Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Carmustine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed1990

Purification and characterization of lipoamide dehydrogenase from Trypanosoma cruzi.

From Trypanosoma cruzi, the causative agent of Chagas' disease, a lipoamide dehydrogenase was isolated. The enzyme, an FAD-cystine oxidoreductase, shares many physical and chemical properties with T. cruzi trypanothione reductase, the key enzyme of the parasite's thiol metabolism. 1. From 60 g epimastigotic T. cruzi cells, 2.7 mg lipoamide dehydrogenase was extracted. The flavoenzyme was purified 3000-fold to homogeneity with an overall yield of 26%. 2. The enzyme is a dimer with a subunit Mr of 55,000. With 1 mM lipoamide (Km approximately 5 mM) and 100 microM NADH (Km = 23 microM), the specific activity at pH 7.0 is 297 U/mg. 3. With excess NADH, the enzyme is reduced to the EH2.NADH complex and, by addition of lipoamide, it is reoxidized, indicating that it can cycle between the oxidized state E and the two-electron-reduced state, EH2. 4. As shown by N-terminal sequencing of the enzyme, 21 out of 30 positions are identical with those of pig heart and human liver lipoamide dehydrogenase. The sequenced section comprises the GGGPGG stretch, which represents the binding site for the pyrophosphate moiety of FAD. 5. After reduction of Eox to the two-electron-reduced state, the enzyme is specifically inhibited by the nitrosourea drug 1,3-bis(2-chloroethyl)-1-nitrosourea (Carmustine), presumably by carbamoylation at one of the nascent active-site thiols. 6. Polyclonal rabbit antibodies raised against T. cruzi lipoamide dehydrogenase and trypanothione reductase are specific for the respective enzyme, as shown by immunoblots of the pure proteins and of cell extracts.

Amino Acid Sequence↗
PubMed1983

Decreased phenytoin level during antineoplastic therapy: a case report.

We report a case of interaction between anticonvulsant and antineoplastic drugs in one male patient with seizures from brain tumour. The patient was treated with phenytoin (PHT), phenobarbital (PB), and an antineoplastic protocol based on a combination regimen with carmustine (BCNU), vinblastin (VLB), methotrexate (MTX), and radiotherapy. Plasma concentrations of PHT fell from 9.4 to 5.6 micrograms/ml 24 h after VLB administration, and remained low for at least 10 days. During this period, partial seizures occurred. Plasma concentrations of PB were unchanged during the period of observation. It is suggested that impaired absorption of PHT, caused by VLB or MTX or both, is responsible for this interaction.

Antineoplastic Agents↗
PubMed1987

Therapy of malignant brain tumors: comparison of the in vitro activities of vidarabin-monophosphate, BCNU and 5-fluorouracil.

BCNU (carmustine), 5-Fluorouracil (5-FU) and Vidarabin-monophosphate (ARA-A5'P) were compared in their activities against 30 cell lines of primary (n = 21) and metastatic (n = 9) brain tumors, which were characterized in tissue culture by cytochemical, immunological and cytogenetic criteria. In vivo achievable concentration-time products were correlated with in vitro pharmacokinetic data. A micro assay was employed to screen for drug toxicity in individual tumor cell lines; cells were exposed to the drugs at exposure doses relevant to in vivo pharmacokinetics. After 5-8 population doubling times of untreated controls, RNA-synthesis, as a parameter of cell metabolism and proliferation, was determined by incorporation of (5, 6-3H)-uridine into cellular RNA (liquid scintillation counting protocol). A tumor stem cell assay was performed under similar conditions. The cytotoxic effect of each drug on individual cell lines was expressed in terms of a sensitivity index SI (SI = 1 indicating complete resistance) to compare effects of different drugs on the individual tumor cell lines. Mean sensitivity indices for ARA-A5'P, BCNU and 5-FU in brain tumor cell lines (in brackets: primary CNS-tumors) were 0.64 (0.59), 0.89 (0.82) and 0.35 (0.33) respectively. 5-FU was significantly more active than BCNU and ARA-A5'P (P less than 0.001), whereas BCNU was significantly less active than ARA-A5'P (P less than 0.001). ARA-A5'P had a suppressive effect on formation of brain tumor stem cell colonies. There was no cross-resistance of ARA-A5'P to either BCNU or 5-FU. We conclude that ARA-A5'P and 5-FU are potent agents in experimental therapy of human brain tumors, compared with BCNU.

Brain Neoplasms↗
PubMed1986

Multiple myeloma in central Norway 1981-1982: a randomized clinical trial of 5-drug combination therapy versus standard therapy.

67 previously untreated patients with multiple myeloma were entered on a randomized clinical trial to determine whether the use of combination chemotherapy including vincristine, carmustine, alkylating agents, and prednisone was more effective than conventional therapy with melphalan and prednisone. The treatment groups did not show significant differences with respect to major prognostic factors. With the 2-drug combination therapy and 5-drug combination therapy, 67 and 74% of the patients achieved remission, respectively. Moreover, no significant difference was found between the two treatment schedules in terms of median survival (30+ months). The survival curves for stage III patients treated with the two regimens did not differ significantly. After 12 months, patients who had achieved remission were randomized to have treatment discontinued or to have maintenance treatment. 7 of 15 patients on maintenance therapy relapsed, whereas 9 of 14 patients who had their therapy discontinued relapsed, and the survival of the two groups was similar.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

M-2 protocol for melphalan-resistant and relapsing multiple myeloma.

33 patients with advanced refractory multiple myeloma received a combination of vincristine, cyclophosphamide, carmustine, melphalan and steroids (M-2 protocol). 20 of them had failed prior chemotherapy with alkylating agents and the remaining 13 patients had relapsed after a response to these drugs. An objective tumour cell mass reduction (greater than or equal to 50%) was achieved in 17% of the patients (6% of previously nonresponders and 33% of previously relapsing), while 9 additional patients improved (30-50% tumour reduction), for an overall response rate of 47% (39% for previously nonresponders and 58% for previously relapsing). The median duration of response was 7 months. Thrombocytopenia was the most common toxicity encountered in the study (39% of cases). Our findings indicate that M-2 protocol is an effective salvage treatment for patients who relapse from previous chemotherapy with alkylating agents. In contrast, results in patients who are primarily resistant to these drugs justify the search for different treatment programmes which can produce greater degrees of tumour reduction.

Adult↗
PubMed1993

High-dose cyclophosphamide, etoposide and BCNU (CVB) with autologous stem cell rescue in malignant lymphomas.

Eighteen patients with malignant lymphoma, 10 non-Hodgkin's and 8 Hodgkin's, were treated with high-dose CVB (cyclophosphamide 4 x 1.5 g/m2, etoposide 4 x 250-400 mg/m2, carmustine 4 x 150-200 mg/m2), followed by autologous peripheral blood stem cells (PBSC, 13 patients) or bone marrow (BM, 5 patients) transplantation. At the time of autograft 6 patients were in complete remission (CR), 3 in partial remission (PR) and 5 in relapse (4 sensitive, 1 resistant), whereas 4 had progressive disease. All CR patients had poor prognostic features at presentation. PBSC were collected at the time of rapid hematologic recovery after intense chemotherapy by means of a cell separator. All patients engrafted. Median time to achieve > or = 0.5 x 10(9)/l polymorphonuclear cells (PMN) and > or = 50 x 10(9)/l platelets was 13 days for both cell types in PBSC autografted patients, versus 20 and 28 days respectively in BM autografted patients. A significant advantage of PBSC over BM was found in terms of time needed to recover either PMN > or = 0.5 and PMN > or = 1 x 10(9)/l (p = 0.01). Autograft-related toxicity consisted mainly of moderate severity interstitial pneumopathy (3 patients), and veno-occlusive disease (1 patient) that resolved completely. Of the 12 patients autografted with detectable disease, 6 (50%) obtained a CR. Seven out of 18 autografted patients (39%) had disease progression within 1 to 5 months of autograft. The projected progression-free survival is over 50% at 4 years and it was significantly longer in patients with sensitive disease than in those with resistant disease (p = 0.01). The efficacy and the low toxicity of CVB suggest that autograft with PBSC may be proposed for the primary treatment of poor prognosis malignant lymphomas.

Adult↗
PubMed2003

Inhibition of telomerase increases resistance of melanoma cells to temozolomide, but not to temozolomide combined with poly (adp-ribose) polymerase inhibitor.

In the present study, we have investigated the influence of telomerase inhibition in chemosensitivity of melanoma cells to temozolomide (TMZ), a methylating agent with promising antitumor activity against metastatic melanoma. In fact, telomerase, a ribonucleoprotein enzyme expressed in the majority of tumors, is presently considered an attractive target for anticancer therapy, with the double aim of reducing tumor growth and increasing chemosensitivity of cancer cells. Susceptibility to TMZ and to other antitumor agents used for treatment of metastatic melanoma was initially assessed in melanoma lines with different basal levels of telomerase activity. Thereafter, chemosensitivity was investigated after inhibition of telomerase by means of stable transfection of a catalytically inactive, dominant-negative mutant of hTERT (DN-hTERT). This study shows for the first time that: a) susceptibility to TMZ of melanoma lines derived from the same patient did not depend on basal telomerase activity; b) inhibition of telomerase by DN-hTERT resulted in reduced growth rate and increased resistance to TMZ and to the chloroethylating agent carmustine, increased sensitivity to cisplatin, and no change in response to tamoxifen or to a selective N3-adenine methylating agent; c) inhibition of poly(ADP-ribose) polymerase (PARP), an enzyme involved in the repair of N-methylpurines, restored sensitivity of DN-hTERT clones to TMZ. These results indicate that a careful selection of the antitumor agent has to be made when antitelomerase therapy is combined with chemotherapy. Moreover, the data presented here suggest that TMZ + PARP inhibitor combination is active against telomerase-suppressed and slowly growing tumors.

Antineoplastic Agents, Alkylating↗
PubMed2004

DNA damage-processing pathways involved in the eukaryotic cellular response to anticancer DNA cross-linking drugs.

We used a panel of isogenic Saccharomyces cerevisiae strains compromised in several different DNA damage-processing pathways to assess in vivo processing of DNA adducts induced by four cross-linking anticancer drugs. By examining cytotoxicity profiles, cell cycle arrest patterns, and determining recombination and mutation frequencies, we found that cisplatin-, nitrogen mustard-, mitomycin-, and carmustine-induced DNA adducts in S. cerevisiae are processed by components of the nucleotide excision repair (NER), recombination repair (RR), and translesion synthesis (TLS) pathways, with substantially different contributions of each pathway for the drugs studied here. In contrast to previous studies that used single pathway-compromised strains to identify genes that mediate sensitivity to DNA cross-linking drugs, we used strains that were compromised in multiple pathways. By doing so, we were able to establish several functions that were previously unknown and interconnections between different DNA damage-processing pathways. To our surprise, we found that for cisplatin-induced cytotoxicity, TLS and RR contribute to survival to a significant extent. In the case of nitrogen mustard DNA adduct processing, equal involvement of two major pathways was established: one that requires functional RR and NER components and one that requires functional TLS and NER components. These data reveal the complexity of DNA cross-link processing that, in many cases, requires interactions of components from several different DNA damage-processing systems. We demonstrate the usefulness of yeast strains with multiple simultaneous defects in DNA damage-processing pathways for studying the modes of action of anticancer drugs.

Antineoplastic Agents↗
PubMed2000

Hematologic toxic reaction to radiation therapy adjuvant to autologous peripheral blood stem cell transplantation for recurrent or refractory Hodgkin disease.

PURPOSE: To evaluate the hematologic toxic reaction to external-beam radiation therapy after high-dose chemotherapy with peripheral blood stem cell (PBSC) support in patients with Hodgkin disease. MATERIALS AND METHODS: A retrospective study of 30 cases of Hodgkin disease in patients who underwent high-dose carmustine, etoposide, and cyclophosphamide chemotherapy with PBSC support was performed. Thirteen patients underwent radiation therapy (28.8-39.0 Gy) a median of 45 days after PBSC repeat infusion. RESULTS: Radiation therapy was delivered as planned, without interruption, in all patients. Five patients developed thrombocytopenia (one with grade 1 thrombocytopenia; two, grade 2; and two, grade 3) and included three with progressive disease prior to radiation therapy and two with a history of prior irradiation. None developed a bleeding complication or required transfusion support. Five patients who underwent irradiation had thrombocytopenia (three with grade 1 and two with grade 2) 100 days after PBSC repeat infusion, compared with three patients (two with grade 1 and one with grade 3) who did not undergo posttransplantation irradiation. At the most recent follow-up, no patient without evidence of disease had a platelet count of less than 100 x 10(9)/L. CONCLUSION: External-beam radiation therapy was well tolerated in the posttransplantation setting in patients with Hodgkin disease. Thrombocytopenia was common but was not related to clinical complications.

Adolescent↗
PubMed2006

Inhibition of vascular endothelial growth factor (VEGF)-A causes a paradoxical increase in tumor blood flow and up-regulation of VEGF-D.

PURPOSE: Vascular endothelial growth factor (VEGF)-A is an important mediator of angiogenesis in almost all solid tumors. The aim of this study was to evaluate the effect of VEGF-A expression on tumor growth, perfusion, and chemotherapeutic efficacy in orthotopic 9L gliosarcomas. EXPERIMENTAL DESIGN: Stable 9L cell lines underexpressing and overexpressing VEGF-A were generated. Anatomic, susceptibility contrast, and continuous arterial spin-labeling magnetic resonance imaging were used to quantify the volume, blood volume, and blood flow of tumors orthotopically grown from these and wild-type 9L cells. Histologic, immunohistochemical, and quantitative reverse transcription-PCR analyses were also done on excised tumors. Finally, the effects of carmustine chemotherapy were also evaluated. RESULTS: Orthotopic tumors underexpressing VEGF-A had slower growth rates (increased median survival), greater blood flow, vessel density, and VEGF-D expression, but no statistical difference in blood volume and chemotherapeutic sensitivity, compared with tumors with wild-type levels of VEGF-A. Tumors overexpressing VEGF-A had faster growth rates, greater blood volume, vessel density, and blood flow but no statistical difference in VEGF-D expression and chemotherapeutic sensitivity compared with wild-type VEGF-A-expressing tumors. CONCLUSION: Blood volume and blood flow are independent and different biomarkers of tumor perfusion. Therefore, both should be measured when characterizing the efficacy of antiangiogenic therapies. Underexpression of VEGF-A does not result in complete inhibition of angiogenesis. Moreover, these tumors have a different perfusion phenotype, suggesting that angiogenesis is mediated by an alternative pathway. The results indicate that VEGF-D is a plausible alternative mediator of this angiogenesis.

Animals↗
PubMed1999

Cutaneous T cell lymphoma: update of treatment.

The state-of-the art therapy of cutaneous T cell lymphoma (CTCL) is reviewed. Commonly used treatments for early-stage (patch/plaque) mycosis fungoides (MF) include topical corticosteroids, mechlorethamine, carmustine, ultraviolet light B and PUVA. Total skin electron beam (TSEB) therapy is indicated for widespread infiltrated plaque and tumor stage disease. Low-dose methotrexate is often useful for resistant patch/plaque MF and erythrodermic CTCL. Interferon alpha (IFN-alpha) is indicated for methotrexate failures and recurrent tumors following TSEB therapy. Photopheresis may be helpful for early-stage erythrodermic CTCL but is very costly. Retinoids may be of value for early and moderately advanced CTCL particularly in combination with other agents such as IFN-alpha and PUVA. Systemic disease usually requires combination chemotherapy such as that used for non-Hodgkin's lymphoma; however, responses are usually short lived.

Administration, Topical↗
PubMedDate not supplied

Primary T cell leptomeningeal lymphoma--successful treatment with systemic chemotherapy.

Primary central nervous system lymphoma (PCNSL) is rare, accounting for only 1-2% of non-Hodgkin's lymphoma, and primary isolated leptomeningeal lymphoma is even rarer. It may create a diagnostic problem, particularly when the tumor cells are of T cell lineage. We herein report a patient with primary T cell leptomeningeal lymphoma. The final diagnosis was confirmed by the cytogenetic study which revealed clonal aberration, isochromosome of long arm of chromosome 7, in the lymphoid cells from CSF. She was treated with a novel protocol of systemic chemotherapy specifically designed for the CNS lymphoma. The regimen consisted of carmustine, vincristine, high-dose methotrexate, etoposide, and methylprednisolone. A total of 5 courses were given and she was still in complete remission at the time of reporting, 21 months after the establishment of diagnosis.

Adult↗
PubMed1987

Experimental combination chemotherapy: intracarotid versus intravenous administration of aziridinylbenzoquinone, BCNU, and cisplatin in dogs.

Sixteen adult beagles (10-12 kg) were used to evaluate combinations of 2,5-diaziridinyl-3,6-biscarboethoxyamino-1,4-benzoquinone (AZQ, aziridinylbenzoquinone), 1,3-bis-2-chloroethyl-1-nitrosourea (BCNU, carmustine), and cis-dichlorodiammineplatinum(II) (CDDP, cisplatin) administered by intravenous or intracarotid infusion. Moderate to severe systemic toxicities resulted from all drug infusions, but no histopathologic changes were found in the central nervous system (CNS) of any of the dogs. Results indicated that the toxicities were not dependent on the route of administration or the recipient's gender, and they were reversible in most cases with intravenous supportive therapy. Cisplatin seemed to have an additive effect when administered in combination with AZQ and/or BCNU.

Animals↗
PubMed1987

Novobiocin enhances alkylating agent cytotoxicity and DNA interstrand crosslinks in a murine model.

DNA-DNA crosslinks are the lethal cellular mechanism of bifunctional alkylating agent cytotoxicity. Novobiocin, an inhibitor of DNA topoisomerase II, impairs eukaryotic DNA repair of alkylating agent adducts and may increase the number of adducts and their resultant cytotoxicity in malignant cells. The effect of novobiocin on clonogenic survival and DNA crosslinking due to cisplatin (cDDP) and carmustine (BCNU) was studied. Novobiocin caused synergistic cytotoxicity in Chinese hamster ovary cells exposed to cDDP or BCNU. Novobiocin and cDDP increased the formation of DNA-DNA interstrand crosslinks six-fold greater than cDDP alone. The effect was schedule dependent. Novobiocin and cDDP or BCNU markedly reduced in vivo growth of a murine fibrosarcoma without increased host toxicity. As a modulating agent of cytotoxicity due to DNA-DNA crosslinking, novobiocin may enhance the clinical effectiveness of the alkylating agents in human cancer and offer insight into new therapeutic strategies.

Alkylating Agents↗
PubMed1987

Sequential treatment with interferon and chemotherapy of metastatic malignant melanoma. Total remission of cutaneous and visceral metastasis, but not of cerebral metastasis.

A woman 35 years of age suffering from cutaneous and visceral metastatic melanoma was treated with recombinant Interferon alpha 2b (rIFN alpha 2b) subcutaneously 3 X 10(6) U/m2 3 times a week for 3 months with no apparent effect on the course of the illness. Two months after IFN therapy the patient developed cerebral metastasis. A cycle of carmustine, 100 mg/day for 3 days, was given, and complete disappearance of the cutaneous and visceral, but not of the cerebral manifestations was observed. Two consolidation cycles based on vincristine, dacarbazine and lomustine were then administered. The patient died 26 months after beginning treatment with IFN and 18 months after chemotherapy for the cerebral metastasis. No trace of tumor at the cutaneous or visceral level was found at autopsy.

Adult↗
PubMedDate not supplied

The feasibility of repetitive courses of high-dose continuous intravenous infusion interleukin-2 and subcutaneous alpha-interferon with polychemotherapy in advanced malignant melanoma.

AIMS AND BACKGROUND: A Phase I study of repetitive courses of chemotherapy (carmustine, cis-platinum, dacarbazine) and immunotherapy (continuous intravenous infusion recombinant interleukin-2 (rIL-2) and subcutaneous (sc) alpha-interferon 2b) plus tamoxifen was performed in order to establish a more efficacious way to sequence this kind of treatment for advanced malignant melanoma. STUDY DESIGN: Patients who had measurable metastatic melanoma, a Karnofsky performance status > or = 80, and no clinically significant hematologic or cardiac disfunction were considered eligible. Treatment consisted of BCNU, 150 mg/m2 i.v. day 1 in alternating cycles; DTIC, 220 mg/m2 i.v. days 1, 2 and 3; CDDP, 25 mg/m2 i.v. days 1, 2 and 3; tamoxifen 10 mg twice/day per os continuously; rIL-2, 18 x 10(6) IU/m2/day continuous i.v. infusion days 5-8 (96 h) and days 19-22 (96 h); alpha-interferon (IFN) s.c. 3 x 10(6) U day 12, 6 x 10(6) U day 14, 9 x 10(6) U days 16, 19, 21, 23, 26, and 28 (from cycle 2, 9 x 10(6) U days 2, 5, 7, 9, 12, 14, 16, 19, 21, 23, 26, and 28). Two consecutive cycles were planned until response evaluation. RESULTS: Three patients were treated according with the protocol; none of them was able to respect the planned dose-intensity schedule. The given dose intensity/planned dose intensity ratios were as follows: DTIC, 0.74 (range, 0.70-0.80); CDDP, 0.77 (0.72-0.80); BCNU, 0.77 (0.72-0.80); rIL-2, 0.65 (0.36-0.80); alpha-IFN, 0.01 (0-0.03); tamoxifen, 1.0. Systemic side effects of rIL-2 and myelotoxicity were the main reasons for treatment delay and/or dose-reduction, and for the long period of hospital care. CONCLUSIONS: We conclude that the treatment schedule is not feasible. However, since we believe that combined chemo-immunotherapy is a potentially active treatment in metastatic malignant melanoma, we have modified it in order to make it more feasible and consequently efficacious.

Adult↗
PubMed2003

Chemotherapy and bio-chemotherapy in patients with advanced melanoma: combination therapy with a nitrosourea.

The treatment of advanced melanoma is still disappointing. In a multicenter randomized clinical trial to compare a chemotherapy (CT) with or without low doses of IL-2 and IFN (Bio-CT), the participating centers chose whether or not to add a nitrosourea, carmustine (BCNU) to the therapy. The aim of the present paper is to report the clinical results of the patients (pts) treated in both arms with BCNU. One hundred and seventy-six pts with advanced melanoma were enrolled in the study from 27 centers and a total of 18 pts also received BCNU in 3 centers. No further changes to the protocol criteria were allowed. One patient refused the treatment. No complete responses were observed. Irrespectively of the treatment arm, 9/17 pts showed a partial response to therapy (53%) (5/9 in the CT and 4/8 in the BioCT arm). The most important adverse events observed were hematological: 12 pts presented grade 3 (6 pts) or grade 4 (6 pts) leukocytopenia and 9 pts had grade 4 thrombocytopenia, all of which resolved spontaneously. The addition of a nitrosourea to CT or Bio-CT appears to improve response rates compared to the same regimens without nitrosourea. Patient tolerability is acceptable. Further studies using this combination are warranted.

Adult↗
PubMed2006

Upfront double high-dose chemotherapy with DICEP followed by BEAM and autologous stem cell transplantation for poor-prognosis aggressive non-Hodgkin lymphoma.

A single center, prospective clinical trial was conducted evaluating 2 cycles of induction high-dose chemotherapy for adults younger than 65 years of age with aggressive non-Hodgkin lymphoma (NHL) and 2 to 3 Age-Adjusted International Prognostic Index risk factors. Patients received one cycle of standard dose cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) followed by one cycle of dose-intensive cyclophosphamide 5.25 g/m(2), etoposide 1.05 g/m(2), cisplatin 105 mg/m(2) (DICEP), then underwent autologous blood stem cell collection, followed by one cycle of high-dose carmustine (BCNU) 300 mg/m(2), etoposide 800 mg/m(2), Ara-C 1600 mg/m(2), melphalan 140 mg/m(2) (BEAM), and autologous stem cell transplantation (ASCT) and radiotherapy to prior bulk. From June 1998 to August 2004, 55 patients aged 20 to 63 years (median 44 years) were accrued, 51 (92%) of whom had diffuse large B-cell NHL. Poor prognostic factors included stage 4 (n = 46), elevated lactate dehydrogenase (LDH; n = 47), Eastern Cooperative Oncology Group (ECOG) performance status 2 to 4 (n = 43), bulky mass more than 10 cm (n = 34), and marrow involvement (n = 16). Only one patient experienced nonrelapse mortality. With a median follow-up of 49 months, 4-year event-free survival (EFS) and overall survival (OS) rates for all 55 patients are 72% (95% confidence interval [CI] = 60%-84%) and 79% (95% CI = 69%-90%), respectively. In conclusion, CHOP-DICEP-BEAM is feasible and gave encouraging EFS and OS for patients with poor-prognosis aggressive NHL.

Adult↗