immune-suppressing medicines after an organ transplant. EBV is present in a sizeable portion of these cases. PubMed

Key shared feature: In all types, a chromosome swap (“translocation”) moves MYC next to immunoglobulin gene control regions, which drives runaway cell growth. The classic swap is t(8;14)(q24;q32), with variants t(2;8) and t(8;22). dceg.cancer.gov+1

Causes and contributing risk factors

Strictly speaking, we know “risk factors and contributors” better than single clear “causes.” Below are well-established drivers or conditions linked to Burkitt lymphoma. For each, I explain how it contributes.

MYC gene translocation.
This is the central biological driver. When MYC is placed under strong immunoglobulin enhancers, cells divide uncontrollably. It is the defining abnormality of Burkitt lymphoma. dceg.cancer.gov
Epstein–Barr virus (EBV).
EBV is present in almost all endemic cases and in a fraction of sporadic and immunodeficiency-related cases. EBV likely helps infected B cells survive and proliferate until other mutations (like MYC) appear. MDPI+1
Chronic malaria exposure (Plasmodium falciparum).
In malaria-endemic regions, repeated malaria infections chronically stimulate the immune system and may reduce immune control of EBV-infected cells, aiding the path to Burkitt lymphoma. PubMed
HIV infection.
HIV weakens immune surveillance. This increases the chance that abnormal B cells expand and gain MYC rearrangements. PubMed
Post-transplant immunosuppression.
Drugs used to prevent organ rejection reduce immune control of abnormal or EBV-infected B cells, raising lymphoma risk. PubMed
Primary (inherited) immunodeficiencies.
Conditions such as X-linked lymphoproliferative disease or ataxia-telangiectasia impair normal immune checks on B cells, which can allow malignant clones to emerge. (Evidence from case series and reviews.) NCBI
High EBV viral load/early EBV infection.
Early-life EBV infection in malaria regions is common and may help set the stage for lymphomagenesis in endemic settings. MDPI
AID (activation-induced cytidine deaminase) activity in germinal centers.
Normal antibody diversification processes can create DNA breaks; misrepair can produce MYC translocations. ScienceDirect
Additional cooperating mutations (e.g., ID3, TCF3, CCND3).
Research shows frequent mutations that support survival and growth of MYC-driven cells. ScienceDirect
Male sex.
Males are affected more often than females; biology is not fully understood, but the pattern is consistent across cohorts. Wikipedia
Childhood and adolescence.
Peak incidence is in children (varies by subtype). Fast-dividing lymphoid tissues in youth may contribute. Wikipedia
Residence in malaria-endemic regions.
Living in equatorial Africa and similar settings correlates with higher endemic BL risk due to malaria-EBV co-factors. PubMed
History of infectious mononucleosis (EBV disease).
Past EBV disease reflects EBV exposure. While most EBV infections do not lead to lymphoma, EBV is part of BL biology, especially endemic cases. MDPI
Immunosuppressive medications (beyond transplant).
Chronic high-dose steroids or other agents can reduce immune surveillance, increasing lymphoma risk in general. (Supported in broader lymphoma data and immunodeficiency-associated BL.) NCBI
Co-infections that strain immunity.
In settings with multiple infections, immune dysregulation may help EBV-infected B cells expand. (Epidemiology supports this in endemic BL.) PubMed
Genetic susceptibility (polygenic background).
Some families or populations may carry variants that slightly change risk, but no single inherited cause is established. (Research inference.) ScienceDirect
Delayed or impaired cytotoxic T-cell responses to EBV.
If antiviral T-cell control is weak, EBV-infected B cells persist longer and can acquire MYC events. MDPI
High antigenic stimulation of B cells.
Repeated immune activation (e.g., chronic infections) increases chances of DNA breaks during antibody gene remodeling. ScienceDirect
Exposure to intense immune stress (e.g., severe malnutrition with infections).
Immune stress may impair EBV control in endemic areas; this is supportive/associative rather than a direct cause. (Epidemiologic context.) PubMed
Prior history of another EBV-related lymphoproliferative disorder.
Some patients with EBV-driven conditions later develop aggressive B-cell lymphomas, including BL, particularly with immunodeficiency. NCBI

Common symptoms and signs

Because Burkitt lymphoma grows very fast, symptoms often appear suddenly and get worse over days to weeks.

Painless swollen lymph nodes.
Lumps in the neck, armpit, or groin that are rubbery and not tender. They enlarge quickly. Mayo Clinic
Jaw or facial swelling (endemic pattern).
In endemic areas, tumors often start in the jaw, causing visible swelling, tooth loosening, or facial asymmetry. PubMed
Abdominal pain or fullness (sporadic pattern).
Tumors often grow in the abdomen and may cause bloating, cramping, or a feeling of pressure. Mayo Clinic
Early satiety and decreased appetite.
A large abdominal mass can press on the stomach or intestines so you feel full after small meals. Mayo Clinic
Bowel changes or obstruction.
Tumors near the ileocecal area can cause constipation, vomiting, or bowel blockage. Mayo Clinic
Fever.
Unexplained fevers reflect inflammation or tumor activity. Mayo Clinic
Night sweats.
Drenching sweats that soak clothing or sheets—one of the classic “B symptoms.” Mayo Clinic
Unintentional weight loss.
Losing weight without trying is another “B symptom” that can signal aggressive lymphoma. Mayo Clinic
Fatigue and weakness.
Fast-growing tumors can cause anemia and high energy use, leading to tiredness. Mayo Clinic
Nausea, vomiting, or GI bleeding.
Abdominal involvement can irritate or invade bowel, causing bleeding or vomiting. Mayo Clinic
Hepatosplenomegaly (enlarged liver/spleen).
Cancer cells can spread to these organs, causing fullness under the ribs. NCBI
Bone marrow symptoms (anemia, easy bruising, infections).
If marrow is involved, you may notice pale skin, frequent infections, or bruising from low blood counts. NCBI
CNS symptoms (headache, confusion, seizures, cranial nerve changes).
Burkitt lymphoma can involve the brain or spinal fluid, causing neurological symptoms. NCBI
Testicular swelling.
In boys and men, testicular involvement can cause painless enlargement. NCBI
Symptoms of tumor lysis (muscle cramps, reduced urine, confusion).
Because the tumor dies rapidly—sometimes even before treatment—chemicals released from cells can upset electrolytes and strain the kidneys. NCBI

Diagnostic tests

A) Physical examination (bedside assessment)

Whole-body lymph node exam.
The doctor gently feels for enlarged nodes in the neck, armpits, and groin. In BL they are often firm, non-tender, and rapidly enlarging. This helps decide what to biopsy and how urgent testing is. Lymphoma Research Foundation
Abdominal exam.
Careful palpation and percussion can reveal abdominal masses, tenderness, or signs of bowel blockage. This guides urgent imaging and surgical consultation if needed. Mayo Clinic
Oral and jaw exam.
Inspection and palpation of the mouth, teeth, and jaw are important in endemic-pattern disease where facial bones are frequently involved. PubMed
Neurologic exam.
Testing strength, sensation, reflexes, and cranial nerves can discover central nervous system involvement that requires immediate imaging and spinal fluid evaluation. NCBI
Testicular exam (males).
A painless enlarged testis can indicate involvement; this prompts scrotal ultrasound and affects staging and therapy. NCBI

B) “Manual” bedside tests and assessments

Performance status scoring (ECOG).
A simple clinician-rated activity scale predicts tolerance of intensive chemotherapy and supports urgent planning. (Widely used across lymphomas.) PubMed
Fecal occult blood card at bedside (if GI symptoms).
A point-of-care test for hidden blood in stool can flag GI involvement while you await imaging and endoscopy as needed. (General oncology practice.) NCBI
Bedside hydration and urine output monitoring.
Strict input/output tracking helps detect tumor lysis and kidney stress early in this ultra-fast lymphoma. (Supportive-care standard in BL). PubMed
Bedside tumor measurements.
Regular tape-measure checks of palpable masses track growth or response during the first critical days of therapy. (Common lymphoma practice.) Lymphoma Research Foundation
Airway assessment (if jaw/facial swelling).
Rapid facial growth can threaten the airway; bedside evaluation determines how urgent imaging and treatment must be. PubMed

C) Laboratory and pathological tests

Complete blood count (CBC) with differential.
Looks for anemia, low platelets, or high/low white cells that suggest marrow or blood involvement. Also provides a baseline before chemotherapy. NCBI
Chemistry panel with kidney tests + tumor lysis labs (uric acid, potassium, phosphate, calcium, creatinine, LDH).
Burkitt lymphoma can trigger tumor lysis; these tests detect it early, guide IV fluids, and guide medicines like allopurinol or rasburicase. LDH also reflects tumor burden. NCBI
HIV testing.
Identifies immunodeficiency-associated BL, affects staging and treatment (antiretroviral coordination is essential). PubMed
EBV testing (serology or EBV DNA).
Supports the diagnosis context, especially in endemic or immunodeficiency settings; not diagnostic alone but clinically helpful. MDPI
Malaria testing (smear or rapid test) in endemic settings.
Assesses an important co-factor that may need treatment alongside BL therapy. PubMed
Excisional lymph node (or mass) biopsy with histology.
This is the definitive test. Pathology shows a “starry-sky” pattern with sheets of medium-sized B cells and many dividing cells. An excisional (whole-node) biopsy is preferred when feasible to preserve architecture. NCBI
Immunophenotyping (IHC and flow cytometry).
Typical pattern: CD20+, CD10+, BCL6+, very high Ki-67 (often near 100%), and usually BCL2-. Flow cytometry confirms a clonal B-cell population. NCBI
Cytogenetics/FISH for MYC rearrangement.
Detects the hallmark MYC translocation (t(8;14) or variants). This anchors the diagnosis and separates BL from other high-grade B-cell lymphomas. dceg.cancer.gov
Bone marrow aspirate/biopsy and CSF cytology.
Check for spread to marrow and spinal fluid. Positive results change staging and add CNS-directed therapy. PubMed
Minimal diagnostic work-up per guidelines (composite).
NCCN pediatric and adolescent/young adult lymphoma guidelines outline a structured set of pathologic, laboratory, and staging tests to begin treatment promptly. NCCN+2PubMed+2

D) Electro-diagnostic tests (focused use)

Electrocardiogram (ECG).
Checks baseline heart rhythm and QT interval before starting certain chemo drugs and during tumor lysis electrolyte shifts that can trigger arrhythmias. PubMed
EEG (only if seizures or encephalopathy).
Used when there are neurologic symptoms to evaluate for seizure activity in CNS involvement. (Supportive neurology practice in lymphoma.) NCBI

E) Imaging tests (staging and planning)

Ultrasound (abdomen, pelvis, testis).
Fast, radiation-free imaging to detect masses, organ enlargement, or testicular disease. Helpful in children and for bedside decisions. PubMed
CT scans of neck/chest/abdomen/pelvis.
Standard for mapping disease in the body at diagnosis; shows lymph nodes, bowel masses, and organ involvement. Mayo Clinic
PET-CT.
Shows metabolically active disease and helps assess early response after therapy begins. Use depends on center and guideline specifics in children vs adults. PubMed
MRI brain and/or spine (if neurologic signs).
Looks for CNS involvement and guides lumbar puncture and intrathecal therapy needs. PubMed
Plain X-ray or dental/jaw imaging (endemic pattern).
May reveal jaw bone changes or tooth displacement when facial bones are involved. PubMed

Non-pharmacological treatments

1) Care at an expert center & fast start of therapy (core strategy).
Purpose: Start full-intensity, BL-specific chemo within days; coordinate CNS prophylaxis and supportive care.
Mechanism: Expert teams follow risk-adapted protocols (e.g., R-CODOX-M/IVAC), manage complications, and avoid dose reductions that hurt cure rates. NCBI+1

2) Tumor lysis syndrome (TLS) prevention bundle.
Purpose: Lower life-threatening electrolyte spikes and kidney injury when chemo kills tumor cells.
Mechanism: Aggressive IV hydration, urine alkalinization when appropriate, close labs; allopurinol or rasburicase per risk. PubMed+2MD Anderson Cancer Center+2

3) Nutritional counseling & energy-protein support.
Purpose: Maintain strength, weight, and treatment tolerance.
Mechanism: Registered dietitian optimizes calorie/protein intake; uses medically supervised oral supplements if needed; follows cancer-specific diet/activity guidance. American Cancer Society+1

4) Infection-risk reduction during neutropenia.
Purpose: Prevent severe infections while white cells are low.
Mechanism: Hand hygiene, food safety, fever education, prompt care if temp ≥38.0°C, vaccines planning with oncology team. CDC+1

5) Oral care to prevent mucositis.
Purpose: Reduce mouth sores, pain, and infection risk.
Mechanism: Best oral care protocols (gentle brushing, bland rinses), evidence-based mucositis measures per MASCC/ISOO. PubMed Central+1

6) Antiemetic planning (before each chemo block).
Purpose: Prevent nausea/vomiting that cause dehydration and poor intake.
Mechanism: Follow ASCO/ESMO risk-based antiemetic regimens and add rescue plans. ASCO Publications+1

7) Fertility preservation counseling (pre-treatment).
Purpose: Protect future fertility when feasible.
Mechanism: Rapid referral for sperm banking, oocyte/embryo cryopreservation, or ovarian suppression where appropriate. ASCO Publications+2ASCO+2

8) Central venous access care education.
Purpose: Reduce line infections/clots and ensure reliable chemo delivery.
Mechanism: Aseptic care, dressing changes, and prompt evaluation of line symptoms—standard oncology protocols. (General supportive-care practice echoed across guidelines.) National Cancer Institute

9) Physical activity as tolerated.
Purpose: Preserve function, reduce fatigue, and support mood.
Mechanism: Light, individualized activity and PT guidance during and between cycles per survivorship guidance. American Cancer Society

10) Psychosocial support.
Purpose: Lower distress and improve adherence.
Mechanism: Access to counseling, peer groups, and practical supports coordinated by the cancer center. American Cancer Society

11) Ommaya reservoir consideration for repeated intrathecal therapy.
Purpose: Comfortable, reliable CNS access when many intrathecal doses are planned.
Mechanism: Surgical reservoir enables repeated CSF sampling and intraventricular chemo. NCBI+1

12) Peri-operative care for acute surgical complications (e.g., intussusception).
Purpose: Rapid relief of obstruction or perforation to enable chemotherapy.
Mechanism: Focused surgery for complications; otherwise, BL is treated medically. PubMed+1

Drug treatments

Notes: Burkitt lymphoma is treated with combinations (blocks) such as CODOX-M/IVAC±rituximab. Doses vary by protocol, renal function, and timing relative to other agents. Always follow your center’s regimen guide. nssg.oxford-haematology.org.uk+1

1) Cyclophosphamide (alkylating agent).
Class: Alkylator. Typical Role: Core in CODOX-M blocks.
Dose/Time: Protocol-specific IV doses within cycles.
Purpose: DNA cross-linking to kill rapidly dividing BL cells.
Mechanism: Forms DNA cross-links → apoptosis.
Key side effects: Myelosuppression, hemorrhagic cystitis (hydrate; consider mesna), infertility risk. FDA Access Data+1

2) Vincristine (VCR).
Class: Vinca alkaloid. Role: With C, D, high-dose MTX in CODOX-M.
Dose/Time: Protocol-specific IV; NEVER intrathecal.
Purpose/Mechanism: Arrests microtubules → mitotic block.
Side effects: Peripheral neuropathy, constipation; fatal if given non-IV. FDA Access Data

3) Doxorubicin (Adriamycin).
Class: Anthracycline.
Purpose/Mechanism: Intercalates DNA, topoisomerase II inhibition, free radicals.
Dose/Time: Protocol-based IV; lifetime dose limits.
Side effects: Myelosuppression, cardiomyopathy risk, mucositis, alopecia. FDA Access Data

4) High-dose Methotrexate (HD-MTX) with leucovorin rescue.
Class: Antimetabolite (folate antagonist).
Purpose/Mechanism: Inhibits DHFR → blocks DNA synthesis; penetrates CNS at high dose.
Dose/Time: Protocol IV infusions (e.g., 1–8 g/m²); must follow timed leucovorin rescue and drug-level monitoring.
Side effects: Renal/hepatic toxicity, mucositis; drug interactions. FDA Access Data

5) Leucovorin (folinic acid) — rescue for HD-MTX.
Class: Reduced folate.
Purpose/Mechanism: “Rescues” normal cells from MTX; does not counteract antitumor effect in tumor cells with transport/retention differences.
Dose/Time: Timed IV/PO starting ~24–36 h post-MTX; titrated by MTX levels.
Side effects: Rare; dosing errors can be dangerous. FDA Access Data+1

6) Cytarabine (Ara-C), including high-dose IV and intrathecal use.
Class: Antimetabolite (pyrimidine analog).
Purpose/Mechanism: Inhibits DNA polymerase; S-phase kill; CNS prophylaxis/treatment at IT doses.
Side effects: Myelosuppression, cerebellar toxicity (esp. high dose/age), conjunctivitis (steroid eye drops). FDA Access Data

7) Ifosfamide.
Class: Alkylator.
Purpose/Mechanism: DNA cross-linking; part of IVAC blocks.
Key co-meds: Mesna + hydration for bladder protection.
Side effects: Myelosuppression, encephalopathy, nephrotoxicity. FDA Access Data+1

8) Etoposide (or etoposide phosphate).
Class: Topoisomerase II inhibitor.
Purpose/Mechanism: DNA strand breaks during replication; IVAC component.
Side effects: Myelosuppression, mucositis; anaphylactoid reactions rarely. FDA Access Data

9) Prednisone/Prednisolone.
Class: Glucocorticoid.
Purpose/Mechanism: Lympholysis; decreases edema/inflammation.
Dose/Time: Protocol oral dosing in induction blocks.
Side effects: Hyperglycemia, immunosuppression, mood changes, GI effects. FDA Access Data+1

10) Rituximab (anti-CD20 monoclonal antibody).
Class: Anti-CD20 biologic.
Purpose/Mechanism: Targets CD20 on BL cells → complement & ADCC.
Use: Frequently added to BL chemo backbones (adults and pediatrics) and improves outcomes in high-grade mature B-cell lymphomas.
Key risks: Infusion reactions, HBV reactivation, PML (boxed). FDA Access Data+2The New England Journal of Medicine+2

11) Rasburicase (for TLS management).
Class: Uricase enzyme.
Purpose/Mechanism: Converts uric acid → allantoin (soluble), rapidly lowering uric acid.
Dose/Time: Given at/before chemo in high-risk TLS; single low-dose strategies used institutionally.
Side effects: Hypersensitivity, hemolysis in G6PD deficiency (screen when indicated). FDA Access Data+1

12) Allopurinol / IV allopurinol (AloPRIM) (TLS prophylaxis).
Class: Xanthine oxidase inhibitor.
Purpose/Mechanism: Prevents new uric acid formation; slower than rasburicase for rapid lowering.
Dose/Time: Start 24–48 h pre-chemo when feasible per TLS algorithm.
Side effects: Rash (including severe), hepatotoxicity; dose adjust in renal impairment. FDA Access Data+1

13) Filgrastim or Pegfilgrastim (G-CSF, per protocol).
Class: Hematopoietic growth factor.
Purpose/Mechanism: Shortens neutropenia duration → lowers febrile neutropenia risk.
Dose/Time: Filgrastim daily SC starting ≥24 h after chemo; pegfilgrastim single 6 mg SC dose per cycle (timed).
Side effects: Bone pain; rare splenic rupture. FDA Access Data+1

Regimen examples and scheduling details (e.g., R-CODOX-M/IVAC, dose timing, leucovorin schedules) are in institutional protocols and national references. nssg.oxford-haematology.org.uk+1

Dietary molecular supplements

Safety note: Many supplements can interact with chemo (e.g., high-dose antioxidants, concentrated herbals). Prioritize correcting measured deficiencies under clinician guidance.

1) Vitamin D (for deficiency).
Dose: Individualized to blood levels (commonly 800–2,000 IU/day; higher short courses for deficiency).
Function/Mechanism: Bone health, calcium balance; supports muscle and immune function. Evidence supports replacing deficiency; avoid excess. Office of Dietary Supplements

2) Omega-3 fatty acids (EPA/DHA).
Dose: Often 1–2 g/day combined EPA/DHA with food (if approved).
Function/Mechanism: May help maintain weight/appetite and cardiometabolic health; anti-inflammatory lipid mediators. Watch bleeding risk with anticoagulants. Office of Dietary Supplements

3) Zinc (only if low).
Dose: Typically 8–11 mg/day from diet; short-term supplementation per clinician for deficiency.
Function/Mechanism: Enzymatic/immune functions; deficiency worsens taste and wound healing. Avoid excessive dosing (can harm copper status). Office of Dietary Supplements

4) Ginger (as adjunct for nausea, if approved).
Dose: Often 0.5–1 g/day standardized extract divided; verify interactions.
Function/Mechanism: 6-gingerol/6-shogaol act on gut and CNS pathways; mixed evidence in chemo-induced nausea. Use only alongside guideline antiemetics. NCCIH+1

5) Protein oral nutrition supplements (ONS).
Dose: Dietitian-guided to hit daily protein targets.
Function/Mechanism: Supplies amino acids to preserve lean mass during intensive chemo. Follow ACS dietary guidance. American Cancer Society

6) Calcium (only with documented need, often with vitamin D).
Dose: Titrate to reach ~1,000–1,200 mg/day total intake from diet + supplement.
Function/Mechanism: Bone health during steroids. Avoid hypercalcemia; coordinate with vitamin D plan. American Cancer Society

7–10) I can add more (e.g., B12/folate only for deficiency; electrolytes during refeeding; thiamine in malnutrition; soluble fiber for gut health) if you want me to continue.

Drugs for immunity booster / regenerative / stem-cell” contexts

1) Filgrastim (G-CSF).
Dose: SC daily starting ≥24 h post-chemo, per protocol.
Function/Mechanism: Expands neutrophil production to reduce infection risk. FDA Access Data

2) Pegfilgrastim (long-acting G-CSF).
Dose: 6 mg SC once per cycle (timed).
Function/Mechanism: Same as above with longer half-life. FDA Access Data

3) Autologous stem-cell rescue (selected relapsed settings).
Dose: Mobilization/collection then high-dose chemo + reinfusion.
Function/Mechanism: Rebuilds marrow after ablation; used selectively in relapse/refractory BL. (Practice varies by center.) National Cancer Institute

4) Allogeneic stem-cell transplant (rare, refractory cases).
Dose: Conditioning then donor stem-cell infusion.
Function/Mechanism: Graft-versus-lymphoma effects; higher risks—specialist decision only. National Cancer Institute

5) Intrathecal methotrexate/cytarabine for CNS prophylaxis/treatment.
Dose: Protocol-based via lumbar puncture or Ommaya.
Function/Mechanism: Direct CSF exposure to prevent/treat CNS disease. FDA Access Data+1

6) IVIG (selected profound hypogammaglobulinemia).
Dose: Weight-based intermittent infusions.
Function/Mechanism: Passive antibody replacement to reduce infections in specific cases; specialist-directed. (General supportive-care concept.) National Cancer Institute

5) Surgeries (procedures & why they’re done)

1) Excisional/incisional biopsy (sometimes image-guided).
Why: Obtain enough tissue for diagnosis (histology, immunophenotype, cytogenetics such as MYC). Fine-needle alone is usually inadequate. Medscape+1

2) Emergency surgery for intussusception/obstruction or perforation.
Why: Life-saving management of acute abdominal complications; enables timely chemotherapy. PubMed+1

3) Ommaya reservoir placement (neurosurgical).
Why: Comfortable, reliable intrathecal access for repeated CNS prophylaxis or therapy. NCBI

(In general, BL is not managed by tumor-debulking surgery; surgery is limited to diagnosis/complications.) NCBI

Preventions

Start treatment fast at a center experienced with BL. NCBI
Follow TLS prevention steps (hydration, uric-acid control, frequent labs). PubMed
Learn neutropenia precautions (hand hygiene, food safety, fever plan). CDC
Keep oral-care routine to lower mucositis/infection risk. PubMed Central
Take antiemetics exactly as prescribed to prevent dehydration. ASCO Publications
Vaccination planning with oncology team (timing matters). CDC
Use growth-factor support when your regimen recommends it. FDA Access Data
Keep scheduled labs and drug-level checks (e.g., HD-MTX). FDA Access Data
Protect your central line (clean, dry, watch for redness/fever). National Cancer Institute
Maintain nutrition and gentle activity as tolerated. American Cancer Society

When to see doctors (or the ER) urgently

Fever ≥38.0°C, chills, or feeling “acutely unwell” during chemo cycles. CDC
New chest pain, shortness of breath, confusion, uncontrolled vomiting/diarrhea, fainting. CDC
Mouth sores so painful you cannot drink, or any bleeding that won’t stop. PubMed Central
Redness/pain/swelling at your central line site or severe new headache/neck stiffness (possible CNS issue). National Cancer Institute
Any sudden severe abdominal pain (concern for obstruction/perforation). PubMed

What to eat / what to avoid

What to eat (examples):

A plant-forward pattern: fruits, colorful vegetables, whole grains, legumes, nuts, and seeds, with lean proteins (fish, poultry, eggs, dairy, tofu). Helps meet calories/protein and micronutrients. American Cancer Society
Small, frequent meals and sips of high-protein shakes if appetite is low. (Dietitian can tailor a plan.) American Cancer Society

What to avoid (or limit):

Unpasteurized dairy/juices, undercooked meats/eggs, and raw sprouts during neutropenia (food-safety focus). CDC
Large, non-prescribed supplement doses or herbal concentrates without oncology approval (interaction risk). American Cancer Society
Excess added sugars and alcohol (can worsen fatigue and nutrition quality). American Cancer Society

FAQs

1) Is Burkitt lymphoma curable?
Yes—many people are cured with modern, intensive chemo (plus CNS prophylaxis), especially when treatment starts quickly at expert centers. PubMed Central

2) Why is treatment so urgent?
BL doubles fast; early, full-dose therapy prevents complications and improves cure rates. NCBI

3) What regimens are commonly used?
Risk-adapted combinations such as CODOX-M/IVAC (often with rituximab); doses and cycle counts vary. nssg.oxford-haematology.org.uk+1

4) Do I really need CNS prophylaxis?
Yes—BL has a high risk of CNS spread; centers use intrathecal therapy and/or high-dose methotrexate. FDA Access Data

5) What is leucovorin “rescue”?
Timed folinic acid after HD-MTX to protect normal cells while keeping the anticancer effect. Precise timing and drug-level checks are essential. FDA Access Data

6) Is rituximab useful in BL?
Adding rituximab to BL chemotherapy improves outcomes in trials/series of mature B-cell lymphomas, including BL. The New England Journal of Medicine

7) Why do I get rasburicase or allopurinol?
To prevent/treat TLS by lowering uric acid—rasburicase works quickly; allopurinol prevents new uric acid formation. FDA Access Data+1

8) Are growth factors (G-CSF) routine?
They’re used per regimen to shorten neutropenia and reduce infection risk; timing matters. FDA Access Data

9) Can surgery remove the lymphoma instead of chemo?
No—BL is treated medically; surgery is for diagnosis and emergencies like obstruction/intussusception. NCBI+1

10) What mouth-care steps help?
Gentle brushing, bland rinses, and guideline-based mucositis measures reduce sores and infections. PubMed Central

11) How do I prevent infections?
Hand hygiene, food safety during neutropenia, fever plan, and vaccine planning with your team. CDC

12) What if I can’t keep food down?
Use your antiemetic plan, try small frequent meals, and ask for dietitian support; report dehydration signs early. ASCO Publications+1

13) Do supplements help cure BL?
No. Some (e.g., vitamin D for deficiency) support overall health, but never replace chemo. Always clear supplements with oncology. Office of Dietary Supplements

14) Will treatment affect fertility?
It can. Ask about rapid fertility preservation options before starting therapy when possible. ASCO Publications

15) Why so many lab tests?
They keep you safe—monitoring for TLS, drug levels (HD-MTX), organ function, and counts guides timely rescue/support. FDA Access Data

SaveSavedRemoved 0