Clofarabine (Clolar)

Number: 0867


Aetna considers clofarabine injection (Clolar) medically necessary for the following indications:

  • Acute myeloid leukemia (AML);
  • Relapsed or refractory acute lymphoblastic leukemia (ALL)
  • Refractory or recurrent childhood (18 years of age or younger) Langerhans cell histiocytosis.

Aetna considers clofarabine experimental and investigational for all other indications including the following (not an all-inclusive list).

  • Breast cancer
  • Central nervous system tumors (e.g., ependymoma)
  • Chronic myelomonocytic leukemia (CMML)
  • Mesothelioma
  • Myelodysplatic syndrome
  • Non-Hodgkin lymphomas (e.g., diffuse large B-cell lymphoma, indolent B-cell lymphomas, and mantle cell lymphoma)

Clolar was approved by the Food and Drug Adminstration (FDA) for acute lymphoblastic leukemia (ALL): "Clolar (clofarabine) Injection is a purine nucleoside metabolic inhibitor indicated for the treatment of pediatric patients 1 to 21 years old with relapsed or refractory acute lymphoblastic leukemia after at least two prior regimens.  Randomized trials demonstrating increased survival or other clinical benefit have not been conducted".

Guidelines from the National Comprehensive Cancer Network (2013) indicate Clolar for the following:

  • Acute Lymphoblastic Leukemia (ALL) -- Salvage therapy for relapsed/refractory Philadelphia chromosone-negative pre-B-cell ALL in patients aged less than or equal to 21 years as a component of clofarabine-containing regimens [2A]
  • Acute Myeloid Leukemia (AML) -- Induction therapy as a single agent for intermediate-intensity therapy for patients age greater than or equal to 60 years with performance status less than or equal to 2 [2B]
  • Acute Myeloid Leukemia (AML) -- Used in combination with cytarabine as
    • Post-induction therapy in patients age less than 60 years with induction failure
    • Salvage chemotherapy [2A]

In a phase I study, Abramson et al (2013) evaluated the effects of clofarabine in patients with relapsed/refractory non-Hodgkin lymphoma (NHL).  Patients were treated once-daily on days 1 through 21 of a 28-day cycle for a maximum of 6 cycles.  The study was conducted with a 3 + 3 design with 10 additional patients treated at the recommended phase II dose.  A total of 30 patients were enrolled including indolent B-cell lymphomas (n = 21), mantle cell lymphoma (n = 6) and diffuse large B-cell lymphoma (n = 3).  The primary toxicities were hematologic including grade 3 to 4 neutropenia (53 %) and thrombocytopenia (27 %); 3 mg was determined to be the recommended phase II dose.  Tumor volume was reduced in 70 % of patients, and the overall response rate (ORR) was 47 % including 27 % complete remissions (CRs).  Responses were seen in indolent B-cell lymphomas and mantle cell lymphoma.  At a median follow-up of 17 months, 68 % of responding patients remain in ongoing remission.  The authors concluded that oral clofarabine was well-tolerated with encouraging efficacy in indolent B-cell lymphomas and mantle cell lymphomas, warranting further investigation.

Lubecka-Pietruszewska et al (2014) stated that clofarabine (2-chloro-2'-fluoro-2'-deoxyarabinosyladenine, ClF) is a second-generation 2'-deoxyadenosine analog that is structurally related to cladribine (2-chloro-2'-deoxyadenosine, 2CdA) and fludarabine (9-beta-d-arabinosyl-2-fluoroadenine, F-ara-A).  It demonstrates potent anti-tumor activity at much lower doses than parent compounds with high therapeutic efficacy in pediatric blood cancers.  Previous studies from these researchers in breast cancer cells indicated that 2CdA and F-ara-A are involved in epigenetic regulation of gene transcription.  These investigators therefore examined if  ClF influences methylation and expression of selected tumor suppressor genes, such as adenomatous polyposis coli (APC), phosphatase and tensin homolog (PTEN), and retinoic acid receptor beta 2 (RARbeta2), as well as expression of p53, p21 and DNA methyltransferase 1 (DNMT1) in MCF-7 and MDA-MB-231 breast cancer cell lines with different invasive potential.  Promoter methylation and gene expression were estimated using methylation-sensitive restriction analysis (MSRA) and real-time PCR, respectively.  Clofarabine demonstrated potent growth inhibitory activity in MCF-7 and MDA-MB-231 cells after 96 hours of treatment with IC50 determined as equal to 640 nM and 50 nM, respectively.  In both breast cancer cell lines, ClF led to hypo-methylation and up-regulation of APC, PTEN and RARbeta2 as well as increase in p21 expression.  Only in non-invasive MCF-7 cells, these changes were associated with down-regulation of DNMT1.  The authors concluded that these results provided first evidence of ClF implications in epigenetic regulation of transcriptional activity of selected tumor suppressor genes in breast cancer.  It seems to be a new important element of ClF anti-cancer activity and may indicate its potential efficacy in epigenetic therapy of solid tumors, especially at early stages of carcinogenesis.

Simko et al (2014) noted that existing therapies for recurrent or refractory histiocytoses, including Langerhans cell histiocytosis (LCH), juvenile xanthogranuloma (JXG), and Rosai-Dorfman disease (RDD), have limited effectiveness.  These researchers reported their experience with using clofarabine as therapy in children with recurrent or refractory histiocytic disorders, including LCH (n = 11), systemic JXG (n = 4), and RDD (n = 3).  Patients treated with clofarabine for LCH, JXG, or RDD by Texas Children's Hospital physicians or collaborators between May 2011 and January 2013 were reviewed for response and toxicity.  Patients were treated with a median of 3 chemotherapeutic regimens prior to clofarabine.  Clofarabine was typically administered at 25 mg/m(2)/day for 5 days.  Cycles were administered every 28 days for a median of 6 cycles (range of 2 to 8 cycles); 17 of 18 patients are alive.  All surviving patients showed demonstrable improvement after 2 to 4 cycles of therapy, with 11 (61 %) complete responses, 4 (22 %) partial responses, and 2 patients still receiving therapy.  Five patients experienced disease recurrence, but 3 of these subsequently achieved complete remission.  All patients with JXG and RDD had complete or partial response at conclusion of therapy.  Side effects included neutropenia in all patients.  Recurring but sporadic toxicities included prolonged neutropenia, severe vomiting, and bacterial infections.  The authors concluded that clofarabine has activity against LCH, JXG, and RDD in heavily pre-treated patients, but prospective multi-center trials are needed to determine long-term efficacy, optimal dosing, and late toxicity of clofarabine in this population.

Guidelines on LCH in children from the National Cancer Institute (PDQ) (NCI, 2015) state that some LCH patients with high-risk multisystem disease develop a “macrophage activation” of their marrow.  The guidelines state that this may be confusing to clinicians who may think the patient has hemophagocytic lymphohistiocytosis and LCH.  The best therapy for this life-threatening manifestation is not clear, because it tends not to respond well to standard hemophagocytic lymphohistiocytosis therapy.  The guidelines state that clofarabine is one option to consider in this situation.  A Euro-Histio-Net guideline on LCH in adults (Girshikofsky et al, 2013) states that clofarabine has been successfully used as salvage therapy for refractory childhood LCH (citing Rodriguez-Galindo, 2008).

By contrast guidelines on LCH from the Histiocyte Society (Minkov et al, 2009), on adult LCH from NCI (2015), and a separate guideline on childhood LCH from members of the Euro Histio Net (Haupt et al, 2013) have no recommendation for clofarabine.  These guidelines have recommendations for steroids, vinblastine, cladribine and cytarabine for multisystem LCH.

Tischer and colleagues (2013) stated that clofarabine is a novel purine nucleoside analog with immunosuppressive and anti-leukemic activity in AML and ALL. This retrospective study was performed to evaluate the feasibility and anti-leukemic activity of a sequential therapy using clofarabine for cytoreduction followed by conditioning for haploidentical hematopoietic stem cell transplantation (HSCT) in patients with non-remission acute leukemia.  Patients received clofarabine (5 × 30 mg/m² IV) followed by a T cell replete haploidentical transplantation for AML (n = 15) or ALL (n = 3).  Conditioning consisted of fludarabine, cyclophosphamide plus either melphalan, total body irradiation (TBI) or treosulfan/etoposide.  High-dose cyclophosphamide was administered for post-grafting immunosuppression.  Neutrophil engraftment was achieved in 83 % and complete remission in 78 % at day +30.  The rate of acute graft versus host disease (GvHD) grade II to IV was 22 %, while chronic GvHD occurred in 5 patients (28 %).  Non-relapse mortality (NRM) after 1 year was 23 %.  At a median follow-up of 19 months, estimated overall survival (OS) and relapse-free survival at 1 year from haploidentical HSCT were 56 and 39 %, respectively.  Non-hematological regimen-related grade III to IV toxicity was observed in 10 patients (56 %) and included most commonly transient elevation of liver enzymes (44 %), mucositis (40 %), and skin reactions including hand-foot syndrome (17 %), creatinine elevation (17 %), and nausea/vomiting (17 %).  The concept of a sequential therapy using clofarabine for cytoreduction followed by haploidentical HSCT proved to be feasible and allowed successful engraftment, while providing an acceptable toxicity profile and anti-leukemic efficacy in patients with advanced acute leukemia.  NRM and rate of GvHD were comparable to results after HSCT from HLA-matched donors.

Rabitsch et al (2014) stated that allogeneic HSCT is the only curative rescue therapy for patients with chemotherapy-refractory acute leukemia.  Disease control prior to HSCT is essential for long-term disease-free survival (DFS) after HSCT.  These investigators retrospectively analyzed the outcome of 20 patients aged 21 to 64 years with refractory leukemia (AML, n = 16; ALL, n = 4) who received debulking therapy with clofarabine (10 mg/m², days 1 to 4) and cyclophosphamide (200 mg/m², days 1 to 4; ClofCy) prior to HSCT.  Clofarabine/cyclophosphamide (1 to 4 cycles) was well-tolerated and resulted in a substantial reduction of leukemic cells in all patients.  Hematopoietic stem cell transplantation was performed in 15 of 20 patients.  After HSCT (myeloablative, n = 9; dose-reduced, n = 6), all patients showed engraftment and full donor chimerism (related donors, n = 4 or unrelated donors, n = 11) and all patients achieved complete hematologic remission (CR).  The median survival after HSCT was 531 days (range of 48 to 1,462 days), and 6 patients were still alive after a median of 1,245 days.  Seven patients died after they had relapsed between days +152 and +1,496.  One patient died from acute graft-versus-host disease (day +48) and 1 from systemic fungal infection (day +87).  The authors concluded that clofarabine/cyclophosphamide is a novel effective treatment approach for patients with chemotherapy-refractory acute leukemia prior to HSCT.  Moreover, they stated that whether this novel debulking protocol leads to improved long-term outcome in patients with refractory leukemias remains to be determined in forthcoming clinical studies.

In a prospective, phase II clinical trial, Chevallier et al (2014) evaluated the safety and effectiveness of a clofarabine, intravenous busulfan and anti-thymocyte globulin-based reduced-toxicity conditioning (CloB2A2) regimen before allogeneic stem cell transplantation.  A total of 30 high-risk patients (median age of 59 years; AML, n = 11, ALL, n =13; myelodysplastic syndrome [MDS] n = 5, bi-phenotypic leukemia n = 1) were included in this study.  At time of their transplant, 20 and 7 patients were in 1st and 2nd CR, respectively, while 3 patients with MDS were responding to chemotherapy or who had not been previously treated.  The CloB2A2 regimen consisted of clofarabine 30 mg/m(2)/day for 4 days, busulfan 3.2 mg/kg/day for 2 days and anti-thymocyte globulin 2.5 mg/kg/day for 2 days.  The median follow-up was 23 months.  Engraftment occurred in all patients.  The 1-year OS, leukemia-free survival, relapse incidence and non-relapse mortality rates were 63 ± 9 %, 57 ± 9 %, 40 ± 9 %, and 3.3 ± 3 %, respectively.  Comparing patients with AML/MDS versus those with ALL/bi-phenotypic leukemia, the 1-year OS and leukemia-free survival rates were 75 ± 10 % versus 50 ± 13%, respectively (p = 0.07) and 69 ± 12 % versus 43 ± 13 %, respectively (p = 0.08), while the 1-year relapse incidence was 25 ± 11 % versus 57 ± 14 %, respectively (p = 0.05).  The authors concluded that the CloB2A2 regimen prior to allogeneic stem cell transplantation is feasible, allowing for full engraftment and low toxicity.  Disease control appears to be satisfactory, especially in patients with AML/MDS.

Ghanem et al (2014) noted that the outcome of patients with MDS and chronic myelomonocytic leukemia (CMML) post-clofarabine is unknown.  These researchers reviewed 109 patients with MDS or CMML with a median age of 67 years, treated with a clofarabine-based chemotherapy as frontline (n = 38) or salvage (n = 71) therapy.  A total of 58 (53 %) patients received salvage therapy after clofarabine failure: 13 allogeneic stem cell transplant (ASCT), 18 high-dose cytarabine-containing regimen, 10 hypomethylating agents and 17 investigational treatments.  A total of 8 patients achieved CR and 3 had stable disease for an overall response rate of 19 %.  With a median follow-up of 3 months from clofarabine failure, 12 patients (11 %) remained alive, 5 remain in CR, 4 of them after ASCT.  The median OS post-clofarabine failure was 4 months with a 1-year survival rate of 23 %.  The authors stated that this outcome is predictable, with patients with high-risk disease at the time of clofarabine failure having the worse survival.  To-date, patients with MDS continue to have a short survival after failure of all available therapies.  Ultimately, patients who are candidates for additional treatments should be offered novel approaches.  They concluded that the outcome of patients with MDS and CMML post-clofarabine failure is poor.  The pattern is similar to patients with MDS post-hypomethylating agent failure and predictable using University of Texas M. D. Anderson Cancer Center global scoring system.

Lee et al (2015) previously demonstrated that resveratrol and clofarabine elicited a marked cytotoxicity on malignant mesothelioma (MM) MSTO-211H cells but not on the corresponding normal mesothelial MeT-5A cells.  Little is known of the possible molecules that could be used to predict preferential chemosensitivity on MSTO-211H cells.  Resveratrol and clofarabine induced down-regulation of Mcl-1 protein level in MSTO-211H cells.  Treatment of cells with cycloheximide in the presence of proteasome inhibitor MG132 suggested that Mcl-1 protein levels were regulated at the post-translational step.  The siRNA-based knockdown of Mcl-1 in MSTO-211H cells triggered more growth-inhibiting and apoptosis-inducing effects with the resultant cleavages of procaspase-3 and its substrate PARP, increased caspase-3/7 activity, and increased percentage of apoptotic propensities.  However, the majority of the observed changes were not shown in MeT-5A cells.  The authors concluded that these studies indicated that the preferential activation of caspase cascade in malignant cells might have important applications as a therapeutic target for MM.

Zoellner and colleagues (2015) noted that prognosis is poor for patients with biologically aggressive non-Hodgkin lymphoma (NHL), refractory to chemotherapy or relapsed after autologous transplantation, especially when no disease control before allogeneic transplantation is achieved. In 16 patients (median age of 53 years, median prior regimens of 5) with relapsed or refractory non-remission NHL, these researchers analyzed retrospectively the effectiveness of a sequential therapy comprising clofarabine re-induction followed by a reduced-intensity conditioning with fludarabine, cyclophosphamide (CY), and melphalan, and T-cell-replete HLA-haploidentical transplantation. High-dose CY was utilized post-transplantation. All patients engrafted. Early response (day +30) was achieved in 94 %. Treatment-related grade III to IV toxicity occurred in 56 %, most commonly transient elevation of transaminases (36 %), while there was a low incidence of infections (19 % cytomegalovirus (CMV) re-activation, 19 % invasive fungal infection) and GVHD (GVHD: acute III to IV: 6 %; mild chronic: 25 %). One-year non-relapse mortality was 19 %. After a median follow-up of 21 months, estimated 1- and 2-year progression-free survival (PFS) was 56 % and 50 %, respectively, with 11 patients (69 %) still alive after 2 years. The authors concluded that sequential therapy is feasible and effective and provided an acceptable toxicity profile in high-risk non-remission NHL. Presumably, cytotoxic re-induction with clofarabine provided enough remission time for the graft-versus lymphoma effect of HLA-haploidentical transplantation to kick in, even in lymphomas that are otherwise chemo-refractory. These preliminary findings need to be validated by well-designed studies.

Central Nervous System Tumors:

To characterize the clofarabine disposition in mice for further pre-clinical efficacy studies, Patel et al (2015) evaluated the plasma and central nervous system disposition in a mouse model of ependymoma. A plasma pharmacokinetic study of clofarabine (45 mg/kg, intra-peritoneal [IP] injection) was performed in CD1 nude mice bearing ependymoma to obtain initial plasma pharmacokinetic parameters. These estimates were used to derive D-optimal plasma sampling time points for cerebral microdialysis studies. A simulation of clofarabine pharmacokinetics in mice and pediatric patients suggested that a dosage of 30 mg/kg IP in mice would give exposures comparable to that in children at a dosage of 148 mg/m(2). Cerebral microdialysis was performed to study the tumor extra-cellular fluid (ECF) disposition of clofarabine (30 mg/kg, IP) in the ependymoma cortical allografts. Plasma and tumor ECF concentration-time data were analyzed using a non-linear mixed effects modeling approach. The median unbound fraction of clofarabine in mouse plasma was 0.79. The unbound tumor to plasma partition coefficient (K pt,uu: ratio of tumor to plasma AUCu,0-inf) of clofarabine was 0.12 ± 0.05. The model-predicted mean tumor ECF clofarabine concentrations were below the in vitro 1-h IC50 (407 ng/ml) for ependymoma neurospheres. The authors concluded that these findings showed the clofarabine exposure reached in the tumor ECF was below that associated with an anti-tumor effect in in-vitro washout study. Thus, clofarabine was de-prioritized as an agent to treat ependymoma, and further pre-clinical studies were not pursued.

Furthermore, National Comprehensive Cancer Network’s clinical practice guideline on “Central nervous system cancers” (Version 1.2015) does not mention clofarabine as a therapeutic option.

CPT Codes / HCPCS Codes / ICD-10 Codes
Information in the [brackets] below has been added for clarification purposes.   Codes requiring a 7th character are represented by "+":
ICD-10 codes will become effective as of October 1, 2015:
Other CPT codes related to the CPB:
96413 Chemotherapy administration, intravenous infusion technique; up to 1 hour, single or initial substance/drug
+96415     each additional hour (List separately in addition to code for primary
HCPCS codes covered if selection criteria are met:
J9027 Injection, clofarabine, 1 mg
ICD-10 codes covered if selection criteria are met:
C91.00 - C91.02 Acute lymphoid leukemia
C92.00, C92.02
C92.40, C92.42
C92.50, C92.52
C92.60, C92.62
C92.A0, C92.A2
Acute myeloid leukemia
C93.00, C93.02 Acute monoblastic/monocytic leukemia
C94.00, C94.02
C94.20, C94.22
Acute erythroid and megakaryoblastic leukemia
E88.89 - E88.9 Other and unspecified metabolic disorders [Recurrent or refractory childhood Langerhans cell histiocytosis]
ICD-10 codes not covered for indications listed in the CPB (not all-inclusive):
C34.00 - C34.92, C38.4 Malignant neoplasm of bronchus, lung, and pleura [mesothelioma]
C50.011 - C50.929 Malignant neoplasm of breast
C83.10 - C83.19 Mantle cell lymphoma
C83.80 - C83.89 Other non-follicular lymphoma
C85.80 - C85.89 Other specified types on non-Hodgkin lymphoma
C93.10 Chronic myelomonocytic leukemia not having achieved remission
C96.5 - C96.6 Multifocal, unisystemic and unifocal Langerhans-cell histiocytosis
D46.0 - D46.9 Myelodysplastic syndromes
E71.39 Other disorders of fatty-acid metabolism
E75.21 - E75.22,
E75.240 - E75.249, E75.3
Other sphingolipidosis
E80.3 Defects of catalase and peroxidase
J84.82 Adult pulmonary Langerhans cell histiocytosis

The above policy is based on the following references:
    1. Fadrel S, Gandhi V, O’Brien S, Results of a phase I - II study of clofarabine in combination with cytarabine (Ara-C) in relapsed and refractory acute leukemia. Blood. 2005;105(3):940-947.
    2. Drugdex. Drug Evaluations: Clofarabine. Thompson Micromedex. 2008. Available at: Accessed 03/16/2010
    3. Childhood Acute Lymphoblastic Leukemia (PDQ®): Treatment (Health Professional Version). National Cancer Institute. Accessed 1/18/2005
    4. Clolar Prescribing Information. Genzyme Corporation. San Antonio, TX. February, 2008.
    5. Micromedex® Healthcare Series. n.d. Thomson Reuters (Healthcare) Inc., Greenwood Village, CO. March 16, 2010. Available at:
    6. National Comprehensive Cancer Network (NCCN). NCCN Clinical Practice Guidelines in Oncology. Acute Myeloid Leukemia. Version.2.2013.
    7. Tischer J, Stemmler HJ, Engel N, et al. Feasibility of clofarabine cytoreduction followed by haploidentical hematopoietic stem cell transplantation in patients with relapsed or refractory advanced acute leukemia. Ann Hematol. 2013;92(10):1379-1388.
    8. Abramson JS, Takvorian RW, Fisher DC, et al. Oral clofarabine for relapsed/refractory non-Hodgkin lymphomas: Results of a phase 1 study. Leuk Lymphoma. 2013;54(9):1915-1920.
    9. Lubecka-Pietruszewska K, Kaufman-Szymczyk A, Stefanska B, et al. Clofarabine, a novel adenosine analogue, reactivates DNA methylation-silenced tumour suppressor genes and inhibits cell growth in breast cancer cells. Eur J Pharmacol. 2014;723:276-287.
    10. Simko SJ, Tran HD, Jones J, et al. Clofarabine salvage therapy in refractory multifocal histiocytic disorders, including Langerhans cell histiocytosis, juvenile xanthogranuloma and Rosai-Dorfman disease. Pediatr Blood Cancer. 2014;61(3):479-487.
    11. Rabitsch W, Böhm A, Bojic M, et al. Clofarabine/cyclophosphamide for debulking before stem cell transplantation. Eur J Clin Invest. 2014;44(8):775-783.
    12. Chevallier P, Labopin M, Socie G, et al. Results from a clofarabine-busulfan-containing, reduced-toxicity conditioning regimen prior to allogeneic stem cell transplantation: The phase 2 prospective CLORIC trial. Haematologica. 2014;99(9):1486-1491.
    13. Ghanem H, Garcia-Manero G, Faderl S, et al. Outcomes of patients with myelodysplatic syndrome and chronic myelomonocytic leukemia post clofarabine failure. Ther Adv Hematol. 2014;5(2):29-34.
    14. Lee YJ, Lee YJ, Lee SH. Resveratrol and clofarabine induces a preferential apoptosis-activating effect on malignant mesothelioma cells by Mcl-1 down-regulation and caspase-3 activation. BMB Rep. 2015;48(3):166-171.
    15. Minkov M., Grois N, McClain K, et al. Langerhans cell histiocytosis. Histiocytosis Society Evaluation and Treatment Guidelines. April 2009.
    16. National Cancer Institute (NCI). Treatment of adult LCH. Langerhans Cell Histiocytosis Treatment (PDQ). Health Professional. Bethesda, MD: NCI; updated January 30, 2015.
    17. National Cancer Institute (NCI). Treatment of childhood LCH. Langerhans Cell Histiocytosis Treatment (PDQ). Health Professional. Bethesda, MD: NCI; updated January 30, 2015.
    18. Haupt R, Minkov M, Astigarraga I, et al.; Euro Histio Network. Langerhans cell histiocytosis (LCH): Guidelines for diagnosis, clinical work-up, and treatment for patients till the age of 18 years. Pediatr Blood Cancer. 2013;60(2):175-184.
    19. Girschikofsky M, Arico M, Castillo D, et al. Management of adult patients with Langerhans cell histiocytosis: Recommendations from an expert panel on behalf of Euro-Histio-Net. Orphanet J Rare Dis. 2013;8:72.
    20. Rodriguez-Galindo C, Jeng M, Khuu P, et al. Clofarabine in refractory Langerhans cell histiocytosis. Pediatr Blood Cancer. 2008;51(5):703-706.
    21. Abraham A, Alsultan A, Jeng M, et al. Clofarabine salvage therapy for refractory high-risk Langerhans cell histiocytosis. Pediatr Blood Cancer. 2013;60(6):E19-E22.
    22. Rudrapatna VK, Morley K, Boucher KM, et al. Phase I trial of low-dose oral clofarabine in myelodysplastic syndromes patients who have failed frontline therapy. Leuk Res. 2015;39(8):835-839
    23. Zoellner AK, Fritsch S, Prevalsek D, et al. Sequential therapy combining clofarabine and T-cell-replete HLA-haploidentical haematopoietic SCT is feasible and shows efficacy in the treatment of refractory or relapsed aggressive lymphoma. Bone Marrow Transplant. 2015;50(5):679-684
    24. Patel YT, Jacus MO, Boulos N, et al. Preclinical examination of clofarabine in pediatric ependymoma: Intratumoral concentrations insufficient to warrant further study. Cancer Chemother Pharmacol. 2015;75(5):897-906
    25. National Comprehensive Cancer Network. Clinical practice guideline: Central nervous system cancers. Version 1.2015. NCCN: Fort Washington, PA.

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