Sunday, July 7, 2019

Neuroblastoma Treatment (PDQ®)—Health Professional Version - National Cancer Institute 6/7

Neuroblastoma Treatment (PDQ®)—Health Professional Version - National Cancer Institute
National Cancer Institute

Neuroblastoma Treatment (PDQ®)–Health Professional Version

Treatment of High-Risk Neuroblastoma

The previously used Children's Oncology Group (COG) neuroblastoma high-risk group assignment criteria are described in Table 13.
Table 13. Children’s Oncology Group (COG) Neuroblastoma High-Risk Group Assignment Schema
INSS Stage  Age  MYCN Status  INPC Histology  DNA Ploidya  Other
DI = DNA index; INPC = International Neuroblastoma Pathologic Classification; INSS = International Neuroblastoma Staging System.
aDNA ploidy: DI >1 is favorable, DI =1 is unfavorable; a hypodiploid tumor (with DI <1 a="" as="" be="" di="" treated="" tumor="" will="" with="">1 (DI <1 be="" considered="" favorable="" hypodiploid="" ploidy="" td="" to="">
bINSS stage 2A/2B symptomatic patients with spinal cord compression, neurologic deficits, or other symptoms are treated with immediate chemotherapy for four cycles.
cINSS stage 3 or stage 4 patients with clinical symptoms as listed above receive immediate chemotherapy.
2A/2Bb Any  Amplified  AnyAnyAny degree of resection
3c ≥547dNonamplified UnfavorableAny  
Any  Amplified Any Any 
4c <365 d="" nbsp="" td="">Amplified Any Any  
365 d to <547 d="" td="">Amplified Any Any  
365 d to <547 d="" td="">Any Any DI =1 
365 d to <547 d="" nbsp="" td="">Any UnfavorableAny  
≥547 dAny Any Any  
4S  <365 d="" nbsp="" td="">Amplified Any Any  Asymptomatic or symptomatic
Table 14 shows the International Neuroblastoma Risk Group (INRG) classification for high-risk neuroblastoma used in ongoing COG studies, including ANBL1531 (NCT03126916).
Table 14. International Neuroblastoma Risk Group (INRG) Pretreatment Classification Schema for High-Risk Neuroblastomaa
ENLARGE
INRG StageHistologic CategoryGrade of Tumor DifferentiationMYCN11q AberrationPloidyPretreatment Risk Group
GN = ganglioneuroma; GNB = ganglioneuroblastoma; NA = not amplified.
aReprinted with permission. © (2015) American Society of Clinical Oncology. All rights reserved. Pinto N et al.: Advances in Risk Classification and Treatment Strategies for Neuroblastoma, J Clin Oncol 33 (27), 2015: 3008–3017.[1]
L1Any, except GN maturing or GNB intermixed Amplified  K (high)
L2 
 Age ≥18 moGNB nodular neuroblastomaPoorly differentiated or undifferentiatedAmplified  N (high)
M 
 Age <18 mo="" td="">  Amplified  O (high)
 Age ≥18 mo     P (high)
MS
 Age <18 mo="" td="">  NAYes Q (high)
Amplified  R (high)
Approximately 8% to 10% of infants with stage 4S disease will have MYCN-amplified tumors and are usually treated on high-risk protocols. The overall event-free survival (EFS) and overall survival (OS) for infants with stage 4 and 4S disease and MYCN-amplification were only 30% at 2 to 5 years after treatment in a European study.[2]
For children with high-risk neuroblastoma, the 5-year OS with current treatments is about 50% for patients diagnosed between 2005 and 2010.[1,3] Children with aggressively treated, high-risk neuroblastoma may develop late recurrences, some more than 5 years after completion of therapy.[4,5]
A study from the INRG database found 146 patients with distant metastases limited to lymph nodes, termed stage 4N, who tended to have favorable-biology disease and a good outcome (5-year OS, 85%), which suggests that for this special subgroup of high-risk, stage 4 patients, less-intensive therapy might be considered.[6]

Treatment Options for High-Risk Neuroblastoma

Outcomes for patients with high-risk neuroblastoma remain poor despite recent improvements in survival in randomized trials.
Treatment options for high-risk neuroblastoma typically include the following:
  1. A regimen of chemotherapy, surgery, tandem cycles of myeloablative therapy and stem cell transplant (SCT), radiation therapy, and dinutuximab with interleukin-2 (IL-2)/granulocyte-macrophage colony-stimulating factor (GM-CSF) and isotretinoin.

Chemotherapy, surgery, tandem cycles of myeloablative therapy and SCT, radiation therapy, and dinutuximab, with IL-2/GM-CSF and isotretinoin

Treatment for patients with high-risk disease is generally divided into the following three phases:
  • Induction (includes chemotherapy and surgical resection).
  • Consolidation (tandem cycles of myeloablative therapy and SCT).
  • Postconsolidation (radiation therapy to the site of the primary tumor and residual metastatic sites, immunotherapy, and retinoid therapy).
Induction phase
The backbone of the most commonly used induction therapy includes dose-intensive cycles of cisplatin and etoposide alternating with vincristine, cyclophosphamide, and doxorubicin.[7] Topotecan and cyclophosphamide were added to this regimen on the basis of the antineuroblastoma activity seen in relapsed patients.[8] Response to therapy after four cycles of chemotherapy or at the end of induction chemotherapy correlates with EFS at the completion of high-risk therapy.[9,10]
After a response to chemotherapy, resection of the primary tumor is usually attempted. Whether a gross-total resection is beneficial either before or after induction chemotherapy is controversial.[11]
Evidence (resection of the primary tumor before or after chemotherapy):
  1. The COG A3973 (NCT00004188) study had central surgical review of 220 patients who underwent attempted gross-total resection after induction chemotherapy. By the surgeon’s estimate, the degree of resection was determined to be 90% or greater versus less than 90%, but only 63% concordance with central review of imaging was found.[12][Level of evidence: 3iiA]
    • Nevertheless, the surgeon’s assessment of 90% or greater resection versus less than 90% resection predicted EFS of 46% versus 38% (P = .01), respectively, and cumulative incidence of local relapse of 8.5% versus 20%, respectively.
    • OS was not significantly different (57% vs. 49%, P = .3).
    • The author's conclusion supports continued efforts to achieve greater than 90% resection in order to decrease local recurrence.
  2. A single-center retrospective study of 87 children with high-risk neuroblastoma demonstrated no significant benefit of gross-total resection compared with near-total (>90%) resection.[13][Level of evidence: 3iiD]
    • However, the results suggest that greater than 90% resection is associated with improved OS compared with less than 90% resection.
The potential benefit of aggressive surgical approaches in high-risk patients with metastatic disease to achieve complete tumor resection, either at the time of diagnosis or after chemotherapy, has not been unequivocally demonstrated. Several studies have reported that complete resection of the primary tumor at diagnosis improved survival; however, the outcome in these patients may be more dependent on the biology of the tumor, which itself may determine resectability, than on the extent of surgical resection.[14-16] In stage 4 patients older than 18 months, controversy exists about whether there is any advantage to gross-total resection of the primary tumor after chemotherapy.[12,15-17]
Consolidation phase
The consolidation phase of high-risk regimens involves myeloablative chemotherapy and SCT, which attempts to eradicate minimal residual disease (MRD) using otherwise lethal doses of ablative chemotherapy rescued by autologous stem cells (collected during induction chemotherapy) to repopulate the bone marrow. Several large randomized controlled studies have shown an improvement in 3-year EFS for treatment with SCT (31% to 47%) versus conventional chemotherapy (22% to 31%).[18-20] Previously, total-body irradiation had been used in SCT conditioning regimens. Most current protocols use tandem chemotherapy and SCT or carboplatin/etoposide/melphalan or busulfan/melphalan as conditioning for SCT.[21][Level of evidence: 3iA]
Evidence (myeloablative chemotherapy and stem cell rescue):
  1. A large European multicenter trial of consolidation therapy randomly assigned patients who had completed a multidrug induction regimen (cisplatin, carboplatin, cyclophosphamide, vincristine, and etoposide with or without topotecan, vincristine, and doxorubicin) and achieved an adequate response to receive either busulfan/melphalan or carboplatin/etoposide/melphalan.[22][Level of evidence: 1iiA]
    • Induction therapy with cisplatin, carboplatin, cyclophosphamide, vincristine, and etoposide, and consolidation for SCT with busulfan/melphalan resulted in an improved EFS, without an effect on OS or severe adverse events.
  2. Two sequential cycles of myeloablative chemotherapy and stem cell rescue given in a tandem fashion was shown to be feasible for patients with high-risk neuroblastoma.[23]
  3. A randomized clinical study (COG-ANBL0532) tested the efficacy of two cycles versus one cycle of myeloablative chemotherapy with stem cell rescue.[24] Children older than 18 months with stage 4 neuroblastoma who had received six cycles of induction chemotherapy were then randomly assigned to receive a single autologous SCT with carboplatin/etoposide/melphalan or tandem transplants with cyclophosphamide/thiotepa followed by reduced-dose carboplatin/etoposide/melphalan. After tumor bed radiation therapy, patients were randomly assigned on a second trial to receive isotretinoin alone or isotretinoin with dinutuximab and immune enhancement.
    • The 3-year EFS was 61% for tandem transplants and 48% for single autologous SCT (P = .008). The 3-year OS was 74% for tandem autologous SCTs and 69% for single autologous SCT (P = .19).
    • For patients who were randomly assigned to not receive dinutuximab and immune enhancement, the 3-year EFS was 74% for tandem SCTs and 56% for single autologous SCT (P = .003); for patients who received dinutuximab and immune enhancement, the 3-year OS was 84% for tandem SCTs and 74% for single SCT (P = .03).
(Refer to the Autologous Hematopoietic Cell Transplantation section in the PDQ summary on Childhood Hematopoietic Cell Transplantation for more information about transplantation.)
Radiation to the primary tumor site (whether or not a complete excision was obtained) is indicated after myeloablative therapy. Treatment of persistently metaiodobenzylguanidine (MIBG)-positive metastatic sites after induction therapy is often performed after myeloablative therapy. The optimal dose of radiation therapy has not been determined, although nonrandomized, retrospective studies suggest doses of 30 Gy to 36 Gy to the primary site improve local control if there is gross residual disease before SCT.[25]
Radiation of metastatic disease sites is determined on an individual basis or according to protocol guidelines for patients enrolled in studies. Metastatic bone relapse in neuroblastoma often occurs at anatomic sites of previous disease. Metastatic sites identified at diagnosis that did not receive radiation during frontline therapy appeared to have a higher risk of involvement at first relapse relative to previously irradiated metastatic sites.[26] These observations support the current paradigm of irradiating metastases that persist by MIBG uptake after induction chemotherapy in high-risk patients. In cases where diffuse bone metastases remain after induction chemotherapy, high-dose chemotherapy is followed by reassessment before consolidative radiation therapy. Irradiation of more than 50% of the bone marrow is not advised.
Preliminary outcomes of proton radiation therapy to treat high-risk neuroblastoma primary tumors have been published, demonstrating acceptable efficacy and toxicity.[27]
Postconsolidation phase
Postconsolidation therapy is designed to treat potential MRD after SCT.[28] Radiation therapy has been used to treat the primary site and sometimes to areas of incompletely resolved metastases. For high-risk patients in remission after SCT, dinutuximab combined with GM-CSF and IL-2 are given in concert with isotretinoin and have been shown to improve EFS.[29,30]
Evidence (all treatments):
  1. A randomized study compared high-dose therapy and purged autologous bone marrow transplant (ABMT) with three cycles of intensive consolidation chemotherapy. In addition, after the completion of either chemotherapy or ABMT, patients on this study were randomly assigned to stop therapy or to receive 6 months of isotretinoin. The EFS and OS results described below reflect outcome from the time of each randomization.[18]; [28][Level of evidence: 1iiA]
    • The 5-year EFS was significantly better in the ABMT arm (30%), than in the consolidation chemotherapy arm (19%; P = .04). There was no significant difference in 5-year OS between the two arms (39% vs. 30%; P = .08).
    • Patients who received isotretinoin had a higher 5-year EFS than did patients who received no maintenance therapy (42% vs. 31%), although the difference was not significant (P = .12). OS was higher for patients randomly assigned to receive isotretinoin (50%) than it was for those who stopped therapy (39%), but this difference was not significant (P = .10).
  2. An updated Cochrane review evaluated three randomized clinical trials comparing ABMT with standard chemotherapy.[18-20,28,31]
    • EFS was significantly better for ABMT, but there was no statistically significant difference in OS.
  3. A retrospective, single-institution, nonrandomized trial compared patients who received GM-CSF and 3F8 anti-GD2 antibody therapy after either autologous SCT or conventional chemotherapy.[32] The patients were a mixture of those referred for initial treatment or further therapy, and included refractory and relapsed patients, some of whom had received autologous SCT at referring institutions. In the autologous SCT group, there was a significantly longer time from first chemotherapy or from autologous SCT to initiation of GM-CSF and 3F8 anti-GD2 antibody treatment. The autologous SCT group also had significantly more ultra–high-risk patients.
    • A trend for better EFS with GM-CSF and 3F8 anti-GD2 antibody therapy and autologous SCT was observed (65% vs. 51%, P = .128), but there was no statistically significant difference in OS between patients who were treated with chemotherapy alone and those who were treated with autologous SCT.
  4. In a separate prospective, randomized study, there was no advantage to purging harvested stem cells of neuroblastoma cells before transplantation.[33]
  5. A review of 147 allogeneic transplant cases submitted to the Center for International Blood and Marrow Transplant Research found no advantage for allogeneic transplant over autologous transplant, even if the allogeneic transplant recipient had received a previous autologous transplant.[34]
  6. In a COG phase III trial after SCT, patients were randomly assigned to receive dinutuximab administered with GM-CSF and IL-2 in conjunction with isotretinoin, versus isotretinoin alone.[29]
    • Immunotherapy together with isotretinoin (EFS, 66%) was superior to standard isotretinoin maintenance therapy (EFS, 46%). As a result, immunotherapy post-SCT is considered the standard of care in COG trials for high-risk disease.
    • As a result of the COG studies, dinutuximab has been approved by the U.S. Food and Drug Administration.
  7. A European study compared dinutuximab-beta (dinutuximab manufactured in hamster cells instead of mouse cells) to dinutuximab-beta plus subcutaneous (SQ) IL-2 administered as maintenance therapy after high-dose chemotherapy with autologous SCT. All patients additionally received isotretinoin. [35]
    • The addition of SQ IL-2 did not improve outcome; the 3-year EFS was 56% for patients treated with dinutuximab-beta and 60% for patients treated with dinutuximab-beta and SQ IL-2 (P = .76).
Radiation therapy to consolidate local control after surgical resection of the primary tumor (whether or not a complete excision was obtained) and myeloablative therapy is often given.[36,37]; [38][Level of evidence: 3iiA] The optimal dose of radiation therapy has not been determined.[25] Extensive lymph node irradiation, regardless of the extent of surgical resection preceding SCT did not provide a benefit to patients for local progression or OS.[39][Level of evidence: 3iii]
Treatment of bony metastatic disease is also considered to maximize disease control, delivered at the time of primary tumor bed irradiation. Radiation therapy to metastatic disease sites is determined on an individual basis or according to protocol guidelines for patients enrolled in studies. Many children present with widespread bony metastases. Because it is not feasible to irradiate all initial sites, the current practice is to treat the sites that have not responded, as assessed by MIBG before SCT.[26,40,41] Metastatic sites identified at diagnosis that did not receive radiation during frontline therapy appeared to have a higher risk of involvement at first relapse relative to previously irradiated metastatic sites.[26] These observations support the current paradigm of irradiating metastases that persist by MIBG uptake after induction chemotherapy in high-risk patients. Irradiation of more than 50% of the bone marrow is not advised.
In cases where diffuse bone metastases remain after induction chemotherapy, high-dose chemotherapy is followed by reassessment before deciding on consolidative radiation therapy.
Preliminary outcomes of proton radiation therapy to treat patients with high-risk neuroblastoma primary tumors have been published, demonstrating acceptable efficacy and toxicity.[27]

Treatment Options Under Clinical Evaluation

Information about National Cancer Institute (NCI)–supported clinical trials can be found on the NCI website. For information about clinical trials sponsored by other organizations, refer to the ClinicalTrials.gov website.
The following is an example of a national and/or institutional clinical trial that is currently being conducted:
  • ANBL1531 (NCT03126916) (A Phase III Study of 131I-MIBG or Crizotinib Added to Intensive Therapy for Children With Newly Diagnosed High-Risk Neuroblastoma): The standard current COG therapy has been described above; it consists of induction chemotherapy, consolidation with surgery and tandem SCT, and postconsolidation radiation therapy with isotretinoin and dinutuximab immune-enhanced immunotherapy. During the 4-week initial induction chemotherapy cycle, patients will be screened for the ALK gene aberration (occurs in approximately 10%–15% of high-risk patients). Before the second cycle of induction chemotherapy, the treatment arm assignment occurs. Most patients enrolled will be MIBG avid and lack the ALKaberration, and will be randomly assigned to one of the following three treatment arms:
    1. Arm A consists of standard COG therapy as described above.
    2. Arm B consists of standard COG therapy but with an MIBG cycle added after the third cycle of induction chemotherapy.
    3. Arm C consists of the same treatment as arm B but the consolidation ablative therapy for SCT will be a single transplant with busulfan/melphalan, rather than the COG standard tandem transplant.
    Patients with the ALK gene mutation or ALK amplification will receive nonrandomized COG current standard induction chemotherapy with the ALK inhibitor crizotinib added, followed by further therapy on the standard COG treatment plan.
    Patients with MIBG nonavid, ALK nonaberrant tumors will receive standard current chemotherapy as in arm A above.
    The classification for the ANBL1531 trial is based on the INRG staging system.
    Boost radiation was discontinued in this trial because no clear benefit over historical controls was apparent.
  • ANBL17P1 (NCT03786783) (Dinutuximab, Sargramostim, and Combination Chemotherapy in Treating Patients With Newly Diagnosed High-Risk Neuroblastoma Undergoing SCT): The need for innovative therapies for children with high-risk neuroblastoma remains critical because many children with high-risk disease experience progressive disease during induction therapy, have persistent metastatic disease, or relapse after the completion of therapy. Recent studies conducted in patients with recurrent or refractory neuroblastoma have demonstrated objective clinical responses after treatment with the combination of an anti-GD2 monoclonal antibody plus chemotherapy and GM-CSF. This limited-institution protocol will evaluate whether the addition of the anti-GD2 monoclonal antibody dinutuximab and GM-CSF to standard induction chemotherapy during cycles three to five for patients with newly-diagnosed neuroblastoma is safe and tolerable.
    Boost radiation was discontinued in this trial because no clear benefit over historical controls was apparent.

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
References
  1. Pinto NR, Applebaum MA, Volchenboum SL, et al.: Advances in Risk Classification and Treatment Strategies for Neuroblastoma. J Clin Oncol 33 (27): 3008-17, 2015. [PUBMED Abstract]
  2. Canete A, Gerrard M, Rubie H, et al.: Poor survival for infants with MYCN-amplified metastatic neuroblastoma despite intensified treatment: the International Society of Paediatric Oncology European Neuroblastoma Experience. J Clin Oncol 27 (7): 1014-9, 2009. [PUBMED Abstract]
  3. Maris JM: Recent advances in neuroblastoma. N Engl J Med 362 (23): 2202-11, 2010. [PUBMED Abstract]
  4. Cotterill SJ, Pearson AD, Pritchard J, et al.: Late relapse and prognosis for neuroblastoma patients surviving 5 years or more: a report from the European Neuroblastoma Study Group "Survey". Med Pediatr Oncol 36 (1): 235-8, 2001. [PUBMED Abstract]
  5. Mertens AC, Yasui Y, Neglia JP, et al.: Late mortality experience in five-year survivors of childhood and adolescent cancer: the Childhood Cancer Survivor Study. J Clin Oncol 19 (13): 3163-72, 2001. [PUBMED Abstract]
  6. Morgenstern DA, London WB, Stephens D, et al.: Metastatic neuroblastoma confined to distant lymph nodes (stage 4N) predicts outcome in patients with stage 4 disease: A study from the International Neuroblastoma Risk Group Database. J Clin Oncol 32 (12): 1228-35, 2014. [PUBMED Abstract]
  7. Kushner BH, LaQuaglia MP, Bonilla MA, et al.: Highly effective induction therapy for stage 4 neuroblastoma in children over 1 year of age. J Clin Oncol 12 (12): 2607-13, 1994. [PUBMED Abstract]
  8. Park JR, Scott JR, Stewart CF, et al.: Pilot induction regimen incorporating pharmacokinetically guided topotecan for treatment of newly diagnosed high-risk neuroblastoma: a Children's Oncology Group study. J Clin Oncol 29 (33): 4351-7, 2011. [PUBMED Abstract]
  9. Decarolis B, Schneider C, Hero B, et al.: Iodine-123 metaiodobenzylguanidine scintigraphy scoring allows prediction of outcome in patients with stage 4 neuroblastoma: results of the Cologne interscore comparison study. J Clin Oncol 31 (7): 944-51, 2013. [PUBMED Abstract]
  10. Yanik GA, Parisi MT, Shulkin BL, et al.: Semiquantitative mIBG scoring as a prognostic indicator in patients with stage 4 neuroblastoma: a report from the Children's oncology group. J Nucl Med 54 (4): 541-8, 2013. [PUBMED Abstract]
  11. De Ioris MA, Crocoli A, Contoli B, et al.: Local control in metastatic neuroblastoma in children over 1 year of age. BMC Cancer 15: 79, 2015. [PUBMED Abstract]
  12. von Allmen D, Davidoff AM, London WB, et al.: Impact of Extent of Resection on Local Control and Survival in Patients From the COG A3973 Study With High-Risk Neuroblastoma. J Clin Oncol 35 (2): 208-216, 2017. [PUBMED Abstract]
  13. Englum BR, Rialon KL, Speicher PJ, et al.: Value of surgical resection in children with high-risk neuroblastoma. Pediatr Blood Cancer 62 (9): 1529-35, 2015. [PUBMED Abstract]
  14. DeCou JM, Bowman LC, Rao BN, et al.: Infants with metastatic neuroblastoma have improved survival with resection of the primary tumor. J Pediatr Surg 30 (7): 937-40; discussion 940-1, 1995. [PUBMED Abstract]
  15. Castel V, Tovar JA, Costa E, et al.: The role of surgery in stage IV neuroblastoma. J Pediatr Surg 37 (11): 1574-8, 2002. [PUBMED Abstract]
  16. Simon T, Häberle B, Hero B, et al.: Role of surgery in the treatment of patients with stage 4 neuroblastoma age 18 months or older at diagnosis. J Clin Oncol 31 (6): 752-8, 2013. [PUBMED Abstract]
  17. Adkins ES, Sawin R, Gerbing RB, et al.: Efficacy of complete resection for high-risk neuroblastoma: a Children's Cancer Group study. J Pediatr Surg 39 (6): 931-6, 2004. [PUBMED Abstract]
  18. Matthay KK, Villablanca JG, Seeger RC, et al.: Treatment of high-risk neuroblastoma with intensive chemotherapy, radiotherapy, autologous bone marrow transplantation, and 13-cis-retinoic acid. Children's Cancer Group. N Engl J Med 341 (16): 1165-73, 1999. [PUBMED Abstract]
  19. Berthold F, Boos J, Burdach S, et al.: Myeloablative megatherapy with autologous stem-cell rescue versus oral maintenance chemotherapy as consolidation treatment in patients with high-risk neuroblastoma: a randomised controlled trial. Lancet Oncol 6 (9): 649-58, 2005. [PUBMED Abstract]
  20. Pritchard J, Cotterill SJ, Germond SM, et al.: High dose melphalan in the treatment of advanced neuroblastoma: results of a randomised trial (ENSG-1) by the European Neuroblastoma Study Group. Pediatr Blood Cancer 44 (4): 348-57, 2005. [PUBMED Abstract]
  21. Elborai Y, Hafez H, Moussa EA, et al.: Comparison of toxicity following different conditioning regimens (busulfan/melphalan and carboplatin/etoposide/melphalan) for advanced stage neuroblastoma: Experience of two transplant centers. Pediatr Transplant 20 (2): 284-9, 2016. [PUBMED Abstract]
  22. Ladenstein R, Pötschger U, Pearson ADJ, et al.: Busulfan and melphalan versus carboplatin, etoposide, and melphalan as high-dose chemotherapy for high-risk neuroblastoma (HR-NBL1/SIOPEN): an international, randomised, multi-arm, open-label, phase 3 trial. Lancet Oncol 18 (4): 500-514, 2017. [PUBMED Abstract]
  23. Seif AE, Naranjo A, Baker DL, et al.: A pilot study of tandem high-dose chemotherapy with stem cell rescue as consolidation for high-risk neuroblastoma: Children's Oncology Group study ANBL00P1. Bone Marrow Transplant 48 (7): 947-52, 2013. [PUBMED Abstract]
  24. Park JR, Kreissman SG, London WB, et al.: A phase III randomized clinical trial (RCT) of tandem myeloablative autologous stem cell transplant (ASCT) using peripheral blood stem cell (PBSC) as consolidation therapy for high-risk neuroblastoma (HR-NB): a Children's Oncology Group (COG) study. [Abstract] J Clin Oncol 34 (Suppl 15): A-LBA3, 2016. Also available online. Last accessed February 11, 2019.
  25. Casey DL, Kushner BH, Cheung NV, et al.: Dose-escalation is needed for gross disease in high-risk neuroblastoma. Pediatr Blood Cancer 65 (7): e27009, 2018. [PUBMED Abstract]
  26. Polishchuk AL, Li R, Hill-Kayser C, et al.: Likelihood of bone recurrence in prior sites of metastasis in patients with high-risk neuroblastoma. Int J Radiat Oncol Biol Phys 89 (4): 839-45, 2014. [PUBMED Abstract]
  27. Hattangadi JA, Rombi B, Yock TI, et al.: Proton radiotherapy for high-risk pediatric neuroblastoma: early outcomes and dose comparison. Int J Radiat Oncol Biol Phys 83 (3): 1015-22, 2012. [PUBMED Abstract]
  28. Matthay KK, Reynolds CP, Seeger RC, et al.: Long-term results for children with high-risk neuroblastoma treated on a randomized trial of myeloablative therapy followed by 13-cis-retinoic acid: a children's oncology group study. J Clin Oncol 27 (7): 1007-13, 2009. [PUBMED Abstract]
  29. Yu AL, Gilman AL, Ozkaynak MF, et al.: Anti-GD2 antibody with GM-CSF, interleukin-2, and isotretinoin for neuroblastoma. N Engl J Med 363 (14): 1324-34, 2010. [PUBMED Abstract]
  30. Cheung NK, Cheung IY, Kushner BH, et al.: Murine anti-GD2 monoclonal antibody 3F8 combined with granulocyte-macrophage colony-stimulating factor and 13-cis-retinoic acid in high-risk patients with stage 4 neuroblastoma in first remission. J Clin Oncol 30 (26): 3264-70, 2012. [PUBMED Abstract]
  31. Yalçin B, Kremer LC, Caron HN, et al.: High-dose chemotherapy and autologous haematopoietic stem cell rescue for children with high-risk neuroblastoma. Cochrane Database Syst Rev 8: CD006301, 2013. [PUBMED Abstract]
  32. Kushner BH, Ostrovnaya I, Cheung IY, et al.: Lack of survival advantage with autologous stem-cell transplantation in high-risk neuroblastoma consolidated by anti-GD2 immunotherapy and isotretinoin. Oncotarget 7 (4): 4155-66, 2016. [PUBMED Abstract]
  33. Kreissman SG, Seeger RC, Matthay KK, et al.: Purged versus non-purged peripheral blood stem-cell transplantation for high-risk neuroblastoma (COG A3973): a randomised phase 3 trial. Lancet Oncol 14 (10): 999-1008, 2013. [PUBMED Abstract]
  34. Hale GA, Arora M, Ahn KW, et al.: Allogeneic hematopoietic cell transplantation for neuroblastoma: the CIBMTR experience. Bone Marrow Transplant 48 (8): 1056-64, 2013. [PUBMED Abstract]
  35. Ladenstein R, Pötschger U, Valteau-Couanet D, et al.: Interleukin 2 with anti-GD2 antibody ch14.18/CHO (dinutuximab beta) in patients with high-risk neuroblastoma (HR-NBL1/SIOPEN): a multicentre, randomised, phase 3 trial. Lancet Oncol 19 (12): 1617-1629, 2018. [PUBMED Abstract]
  36. Haas-Kogan DA, Swift PS, Selch M, et al.: Impact of radiotherapy for high-risk neuroblastoma: a Children's Cancer Group study. Int J Radiat Oncol Biol Phys 56 (1): 28-39, 2003. [PUBMED Abstract]
  37. Casey DL, Kushner BH, Cheung NK, et al.: Local Control With 21-Gy Radiation Therapy for High-Risk Neuroblastoma. Int J Radiat Oncol Biol Phys 96 (2): 393-400, 2016. [PUBMED Abstract]
  38. Gatcombe HG, Marcus RB Jr, Katzenstein HM, et al.: Excellent local control from radiation therapy for high-risk neuroblastoma. Int J Radiat Oncol Biol Phys 74 (5): 1549-54, 2009. [PUBMED Abstract]
  39. Braunstein SE, London WB, Kreissman SG, et al.: Role of the extent of prophylactic regional lymph node radiotherapy on survival in high-risk neuroblastoma: A report from the COG A3973 study. Pediatr Blood Cancer : e27736, 2019. [PUBMED Abstract]
  40. Li R, Polishchuk A, DuBois S, et al.: Patterns of Relapse in High-Risk Neuroblastoma Patients Treated With and Without Total Body Irradiation. Int J Radiat Oncol Biol Phys 97 (2): 270-277, 2017. [PUBMED Abstract]
  41. Mazloom A, Louis CU, Nuchtern J, et al.: Radiation therapy to the primary and postinduction chemotherapy MIBG-avid sites in high-risk neuroblastoma. Int J Radiat Oncol Biol Phys 90 (4): 858-62, 2014. [PUBMED Abstract]
Posted by at

No comments:

Post a Comment

Subscribe to: Post Comments (Atom)