HODGKIN LYMPHOMA — COMPLETE STUDY GUIDE
CLASSIFICATION, STAGING, TREATMENT, EXTRAVASATION, AND SUPPORTIVE CARE
CONCEPTUAL SUMMARY
DEFINITION AND OVERVIEW: Hodgkin lymphoma (HL) is a lymphoid malignancy characterized by clonal malignant Hodgkin/Reed-Sternberg (HRS) cells within a reactive cellular background of granulocytes, plasma cells, and lymphocytes. HRS cells are of B-cell lineage (confirmed by PCR) and arise from germinal center B-cells — but despite this origin, they LOSE phenotypic B-cell features. Reed-Sternberg cells represent only 1–10% of cells in involved lymph nodes — they are a MINORITY, not the majority. The classic Reed-Sternberg cell is large and binucleated with prominent nucleoli, giving an "owl's eyes" appearance. Bimodal age distribution: peaks at 15–35 years and > 55 years; slight male predominance. Highly curable — 5-year survival 85–90%. The high cure rate has shifted clinical focus to managing LONG-TERM TOXICITIES.
SUBTYPES AND IMMUNOPHENOTYPE: Classical HL (cHL) — approximately 95% of cases. Reed-Sternberg cell immunophenotype: CD15+ (85%), CD30+ (virtually 100%), PAX5+. LACKS CD19, CD20, CD79a (pan-B markers) and CD3, CD7 (pan-T markers). Absence of CD15 alone does NOT exclude cHL. Missing BOTH CD15 and CD30 with CD20+ → consider NLPHL or large B-cell NHL. cHL subtypes by frequency and prognosis: Nodular sclerosing (most common; frequent mediastinal involvement), mixed cellularity (EBV association), lymphocyte-rich (good prognosis), lymphocyte-depleted (worst prognosis among cHL subtypes).
Nodular Lymphocyte-Predominant HL (NLPHL) — distinct from cHL: Malignant cells = "POPCORN CELLS" (lymphocytic and histiocytic / L&H cells). Immunophenotype: CD20+, CD45+, CD19+, CD22+, CD79a+; LACKS CD15 and CD30 — OPPOSITE of Reed-Sternberg cells in cHL. Approximately 70–80% present with EARLY-STAGE disease at diagnosis. Less mediastinal involvement and FEWER B symptoms compared to cHL. Typically asymptomatic lymphadenopathy with indolent course. CD20+ → rituximab is foundational for NLPHL therapy — rituximab is NOT used in standard cHL.
CLINICAL PRESENTATION: Constitutional B symptoms: fever, night sweats, weight loss > 10%. Fatigue, pruritus, dyspnea on exertion. Painless lymphadenopathy (commonly supraclavicular, mediastinal, cervical). Bulky mediastinal mass common in advanced disease. Alcohol-induced pain at lymph nodes — rare but SPECIFIC to HL. NLPHL: typically asymptomatic; B symptoms less common.
DIAGNOSIS: Excisional lymph node biopsy REQUIRED — needle biopsy alone is insufficient. Positive for Reed-Sternberg cells on histology. IHC: CD30+, CD15+, PAX5+. PET/CT scan for staging — superior to CT alone for identifying active disease. Labs: CBC, renal/hepatic panels, pulmonary function tests (bleomycin baseline), LVEF/ejection fraction (doxorubicin baseline).
STAGING (ANN ARBOR): Stage I = single lymph node region. Stage II = ≥ 2 lymph node regions, same side of diaphragm. Stage III = both sides of diaphragm. Stage IV = extranodal involvement (e.g., bone marrow). Suffix B = B symptoms present; suffix A = absent. Bulky disease = mass ≥ 10 cm OR mediastinal mass > 1/3 thoracic diameter → affects treatment intensity.
PET-CT AND DEAUVILLE CRITERIA: PET/CT timing after chemotherapy: wait ≥ 3 WEEKS (to avoid false positives from treatment-induced inflammation — inflammation increases FDG uptake). Post-radiotherapy: wait ≥ 6 weeks. Post-G-CSF: wait ≥ 2 weeks. End-of-treatment: some protocols recommend 6–8 weeks. Elevated blood glucose → DECREASED FDG uptake → FALSE-NEGATIVE risk — delay scan until glucose < 200 mg/dL. Use oral hypoglycemics (not insulin) near FDG administration. False-positive causes: rebound thymic hyperplasia, infection, inflammation, brown fat, extramedullary hematopoiesis.
Deauville Criteria (visual interpretation of PET-CT — NOT histological grading, NOT clinical/lab prognostic scoring — that is the International Prognostic Score/IPS): Score 1 = no uptake. Score 2 = uptake ≤ mediastinum → NEGATIVE (optimal). Score 3 = uptake > mediastinum but ≤ liver → good prognosis in most HL; interpret in clinical context. Score 4 = uptake moderately > liver → POSITIVE. Score 5 = uptake markedly > liver → POSITIVE. Scores 1–3 interim = optimal response → may DE-ESCALATE (e.g., drop bleomycin → continue as AVD). Scores 4–5 = sub-optimal → consider intensification; BIOPSY before starting second-line to confirm residual disease and exclude false-positive.
FIRST-LINE TREATMENT REGIMENS: ABVD components: A = Doxorubicin (Adriamycin), B = Bleomycin, V = Vinblastine, D = Dacarbazine. Administered every 28 days × 4–6 cycles. AVD = ABVD minus bleomycin (removed to reduce pulmonary toxicity).
Treatment by stage: Early-stage (I–II) unfavorable or IIB with bulk: ABVD × 2 cycles → PET-adapted (add ISRT or escalate if poor response). Advanced-stage (III–IV): ABVD × 2 cycles → AVD × 4 cycles ± ISRT (PET-adapted; drop bleomycin if optimal interim PET response); OR A+AVD × 6 cycles (brentuximab + AVD; ECHELON-1 trial; Category 1); OR BEACOPP escalated × 6 ± ISRT. NLPHL Stage IA: Radiotherapy alone. NLPHL other stages: Chemotherapy per cHL protocols with rituximab (CD20+).
KEY TREATMENT RULES — HIGH YIELD: CHOP = NHL regimen — NOT for HL. Stanford V = REMOVED from NCCN Guidelines — no longer recommended. ISRT alone = no longer recommended as standalone initial therapy. Brentuximab vedotin as single agent = NOT recommended frontline. LEUKOPENIA IS NOT A REASON TO REDUCE ABVD DOSE — proceed at full doses; 5-year EFS and OS are comparable with or without prophylactic G-CSF. G-CSF: NOT routinely recommended for ABVD; IS recommended for A+AVD and BEACOPP escalated. G-CSF with bleomycin-containing regimens (ABVD) → may INCREASE bleomycin pulmonary toxicity (BPT) risk.
BRENTUXIMAB VEDOTIN: Anti-CD30 antibody-drug conjugate (ADC). Payload: MMAE (monomethyl auristatin E) → blocks microtubule-dependent cell division. Used in ALL settings: frontline early-stage, frontline advanced-stage, AND relapsed/refractory. Frontline advanced-stage (III–IV): A+AVD (ECHELON-1 trial) — Category 1; improved PFS and OS vs ABVD. Relapsed/refractory: post-ASCT consolidation (AETHERA trial), salvage before transplant, palliation. Key toxicities: peripheral neuropathy (DOSE-LIMITING, ≥ 20%), neutropenia, fatigue, nausea. CONTRAINDICATED in patients with PRE-EXISTING NEUROPATHY. DO NOT combine brentuximab vedotin with bleomycin — unacceptable risk of FATAL pulmonary toxicity.
EXTRAVASATION MANAGEMENT IN ABVD: ABVD contains TWO vesicants: doxorubicin (anthracycline) + vinblastine (vinca alkaloid). When agent is UNKNOWN → ALWAYS treat for the ANTHRACYCLINE (more severe). Anthracyclines = DNA-binding vesicants causing continuous cycle of tissue necrosis — greatest vesicant potential among chemotherapy agents. Steps: aspirate remaining fluid → remove IV line → apply ICE PACKS + administer DEXRAZOXANE. Dexrazoxane (Totect): FDA-approved for anthracycline extravasation; 98.2% effective in preventing surgical necrosis when given within 6 hours. HEAT should NEVER be applied to anthracycline extravasation — increases blood flow and worsens tissue damage. DMSO: historical alternative; CANNOT be used concurrently with dexrazoxane; no longer preferred. Vinca alkaloid (vinblastine) extravasation: hyaluronidase + WARM compresses. Cannot apply both cold AND warm compresses simultaneously → anthracycline always takes priority.
KEY TOXICITIES AND MONITORING: Doxorubicin: cardiotoxicity → monitor LVEF/ejection fraction. Bleomycin: pulmonary toxicity (BPT) → monitor PFTs (DLCO); avoid in older adults or pre-existing lung disease; avoid G-CSF with bleomycin; do NOT combine with brentuximab vedotin. Vinblastine: peripheral neuropathy, constipation, myelosuppression → monitor neurologic assessment and CBC. Brentuximab vedotin: peripheral neuropathy (dose-limiting), neutropenia → monitor neurologic assessment and CBC. Long-term: secondary malignancy, hypothyroidism (post-neck radiation), cardiopulmonary toxicity, infertility.
PRACTICE QUESTIONS — HODGKIN LYMPHOMA
KU is a 31-year-old non-smoking female with fatigue, low-grade fevers, 10-pound weight loss, pruritus, and mild dyspnea on exertion. PET/CT reveals left supraclavicular adenopathy, a bulky 11 cm mediastinal mass, and retroperitoneal lymphadenopathy. Excisional biopsy is positive for Reed-Sternberg cells. She is diagnosed with Stage IIB classical Hodgkin lymphoma with bulky disease.
Which of the following is the most appropriate initial treatment option for KU?
A. ISRT
B. ABVD
C. Brentuximab vedotin
D. Stanford V
Answer: B. ABVD
Explanation: KU has Stage IIB cHL with bulky disease (mass ≥ 10 cm) and B symptoms (weight loss, fevers) — this classifies her as Stage I–II UNFAVORABLE disease. For early-stage unfavorable cHL, the standard initial treatment is ABVD × 2 cycles, followed by PET-adapted therapy (additional ABVD cycles + ISRT, or intensification if poor interim PET response). ISRT alone (option A) was a historical standard but is NO LONGER recommended as standalone initial therapy due to long-term toxicities including heart disease and secondary malignancies. Brentuximab vedotin (option C) — frontline A+AVD (Category 1) is specifically for Stage III–IV advanced disease; KU has Stage II disease and does not meet standard criteria for frontline brentuximab single-agent use. Stanford V (option D) — recently REMOVED from NCCN Guidelines and is no longer a recommended regimen. Clinical pharmacist note: If KU develops leukopenia (e.g., ANC 0.5) during cycle 2, the correct action is to PROCEED WITH FULL DOSES — leukopenia is NOT a reason to reduce dose intensity in ABVD for curative-intent HL therapy.
[/expand]KU returns for cycle 2 of ABVD. All labs are within normal limits except ANC = 0.5. The attending physician asks whether KU's chemotherapy doses should be reduced.
Which of the following is appropriate for KU at this time?
A. Hold chemotherapy and add growth factor support
B. Reduce all chemotherapy doses by 25%
C. Reduce the dose of doxorubicin by 25%
D. Proceed with chemotherapy at full doses
Answer: D. Proceed with chemotherapy at full doses
Explanation: Leukopenia/neutropenia is NOT a contraindication to and NOT a reason for dose reduction in patients with cHL receiving ABVD. Key principles: ABVD can be safely administered at full-dose intensity without routine growth factor support. Five-year EFS and OS are comparable in patients who receive ABVD at full doses with or without prophylactic G-CSF. G-CSF is NOT routinely recommended during initial ABVD therapy. Additionally, a retrospective analysis found that G-CSF use with bleomycin-containing regimens may increase the risk of bleomycin pulmonary toxicity (BPT). Holding chemotherapy (option A) or dose reducing (options B and C) would compromise the curative intent of treatment — dose intensity must be maintained for optimal outcomes in HL.
[/expand]KU has just completed her ABVD infusions and reports warmth and burning around her central line site. Since all infusions are completed, it is unclear which agent may have extravasated.
How should extravasation antidotes be directed in this case?
A. Treat the anthracycline extravasation
B. Treat the vinca alkaloid extravasation
C. Treat both the anthracycline and vinca alkaloid extravasations simultaneously
D. Treatment is not necessary since extravasation has not been definitively confirmed
Answer: A. Treat the anthracycline extravasation
Explanation: ABVD contains TWO vesicants: doxorubicin (anthracycline) and vinblastine (vinca alkaloid). When the causative agent is unknown, management MUST be directed toward the ANTHRACYCLINE because it is the more severe of the two. Anthracyclines are DNA-binding vesicants that bind to healthy tissue and cause a continuous cycle of cell death and severe necrosis — they carry the greatest vesicant potential among chemotherapy agents. Treating both simultaneously (option C) is physically IMPOSSIBLE — anthracycline extravasation requires COLD compresses + dexrazoxane, while vinca alkaloid requires WARM compresses + hyaluronidase; these are mutually exclusive treatments and cold always takes priority. Withholding treatment (option D) is NEVER appropriate — vesicant injuries can progress to involve joints and tendons. Summary: anthracycline = cold compress + dexrazoxane; vinca alkaloid = warm compress + hyaluronidase.
[/expand]Towards the end of her ABVD infusions, KU complains of warmth and burning around her central line site. After the nurse has aspirated any remaining fluid and removed the IV line, what would be the standard next step in treating this extravasation?
A. Heat packs
B. Heat packs and topical DMSO
C. Ice packs and hyaluronidase
D. Ice packs and dexrazoxane
Answer: D. Ice packs and dexrazoxane
Explanation: After aspirating remaining fluid and removing the IV line, the standard next steps for ABVD extravasation (treating as anthracycline extravasation) are: Ice packs (cold compresses) — cause vasoconstriction, localizing the drug and preventing spread to adjacent healthy tissue. Dexrazoxane (Totect) — FDA-approved antidote for anthracycline extravasation; 98.2% effective in preventing the need for surgical intervention when administered within 6 hours of the event. HEAT PACKS (options A and B) are NEVER applied to anthracycline extravasation — heat increases blood flow and drug distribution, worsening tissue damage. DMSO (option B) — a historical alternative for anthracycline extravasation; CANNOT be used concurrently with dexrazoxane and is no longer the preferred standard of care. Hyaluronidase + warm compresses (option C) — correct treatment for VINCA ALKALOID (vinblastine) extravasation only; not appropriate when anthracycline is the priority.
[/expand]KU is a 24-year-old female with fatigue, low-grade fevers, 10-pound weight loss, pruritus, and mild dyspnea on exertion. CT reveals left supraclavicular adenopathy, a bulky 15 cm mediastinal mass, and retroperitoneal lymphadenopathy. Bone marrow biopsy reveals marrow involvement. Excisional biopsy is positive for Reed-Sternberg cells. She is diagnosed with Stage IIIB classical Hodgkin lymphoma.
Which of the following is the most appropriate treatment option for KU at this time?
A. CHOP × 6 cycles + ISRT
B. ABVD × 2 cycles + ISRT
C. ABVD × 2 cycles followed by AVD × 4 cycles
D. Stanford V × 8 weeks
Answer: C. ABVD × 2 cycles followed by AVD × 4 cycles
Explanation: KU has Stage IIIB cHL — ADVANCED-STAGE disease (lymphadenopathy on both sides of the diaphragm + bone marrow involvement + B symptoms). For advanced-stage cHL (III–IV), the preferred PET-adapted approach is ABVD × 2 cycles → if interim PET shows optimal response (Deauville 1–3), DE-ESCALATE by dropping bleomycin → continue AVD × 4 cycles. This approach minimizes bleomycin pulmonary toxicity while maintaining efficacy. CHOP × 6 + ISRT (option A) — CHOP is a foundational regimen for NON-HODGKIN LYMPHOMA; it is NOT recommended for cHL. ABVD × 2 + ISRT (option B) — abbreviated chemotherapy + radiation is for EARLY-STAGE FAVORABLE disease; insufficient for Stage IIIB advanced disease. Stanford V × 8 weeks (option D) — Stanford V requires 12 weeks when combined with ISRT (not 8 weeks); moreover, Stanford V has been REMOVED from NCCN Guidelines for certain cHL stages.
[/expand]"Popcorn appearance" of malignant cells is seen in which subtype of Hodgkin lymphoma?
A. Nodular lymphocyte-predominant Hodgkin lymphoma
B. Nodular sclerosing Hodgkin lymphoma
C. Lymphocyte-rich Hodgkin lymphoma
D. Lymphocyte-depleted Hodgkin lymphoma
Answer: A. Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL)
Explanation: NLPHL is characterized by large malignant cells called "POPCORN CELLS" (also known as lymphocytic and histiocytic / L&H cells), named for their nuclear appearance with increased nucleoli resembling popcorn. These are distinct from the Reed-Sternberg cells of cHL, which have a binucleated "owl's eyes" appearance. Immunophenotype of popcorn cells: CD20+, CD45+, CD19+, CD22+, CD79a+ — LACKS CD15 and CD30 (opposite of cHL Reed-Sternberg cells). The CD20 expression is clinically critical: rituximab is a foundational component of NLPHL therapy but is NOT used in standard cHL protocols. Nodular sclerosing (B), lymphocyte-rich (C), and lymphocyte-depleted (D) are all classical HL subtypes with Reed-Sternberg cells — they do NOT show popcorn cells.
[/expand]Which of the following statements is/are TRUE regarding nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL)?
A. 80% of cases present with early-stage disease
B. Compared with classical Hodgkin lymphoma, mediastinal involvement and B symptoms are less common
C. Positive for CD20
D. All of the above
Answer: D. All of the above
Explanation: All three statements accurately describe NLPHL: Approximately 70–80% of NLPHL cases present with early-stage (Stage I or II) disease — the disease is often localized at diagnosis. Mediastinal involvement and B symptoms are LESS COMMON in NLPHL compared to cHL — NLPHL typically presents with asymptomatic peripheral lymphadenopathy and follows an indolent course. NLPHL cells are CD20 POSITIVE — the popcorn cells express CD20, CD45, CD19, CD22, and CD79a, while LACKING CD15 and CD30 (the opposite of cHL Reed-Sternberg cells). The clinical implication of CD20 positivity: rituximab is a foundational treatment component for NLPHL — unlike standard cHL where rituximab is not used. NLPHL may also relapse as large-cell lymphoma, which is a distinctive clinical feature.
[/expand]How long after chemotherapy should a PET-CT scan be performed to avoid false-positive results?
A. Within a week
B. After 1 week
C. After 2 weeks
D. After 3 weeks
Answer: D. After 3 weeks (≥ 3 weeks)
Explanation: PET/CT should be performed at least 3 WEEKS after completion of a chemotherapy cycle before restaging. This waiting period is necessary because chemotherapy-induced inflammation causes increased FDG (fluorodeoxyglucose) uptake in treated tissues, which can produce FALSE-POSITIVE results — suggesting residual disease when none is present. Additional timing rules: post-radiotherapy: wait ≥ 6 weeks; post-G-CSF: wait ≥ 2 weeks (activated bone marrow takes up FDG); end-of-treatment assessment: some protocols recommend 6–8 weeks. Other false-positive causes: rebound thymic hyperplasia, infection, brown fat, extramedullary hematopoiesis. Important metabolic consideration: elevated blood glucose → DECREASED FDG uptake → FALSE-NEGATIVE result. Delay scan until glucose < 200 mg/dL; use oral hypoglycemics (not insulin) near FDG administration in diabetic patients.
[/expand]Brentuximab vedotin is used as:
A. Frontline treatment for classic early-stage HL
B. Frontline treatment for classic late-stage (advanced) HL
C. Relapsed/refractory HL
D. All of the above
Answer: D. All of the above
Explanation: Brentuximab vedotin is an anti-CD30 ADC (payload = MMAE) with established roles across ALL settings in cHL: Frontline advanced-stage (III–IV): A+AVD regimen (brentuximab + AVD) is a Category 1 NCCN recommendation based on the ECHELON-1 trial — demonstrated improved PFS and OS compared to ABVD. Frontline early-stage unfavorable: Used in select early-stage scenarios (Category 2A/2B), PET-adapted therapy, or for patients > 60 years or those for whom bleomycin is contraindicated. Relapsed/refractory cHL: Post-ASCT consolidation (AETHERA trial — improved PFS in high-risk patients); salvage therapy before transplant; palliation in transplant-ineligible patients. Key safety rules: CONTRAINDICATED in patients with pre-existing neuropathy (peripheral neuropathy is dose-limiting). Do NOT combine with bleomycin — unacceptable risk of FATAL pulmonary toxicity.
[/expand]The Deauville criteria are used for which of the following?
A. Visual interpretation of PET-CT
B. Histological grading of Hodgkin lymphoma
C. Prognostic scoring of HL by clinical markers
D. Prognostic scoring of HL by laboratory markers
Answer: A. Visual interpretation of PET-CT
Explanation: The Deauville criteria are a 5-point visual scoring system for interpreting PET-CT scans in lymphoma patients — they are based on a radiologist's visual assessment of FDG uptake compared to reference organs (mediastinum and liver). The five scores: 1 = no uptake; 2 = uptake ≤ mediastinum (NEGATIVE — optimal response); 3 = uptake > mediastinum but ≤ liver (good prognosis in most HL; interpret in context); 4 = uptake moderately > liver (POSITIVE); 5 = uptake markedly > liver (POSITIVE). Clinical application in HL: Deauville 1–3 on interim scan = optimal response → de-escalate (e.g., drop bleomycin → continue as AVD). Deauville 4–5 = sub-optimal → consider intensification; BIOPSY first to confirm residual disease and exclude false-positive before changing to second-line therapy. Important distinctions: Deauville criteria are NOT histological grading (option B), NOT clinical prognostic scoring (option C), and NOT laboratory-based scoring (option D). Those functions belong to the International Prognostic Score (IPS), which uses clinical and laboratory markers at diagnosis.
[/expand]Approximately what percentage of patients are cured of Hodgkin lymphoma?
A. 55–60%
B. 65–70%
C. 75–80%
D. 85–90%
Answer: D. 85–90%
Explanation: Hodgkin lymphoma is one of the most curable malignancies — modern treatment achieves cure in up to 85–90% of patients. This extraordinary cure rate has fundamentally shifted clinical priorities: because the overwhelming majority of newly diagnosed patients will be cured, clinical management now heavily focuses on minimizing LONG-TERM TOXICITIES from therapy including: secondary malignancies, cardiotoxicity (doxorubicin), pulmonary toxicity (bleomycin), infertility, and hypothyroidism (post-neck radiation). This "toxicity-reduction" philosophy drives modern treatment strategies such as PET-adapted de-escalation (dropping bleomycin with good interim response), preference for ISRT over extended-field radiation, and avoidance of unnecessary consolidation radiotherapy in early-stage favorable responders.
[/expand]Which one of the following statements is NOT TRUE regarding the Reed-Sternberg cell?
A. It is thought to be of B-cell lineage
B. It is multinucleate
C. It represents the majority of cells in a lymph node of Hodgkin lymphoma
D. It usually expresses CD15 and CD30
Explanation: This is FALSE — Reed-Sternberg cells represent only 1–10% of the cells in an involved lymph node. They are a MINORITY of cells; the vast majority of cells in HL-involved nodes are non-malignant reactive cells (granulocytes, plasma cells, lymphocytes) that constitute the inflammatory background. The other statements are all TRUE: B-cell lineage (option A) — molecular PCR studies confirmed HRS cells are clonal pre-apoptotic germinal center-derived B-lymphocytes; despite this B-cell origin, RS cells LOSE B-cell phenotypic features (they are CD20 negative in cHL). Multinucleate (option B) — classic RS cell is large and binucleated with prominent nucleoli giving the hallmark "owl's eyes" appearance under microscopy. CD15 and CD30 expression (option D) — in cHL, RS cells consistently express CD30 (virtually 100%) and CD15 (approximately 85%), which are the defining immunophenotypic markers used for diagnosis; they are typically negative for CD20 (unlike NLPHL popcorn cells).
[/expand]41. ABVD was prescribed for a newly diagnosed patient with Hodgkin disease. What does the acronym ABVD mean?
- A. Adriamycin, bleomycin, vinblastine, dexamethasone (11%)
- B. Adriamycin, bleomycin, vincristine, dexamethasone (27%)
- C. Adriamycin, bleomycin, vincristine, dacarbazine (19%)
- D. Adriamycin, bleomycin, vinblastine, dacarbazine (43%)
[expand] Answer (d) ABVD - Adriamycin or doxorubicin. Bleomycin, Vinblastine, and Dacarbazine
[/expand]106. The BEAM regimen used to treat lymphoma includes:
- A Bleomycin, etoposide, Adriamycin, and methotrexate (23%)
- B BCNU, etoposide, Adriamycin, and melphalan (14%)
- C BCNU, etoposide, cytarabine, and methotrexate (13%)
- D BCNU, etoposide, ARA-C, and melphalan (60%)
BCNU = carmustine, etoposide, ARA-C = cytarabine, melphalan
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