Neuroblastoma |
![]() ![]() |
Neuroblastoma is one of the most common solid tumours of early childhood usually found in babies or young children. The disease originates in the adrenal medulla or other sites of sympathetic nervous tissue. The most common site is the abdomen (near the adrenal gland) but can also be found in the chest, neck, pelvis, or other sites. Most patients have widespread disease at diagnosis. This page contains links to information specifically related to Neuroblastoma, other relevant resources are availible via the Main Menu of Children's Cancer Web.
Menu: Neuroblastoma




Information Patients and Family (15 links)
Understanding Neuroblastoma
Children's Hospital Boston
Suzanne Shusterman, MD, Attending Physician at Children's Hospital Boston and Dana-Farber Cancer Institute, explains the type of cancer known as a neuroblastoma.
National Cancer InstitutePDQ summaries are written and frequently updated by editorial boards of experts Further info.
Cancer Research UKCancerHelp information is examined by both expert and lay reviewers. Content is reviewed every 12 to 18 months. Further info.
Questions and answers
Macmillan Cancer SupportContent is developed by a team of information development nurses and content editors, and reviewed by health professionals. Further info.
Associazione Italiana per la Lotta al Neuroblastoma | Italian Neuroblastoma Association - Italiana - English
A national association initially founded by parents in 1993.
Children's Neuroblastoma Cancer Foundation
CNCF
CNCF is a non-profit national organization committed to finding a cure for neuroblastoma through research, education, awareness and advocacy. Founded in 2000 by parents. The site includes news, details of events information for newly diagnosed, in-treatment and post-treatment.
FAN: Families Against Neuroblastoma
A UK charity dedicated to providing support for families affected by Neuroblastoma through every stage of their journey.
N-BLASTOMA- The Neuroblastoma Online Support Group
ACOR
Email list, includes details of how to join etc.
Childrens' Oncology Group
Includes information, with sections on newly diagnosed, in treatment and after treatment.
A charity which helps children and families affected by neuroblastoma in the UK by providing financial assistance for children's clinical treatment; supporting families affected by the disease and raise money to fund neuroblastoma research.
A non-profit organisation aimong to raise awareness of neuroblastoma, raise funds for research and provide support and advice to patients and families.
Neuroblastoma Canada is a national community-based organization dedicated to uniting Canadian neuroblastoma families. Support includes a Family Mentoring Program.
New Approaches to Neuroblastoma Therapy
NANT
A group of institutions throughout North America, committed to working together on clinical trials of novel approaches to treating high-risk neuroblastoma. The Website includes information about neuroblastoma and about the NANT clinical trials.
The James Fund for Neuroblastoma Research
James Fund
An organisation set up by parents which raising funds for neuroblastoma, while supporting families. The site includes details of events, information and a blog.
The Neuroblastoma Society is a charity, formed in 1982, which raises funds for medical research into improving both diagnosis and treatment of the disease. The Society also offers an opportunity for parents to give each other mutual help, support and comfort.
Information for Health Professionals / Researchers (8 links)
- PubMed search for publications about Neuroblastoma - Limit search to: [Reviews]
PubMed Central search for free-access publications about Neuroblastoma
MeSH term: NeuroblastomaUS National Library of Medicine
PubMed has over 22 million citations for biomedical literature from MEDLINE, life science journals, and online books. Constantly updated.
National Cancer InstitutePDQ summaries are written and frequently updated by editorial boards of experts Further info.
Advances in Neuroblastoma Research
An international conference held every 2 years, alternating between Europe and the USA. These meetings provide for an exchange of information among investigators studying neuroblastoma biology, diagnosis, prognosis, and therapy.
Clinical Trials - Neuroblastoma
National Cancer Institute
Search of the NCI's database of 12,000+ clinical trials from around the world.
Network for Neuroblastoma and CNS tumor research in children
New Approaches to Neuroblastoma Therapy
NANT
A group of institutions throughout North America, committed to working together on clinical trials of novel approaches to treating high-risk neuroblastoma. The Website includes information about neuroblastoma and about the NANT clinical trials.
SIOP
International Society of Paediatric Oncology European Neuroblastoma Research Network. This aims to optimise the use of European pre-existing infrastructures in the individual countries and to improve their consistency and complementarity on a European level. The pooling of data will contribute to harmonised standard procedures and integrate the research efforts to reach a critical mass.
Sympathetic Nervous System Tumors
SEER, National Cancer Institute
Part of a SEER report on statistical trends and risk factors associated with childhood cancers. From: Cancer Incidence and Survival Among Children and Adolescents: United States SEER Program 1975-1995. (PDF)

Latest Research Publications
This list of publications is regularly updated (Source: PubMed).
Proteomic Profiling of Neuroblastoma Cells Adhesion on Hyaluronic Acid-Based Surface for Neural Tissue Engineering.
Biomed Res Int. 2016; 2016:1917394 [PubMed] Free Access to Full Article Related Publications
Related:

Elevated MIBG Activity at the Site of Erythema of Unknown Etiology.
Clin Nucl Med. 2017; 42(3):227-230 [PubMed] Related Publications
Pancreaticoduodenectomy for pediatric and adolescent pancreatic malignancy: A single-center retrospective analysis.
J Pediatr Surg. 2017; 52(2):299-303 [PubMed] Article available free on PMC after 01/02/2018 Related Publications
METHODS: Our analytic cohort included all consecutive patients ≤18years of age treated at our institution from 1993 to 2015 who underwent PD. Patient data (demographics, disease characteristics, surgical and adjuvant treatment, length of hospital stay, and postoperative course) were extracted from the medical records.
RESULTS: We identified 12 children with a median age of 9years (7 female, 5 male). Final diagnoses were pancreatoblastoma (n=3), solid pseudopapillary tumor (n=3), neuroblastoma (n=2), rhabdomyosarcoma (n=2), and neuroendocrine carcinoma (n=2). Four patients underwent PD for resection of recurrent disease. 75% (9/12 patients) received neoadjuvant therapy. The median operative time was approximately 7hours with a mean blood loss of 590cm(3). The distal pancreas was invaginated into the posterior stomach (n=3) or into the jejunum (n=5) or was directly sewn to the jejunal mucosa (n=4). There were no operative deaths. There were 4 patients (34%) with grade II complications, 1 with a grade IIIb complication (chest tube), and 1 with a grade IV complication (reexploration). The most common long-term morbidity was pancreas exocrine supplementation (n=10; 83%). Five patients (42%) diagnosed with either solid pseudopapillary tumor or rhabdomyosarcoma are currently alive with a mean survival of 77.4months.
CONCLUSION: Pancreaticoduodenectomy is a feasible management strategy for pediatric pancreatic malignancies and is associated with acceptable morbidity and overall survival. Long-term outcome is mostly dependent on histology of the tumor.
LEVEL OF EVIDENCE: Level IV; retrospective study with no comparison group.
Related:



Lack of Associations between XPC Gene Polymorphisms and Neuroblastoma Susceptibility in a Chinese Population.
Biomed Res Int. 2016; 2016:2932049 [PubMed] Article available free on PMC after 01/02/2018 Related Publications
Primary Neuroblastoma Involving Spinal Canal.
Clin Nucl Med. 2016; 41(12):986-988 [PubMed] Related Publications
Children Undergoing Chemotherapy: Is It Too Late for Dental Rehabilitation?
J Clin Pediatr Dent. 2016; 40(6):503-505 [PubMed] Related Publications
Telomere biology including TERT rearrangements in neuroblastoma: a useful indicator for surgical treatments.
J Pediatr Surg. 2016; 51(12):2080-2085 [PubMed] Related Publications
METHODS: In 121 NBLs, including 67 cases detected by mass-screening whose telomere length, telomerase activity, ALT with ATRX/DAXX alterations, and MYCN amplification were already known, TERT rearrangements were examined using GeneChip SNP arrays.
RESULTS: The 11 ATRX/DAXX mutated ALT cases and 29 cases with high telomerase activity showed poor prognosis. MYCN amplification and TERT rearrangements were independently detected in 16 and 13 cases, respectively, and these alterations were significantly correlated with high telomerase activity. In 81 infant cases, MYCN amplification, TERT rearrangements and ATRX mutations were detected in 3, 4, and 3 cases, respectively. Among them, 6 cases showed progression or recurrences.
CONCLUSIONS: Telomere stabilization in NBLs is acquired by telomerase activation through MYCN amplification, TERT rearrangements or by ALT. Since these tumors usually show progression and recurrence, complete resection should be considered, even in infant cases.
LEVEL OF EVIDENCE: Prognosis study, level III.
Related:

miR-1303 promotes the proliferation of neuroblastoma cell SH-SY5Y by targeting GSK3β and SFRP1.
Biomed Pharmacother. 2016; 83:508-513 [PubMed] Related Publications
Related:

dl-3-n-Butylphthalide attenuation of methamphetamine-induced neurotoxicity in SH-SY5Y neuroblastoma cells.
Life Sci. 2016; 165:16-20 [PubMed] Related Publications
MAIN METHODS: Experiments were carried out on SH-SY5Y cells. Neuronal injury and apoptotic cell death were detected by MTT assay and analysis of nuclear morphology. Intracellular reactive oxygen species (ROS) was evaluated by dichloro-dihydro-fluorescein diacetate (DCFH-DA) assay and protein expression levels of the apoptosis-related cleaved caspase-3, bcl2 and Bax were determined by western blotting.
KEY FINDINGS: Treatment of SH-SY5Y cells with Meth induced cell injury and apoptosis. NBP attenuated Meth-associated cell injury and apoptosis via blockage of Meth-mediated upregulation of intracellular ROS production and inhibition of Meth-induced decrease of cleaved caspase-3/caspase-3 and Bcl-2/Bax ratios.
SIGNIFICANCE: The results presented in this study indicate that NBP may have therapeutic benefits in the treatment of Meth-induced neuronal injury in the central nervous system.
Related:

Congenital Adrenal Neuroblastoma With and Without Cystic Change: Differentiating Features With an Emphasis on the of Value of Ultrasound.
AJR Am J Roentgenol. 2016; 207(5):1105-1111 [PubMed] Related Publications
MATERIALS AND METHODS: A total of 41 patients with surgically confirmed congenital adrenal neuroblastoma were enrolled. We divided the patients into two groups according to presence or absence of cystic change in the tumor, as determined from the initial ultrasound findings. Clinical and laboratory findings, disease stage, and patient outcome were investigated with a statistical comparison between the two groups. The imaging findings for cystic congenital adrenal neuroblastoma were reviewed to compare the additional diagnostic value of CT and MRI when paired with ultrasound.
RESULTS: There were 22 patients (54%) in the group without cystic changes and 19 patients (46%) in the group with cystic changes. Prenatal detection and absence of metastasis were significantly more common in the cystic group than in the noncystic group (p < 0.05). Sensitivities of tumor marker levels were also significantly lower in the cystic group. Patient outcome was excellent, and there was no significant difference between the groups. With regard to imaging of cystic congenital adrenal neuroblastoma, in the 15 cases in which CT or MRI was paired with ultrasound, no additional diagnostic information was discerned with CT or MRI.
CONCLUSION: Nearly one-half of congenital adrenal neuroblastomas are cystic, and these tumors have clinical and laboratory features that distinguish them from noncystic congenital adrenal neuroblastoma. Diagnostic tests, including CT, MRI, and assessment of tumor markers, have low diagnostic value in the evaluation of cystic congenital adrenal neuroblastoma.
A nanoporous surface is essential for glomerular podocyte differentiation in three-dimensional culture.
Int J Nanomedicine. 2016; 11:4957-4973 [PubMed] Article available free on PMC after 01/02/2018 Related Publications
Aggressive esthesioneuroblastoma with divergent differentiation: A taxonomic dilemma.
Orbit. 2016; 35(6):357-359 [PubMed] Related Publications
Cytotoxicity of lipid-soluble ginseng extracts is attenuated by plasma membrane redox enzyme NQO1 through maintaining redox homeostasis and delaying apoptosis in human neuroblastoma cells.
Arch Pharm Res. 2016; 39(10):1339-1348 [PubMed] Related Publications
Related:


MEK inhibitors as a novel therapy for neuroblastoma: Their in vitro effects and predicting their efficacy.
J Pediatr Surg. 2016; 51(12):2074-2079 [PubMed] Related Publications
METHOD: Five neuroblastoma cell lines were treated with trametinib (MEK inhibitor) or CH5126766 (RAF/MEK inhibitor). Growth inhibition was analyzed using a cell viability assay. ERK phosphorylation and the MYCN expression were analyzed by immunoblotting or immunohistochemistry. RAS/RAF mutations were identified by direct sequencing or through the COSMIC database.
RESULTS: Both MEK inhibitors showed growth inhibition effects on cells with ERK phosphorylation, but almost no effect on cells without. In immunoblotting analyses, ERK phosphorylation and MYCN expression were suppressed in ERK active cells by these drugs. Furthermore, phosphorylated-ERK immunohistochemistry corresponded to the drug responses. Regarding the relationship between RAS/Raf mutations and ERK phosphorylation, ERK was phosphorylated in one cell line (NLF) without RAS/Raf mutations.
CONCLUSION: MEK inhibitors are a promising molecular-targeted therapeutic option for ERK active neuroblastomas. The efficacy of MEK inhibitors corresponds to ERK phosphorylation, while RAS/RAF mutations are not always detected in drug-sensitive cells. Phosphorylated-ERK immunohistochemistry is thus a useful method to analyze ERK activity and predict the therapeutic effects of MEK inhibitors.
Related:

Tumor-homing effect of human mesenchymal stem cells in a TH-MYCN mouse model of neuroblastoma.
J Pediatr Surg. 2016; 51(12):2068-2073 [PubMed] Related Publications
METHODS: hMSCs (3×10(6)) labeled with DiR, a lipophilic near-infrared dye, were intraperitoneally (i.p.) or intravenously (i.v.) administered to the TH-MYCN mice. hMSC in vivo kinetics were assayed using the IVIS® imaging system for 24h after injection. Immunohistochemistry using human CD90 antibody was also performed to confirm the location of hMSCs in various organs and tumors. Furthermore, the survival curve of TH-MYCN mice treated with hMSCs was compared to a control group administered PBS.
RESULTS: i.p. hMSCs were recognized in the tumors of TH-MYCN mice by IVIS. hMSCs were also located inside the tumor tissue. Conversely, most of the i.v. hMSCs were captured by the lungs, and migration into the tumors was not noted. There was no significant difference in the survival between the hMSC and control groups.
CONCLUSION: The present study suggested that hMSCs may be potential tumor-specific therapeutic delivery vehicles in NB according to their homing potential to tumors.
In vivo expansion and activation of γδ T cells as immunotherapy for refractory neuroblastoma: A phase 1 study.
Medicine (Baltimore). 2016; 95(39):e4909 [PubMed] Article available free on PMC after 01/02/2018 Related Publications
METHODS: Patients 2 to 21 years of age with refractory neuroblastoma with no known curative therapeutic options received ZOL on day 1, and IL-2 on days 1 to 5 and 15 to 19 of each 28-day cycle (n = 4). Lymphocyte immunophenotyping was assessed weekly. Immunophenotyping studies from the treatment group were compared with healthy pediatric controls (n = 16; range, 5y-15y) and of untreated NB disease controls (n = 9; range, 4m-18y).
RESULTS: Treatment was well tolerated with no unexpected grade 3 and 4 toxicities. Lymphocyte subset counts did not differ significantly between volunteers and disease controls with the exception of γδ+ T cell counts that were significantly higher in healthy volunteers (212 + 93 vs. 89 + 42, P = 0.05). Study patients showed increases in circulating γδ+ T cell count (3-10 fold) after the first week, increasing into the range seen in healthy volunteers (125 + 37, P = 0.1940). Interestingly, all ZOL + IL-2 treated patients showed significant increases in CD3+CD4+CD27CD127 T cells that rose weekly in 2 patients throughout the 4 weeks of observation (maximum 41% and 24% of total CD3+CD4+ T cells, respectively).
CONCLUSIONS: In summary, combined ZOL and IL-2 is well tolerated and restored γδ+ T cell counts to the normal range with a moderate expansion of Natural Killer cells. Progressive increases in circulating CD4+ T cells with a regulatory phenotype cells may offset beneficial effects of this therapy.
Related:



(123)I-mIBG scintigraphy in neuroblastoma: development of a SIOPEN semi-quantitative reporting ,method by an international panel.
Eur J Nucl Med Mol Imaging. 2017; 44(2):234-241 [PubMed] Article available free on PMC after 01/02/2018 Related Publications
METHOD: Patterns of abnormal skeletal (123)I-mIBG uptake were defined and assigned numerical scores [0-6] based on disease extent within 12 body segments. Uptake intensity was excluded from the analysis. Data sets from 82 patients were scored independently by six experienced specialists as unblinded pairs (pre- and post-induction chemotherapy) and in random order as a blinded study. Response was defined as ≥50 % reduction in post induction score compared with baseline.
RESULTS: In total, 1968 image sets were reviewed individually. Response rates of 88 % and 82 % were recorded for patients with baseline skeletal scores ≤23 and 24-48 respectively, compared with 44 % response in patients with skeletal scores >48 (p = 0.02). Reducing the number of segments or extension scale had a small but statistically negative impact upon the number of responses detected. Intraclass correlation coefficients [ICCs] calculated for the unblinded and blinded study were 0.95 at diagnosis and 0.98 and 0.99 post-induction chemotherapy, respectively.
CONCLUSIONS: The SIOPEN mIBG score method is reproducible across the full spectrum of disease in high risk neuroblastoma. Numerical assessment of skeletal disease extent avoids subjective evaluation of uptake intensity. This robust approach provides a reliable means with which to examine the role of 123I mIBG scintigraphy as a prognostic indicator in neuroblastoma.
Related:

68Ga-DOTATOC and FDG PET Imaging of Preclinical Neuroblastoma Models.
Anticancer Res. 2016; 36(9):4459-66 [PubMed] Related Publications
MATERIALS AND METHODS: Three cell lines of human NB with different levels of expression of SSTR2 were grafted into nude mice. Animals were imaged with FDG and (68)Ga-DOTATOC and the maximum standardized uptake value (SUVmax) was determined to quantify tracer uptake. Ex vivo biodistribution of (68)Ga-DOTATOC and immunohistochemical analysis of NB xenografts were performed.
RESULTS: Compared with FDG, the SUVmax of (68)Ga-DOTATOC uptake by the tumour was lower but the ratio to background was higher; there was a strong positive correlation between SUVmax values observed with the two tracers (r(2)=0.65). Sorting the cell lines according to uptake of FDG or (68)Ga-DOTATOC, injected activity per gram of tissue, Ki67 index or expression of SSTR2 assessed visually led to the same classification.
CONCLUSION: (68)Ga-DOTATOC allows preclinical imaging of NB according to the intensity of the expression of SSTR2. In contrast with what has been reported for neuroendocrine tumours, in this NB model, the (68)Ga-DOTATOC uptake was positively correlated with FDG uptake and with Ki67 index, usual markers of tumour aggressiveness. If confirmed in humans, this result would favour a theranostic application of (68)Ga-DOTATOC in NB, even in advanced stages.
Related:

Oxygen and differentiation status modulate the effect of X-ray irradiation on physiology and mitochondrial proteome of human neuroblastoma cells.
Arch Physiol Biochem. 2016; 122(5):257-265 [PubMed] Related Publications
Related:

Exogenous heat shock protein HSP70 reduces response of human neuroblastoma cells to lipopolysaccharide.
Dokl Biochem Biophys. 2016; 469(1):239-43 [PubMed] Related Publications
Related:

Expression pattern of ISL-1, TTF-1 and PAX5 in olfactory neuroblastoma.
Pol J Pathol. 2016; 67(2):130-5 [PubMed] Related Publications
A rare case of Ganglioneuroblastoma Encapsulated in Pheochromocytoma.
Acta Medica (Hradec Kralove). 2016; 59(2):67-9 [PubMed] Related Publications
MRI-guided radiotherapy of the SK-N-SH neuroblastoma xenograft model using a small animal radiation research platform.
Br J Radiol. 2017; 90(1069):20160427 [PubMed] Related Publications
METHODS: As part of a tumour growth inhibition study, SK-N-SH xenografts were generated in BALB/c nu/nu mice. Mice (n = 8) were placed in a printed MR- and CT-compatible plastic cradle, imaged using a 4.7-T MRI scanner and then transferred to a small animal radiation research platform (SARRP) irradiator with on-board CBCT. MRI/CBCT co-registration was performed to enable RT planning using the soft-tissue contrast afforded by MRI prior to delivery of RT (5 Gy). Tumour response was assessed by serial MRI and calliper measurements.
RESULTS: SK-N-SH xenografts formed soft, deformable tumours that could not be differentiated from surrounding normal tissues using CBCT. MR images, which allowed clear delineation of tumours, were successfully co-registered with CBCT images, allowing conformal RT to be delivered. MRI measurements of tumour volume 4 days after RT correlated strongly with length of survival time.
CONCLUSION: MRI allowed precision RT of SK-N-SH tumours and provided an accurate means of measuring tumour response. Advances in knowledge: MRI-based RT planning of murine tumours is feasible using an SARRP irradiator.
Attenuation of Aβ toxicity by promotion of mitochondrial fusion in neuroblastoma cells by liquiritigenin.
Arch Pharm Res. 2016; 39(8):1137-43 [PubMed] Related Publications
PLGA nanoparticles from nano-emulsion templating as imaging agents: Versatile technology to obtain nanoparticles loaded with fluorescent dyes.
Colloids Surf B Biointerfaces. 2016; 147:201-9 [PubMed] Related Publications
Maturation toward neuronal tissue in a Ewing sarcoma of bone after chemotherapy.
Diagn Pathol. 2016; 11(1):74 [PubMed] Article available free on PMC after 01/02/2018 Related Publications
CASE PRESENTATION: An 8-year old boy was diagnosed with a Ewing sarcoma in the left femur. On biopsy the morphology was typical and there was an EWSR1-FLI1 gene fusion. He underwent neo-adjuvant chemotherapy and resection of the tumor. On microscopic evaluation, part of the tumor showed ganglioneuroblastoma-like differentiation with expression of neuronal markers. The continued presence of EWSR1 rearrangement in both the blue round cell component and the ganglioneuroblastoma-like component was shown by FISH analysis.
CONCLUSIONS: In conclusion, this case describes the possibility of a Ewing sarcoma to differentiate into a ganglioneuroblastoma-like lesion after neo-adjuvant chemotherapy treatment; the prognostic value of this phenomenon remains questionable.
Related:






Different infusion durations for preventing platinum-induced hearing loss in children with cancer.
Cochrane Database Syst Rev. 2016; (8):CD010885 [PubMed] Related Publications
OBJECTIVES: To assess the effects of different durations of platinum infusion to prevent hearing loss or tinnitus, or both, in children with cancer. Secondary objectives were to assess possible effects of these infusion durations on: a) anti-tumour efficacy of platinum-based therapy, b) adverse effects other than hearing loss or tinnitus, and c) quality of life.
SEARCH METHODS: We searched the electronic databases Cochrane Central Register of Controlled Trials (CENTRAL; The Cochrane Library 2016, Issue 4), MEDLINE (PubMed) (1945 to 18 May 2016) and EMBASE (Ovid) (1980 to 18 May 2016). In addition, we handsearched reference lists of relevant articles and we assessed the conference proceedings of the International Society for Paediatric Oncology (2009 up to and including 2015) and the American Society of Pediatric Hematology/Oncology (2014 and 2015). We scanned ClinicalTrials.gov and the World Health Organization International Clinical Trials Registry Platform (WHO ICTRP; apps.who.int/trialsearch) for ongoing trials (searched on 20 May 2016 and 24 May 2016 respectively).
SELECTION CRITERIA: Randomised controlled trials (RCTs) or controlled clinical trials (CCTs) comparing different platinum infusion durations in children with cancer. Only the platinum infusion duration could differ between the treatment groups.
DATA COLLECTION AND ANALYSIS: Two review authors independently performed the study selection, risk of bias assessment and GRADE assessment of included studies, and data extraction including adverse effects. Analyses were performed according to the guidelines of the Cochrane Handbook for Systematic Reviews of Interventions.
MAIN RESULTS: We identified one RCT and no CCTs; in this update no additional studies were identified. The RCT (total number of children = 91) evaluated the use of a continuous cisplatin infusion (N = 43) versus a one-hour bolus cisplatin infusion (N = 48) in children with neuroblastoma. For the continuous infusion, cisplatin was administered on days 1 to 5 of the cycle but it is unclear if the infusion duration was a total of 5 days. Methodological limitations were present. Only results from shortly after induction therapy were provided. No clear evidence of a difference in hearing loss (defined as asymptomatic and symptomatic disease combined) between the different infusion durations was identified as results were imprecise (risk ratio (RR) 1.39, 95% confidence interval (CI) 0.47 to 4.13, low quality evidence). Although the numbers of children were not provided, it was stated that tumour response was equivalent in both treatment arms. With regard to adverse effects other than ototoxicity we were only able to assess toxic deaths. Again, the confidence interval of the estimated effect was too wide to exclude differences between the treatment groups (RR 1.12, 95% CI 0.07 to 17.31, low quality evidence). No data were available for the other outcomes of interest (i.e. tinnitus, overall survival, event-free survival and quality of life) or for other (combinations of) infusion durations or other platinum analogues.
AUTHORS' CONCLUSIONS: Since only one eligible RCT evaluating the use of a continuous cisplatin infusion versus a one-hour bolus cisplatin infusion was found, and that had methodological limitations, no definitive conclusions can be made. It should be noted that 'no evidence of effect', as identified in this review, is not the same as 'evidence of no effect'. For other (combinations of) infusion durations and other platinum analogues no eligible studies were identified. More high quality research is needed.
Related:



Suppression of miR-19b enhanced the cytotoxic effects of mTOR inhibitors in human neuroblastoma cells.
J Pediatr Surg. 2016; 51(11):1818-1825 [PubMed] Related Publications
METHODS: AZD8055 (a new mTOR inhibitor)- or rapamycin-induced cytotoxic effects on neuroblastoma cells were studied. Western blotting was used to investigate the expression of various proteins in the mTOR pathway. MicroRNA precursors and antagomirs were transfected into cells to manipulate the expression of target microRNA.
RESULTS: AZD8055 exerted stronger cytotoxic effects than rapamycin in neuroblastoma cells (p<0.03). In addition, AZD8055 suppressed the mTOR pathway and increased the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in the neuroblastoma cells. AZD8055 significantly decreased miR-19b expression (p<0.005); in contrast, rapamycin increased miR-19b expression (p<0.05). Transfection of miR-19b antagomir into the neuroblastoma cells mimicked the effects of AZD8055 treatment, whereas miR-19b overexpression reversed the effects of AZD8055. Combination of miR-19b knockdown and rapamycin treatment significantly improved the sensitivity of neuroblastoma cells to rapamycin (p<0.02).
CONCLUSION: Suppression of miR-19b may enhance the cytotoxic effects of mTOR inhibitors in neuroblastoma cells.
Related:


Inconspicuous Presentation of Metastatic Neuroblastoma.
W V Med J. 2016 Jul-Aug; 112(4):38-41 [PubMed] Related Publications
Cytosolic Ku70 regulates Bax-mediated cell death.
Tumour Biol. 2016; 37(10):13903-13914 [PubMed] Article available free on PMC after 01/02/2018 Related Publications
Related:


Monitor this page |
powered by ChangeDetection |
This page last updated: 9th March 2017
Displaying links verified within last 2 weeks at time of update.