جستجوی مقالات مرتبط با کلیدواژه "neuroblastoma" در نشریات گروه "پزشکی"
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The most frequent type of extracranial solid tumor in pediatric cases is neuroblastoma (NB), almost always arising in tissues with sympathetic innervation with only a few reported cases arising in other organs. NBs with hepatic involvement are typically metastatic lesions as primary hepatic NBs are extremely rare. This study presents a 5.5-month-old boy with primary hepatic NB. This case study describes a male 5.5-month-old preterm infant who presented with overt hepatomegaly. Laboratory tests showed an abnormally high level of alpha-fetoprotein. A sonography-guided liver needle biopsy was performed, so histopathological examination suggested the diagnosis of a small round-cell tumor. Immunohistochemical staining demonstrated evidence of neuronal differentiation in the tumor. The sum of these findings was in favor of the diagnosis of NB. Bone marrow aspiration and biopsy were normal. The full-body computed tomography scan revealed a large intrahepatic mass measuring 82×70×74 mm with mild peripheral enhancement. A metaiodobenzylguanidine (MIBG) scintiscan confirmed a huge round MIBG-avid hepatic lesion without other remarkable lesions at other sites in the body. Chemotherapy treatment was started for the patient, and after 4 sessions of chemotherapy, an ultrasound showed that the mass size had decreased to 55×36 mm. This report describes the first primary hepatic NB in a pediatric patient with detailed clinicopathological details. Primary hepatic NB is extremely rare. It is important to consider neuroendocrine tumors as a possibility when faced with a single hepatic tumor that has a similar histological appearance.
Keywords: Liver neoplasms, Neuroblastoma, Pediatrics -
BackgroundNeuroblastoma is the most common extracranial solid tumor in children. MYCN gene amplification (MNA) is an independent prognostic factor for rapid tumor progression and poor prognosis, regardless of age and clinical stage. Gain of the MYCN gene locus on the short arm of chromosome 2 can also be found in neuroblastoma.MethodIn this retrospective descriptive analysis of genetic alterations in neuroblastoma tumor samples, both before and after standard chemotherapy, we examined the MYCN gene copy number status in 20 neuroblastic tumor samples using the fluorescence in situ hybridization (FISH) method. We also evaluated its relationship with clinical variables and tumor maturation after standard chemotherapy treatment. Additionally, we compared disease outcomes among different MYCN copy number categories.ResultsAmong the tumor samples, four (25%) exhibited increased MYCN copy numbers, 20% showed MYCN amplification, and 5% displayed MYCN gain. We observed decreased survival rates in advanced stages of neuroblastoma. Furthermore, in male patients, we noted an association between increased MYCN copy number and metastatic tumors.ConclusionWe found that increased MYCN copy number is moderately associated with an immature phenotype and correlated with lower event-free survival. However, we did not detect a statistically significant difference.Keywords: Neuroblastoma, MYCN amplification, Chemotherapy, Refractory, Progression-free survival
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Dinutuximab, which is a monoclonal antibody targeting GD2 expressed in neuroblasts, improves survival when included in the therapy regimen. This article reviews the importance of dinutuximab in managing neuroblastoma (NB). Dinutuximab targets high levels of GD2 expression in NB cells, thus increasing event?free survival when used in the maintenance therapy of high?risk patients with NB. Although several collaborative studies have set the standard of care for maintenance therapy, the long?term follow?up and continuous evaluation of the use of antibodies and the co?administration of other pharmacological or immunomodulatory drugs remain to be studied. Trials have shown that the use of dinutuximab for maintenance therapy can prolong the time before the first relapse and improve overall survival. However, there is uncertainty in the function of cytokines co?administered with dinutuximab,which may lead to increased toxicity without additional benefits. Recent studies on relapsed and refractory NB have shown the potential efficacy of dinutuximab. Further research is required to properly incorporate Dinutuximab in current treatment modalities.
Keywords: Dinutuximab, GD2, monoclonal antibody, neuroblastoma -
Objective(s)Cerebral ischemia/reperfusion (I/R) injury inevitably aggravates the initial cerebral tissue damage following a stroke. Peroxiredoxin 1 (Prdx1) is a representative protein of the endogenous antioxidant enzyme family that regulates several reactive oxygen species (ROS)-dependent signaling pathways, whereas the JNK/caspase-3 proapoptotic pathway has a prominent role during cerebral I/R injury. This study aimed to examine the potential mechanism of Prdx1 in Neuro 2A (N2a) cells following oxygen–glucose deprivation and reoxygenation (OGD/R) injury.Materials and MethodsN2a cells were exposed to OGD/R to simulate cerebral I/R injury. Prdx1 siRNA transfection and the JNK inhibitor (SP600125) were used to interfere with their relative expressions. CCK-8 assay, flow cytometry, and lactate dehydrogenase (LDH) assay were employed to determine the viability and apoptosis of N2a cells. The intracellular ROS content was assessed using ROS Assay Kit. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analyses were conducted to detect the expression levels of Prdx1, JNK, phosphorylated JNK (p-JNK), and cleaved caspase-3.ResultsFirstly, Prdx1, p-JNK, and cleaved caspase-3 expression were significantly induced in OGD/R-exposed N2a cells. Secondly, the knockdown of Prdx1 inhibited cell viability and increased apoptosis rate, expression of p-JNK, and cleaved caspase-3 expression. Thirdly, SP600125 inhibited the JNK/caspase-3 signaling pathway and mitigated cell injury following OGD/R. Finally, SP600125 partially reversed Prdx1 down-regulation-mediated cleaved caspase-3 activation and OGD/R damage in N2a cells.ConclusionPrdx1 alleviates the injury to N2a cells induced by OGD/R via suppressing JNK/caspase-3 pathway, showing promise as a potential therapeutic for cerebral I/R injury.Keywords: Caspase-3, Cell Hypoxia, c-Jun N-terminal kinase, Mice, Neuroblastoma, Peroxiredoxin 1, Reperfusion injury
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In this cross-sectional study, we aimed to evaluate epidemiologic data, survival, and prognosis of pediatric patients diagnosed with neuroblastoma who were referred to Mahak Pediatric Cancer Treatment and Research Center (MPCTRC). One-hundred thirty-seven children younger than 15 years with neuroblastoma from April 2008 to March 2020 were included in this study. Data were retrospectively extracted from their documents, and follow-up was done for alive individuals. Collected data were analyzed using SPSS software version 25 for parametric and non-parametric variables. Of all patients, 51.82% (n=71) were male (M/F ratio was 1.07:1) with a mean age of 2.48±0.26 years. According to the International Neuroblastoma Staging System (INSS), more than 70% of patients were diagnosed with stages 3, 4, and 4S. Primary tumors were located mostly in the adrenal glands (42.34%) and abdomen (29.20%), respectively. Additionally, 62% of children experienced metastasis, with the most common site being bone marrow. Moreover, patients' overall survival, progression-free survival, and event-free survival were 55.2%±5.6, 41.0%±7.9, and 30.0%±5.1, respectively. Early diagnosis and effective treatment of neuroblastoma can directly influence patients' survival, and those who are diagnosed with neuroblastoma within one month of its symptoms onset are more likely to have higher survival rates.
Keywords: Neuroblastoma, Pediatric oncology, Survival rates, Delayed diagnosis, treatment -
Introduction
Neuroblastoma (NB) is one of the most common malignant extracranial solid tumors in children, mainly detected in children between the ages of 22 months to five years. It can develop in any location of the sympathetic nervous system. Although it has a broad spectrum of signs and symptoms, it is hard to find cases with major respiratory manifestations.
Case PresentationOur case report presents a 50-day-old male admitted to a local hospital with respiratory distress and cyanosis. Then, he was intubated and transferred to our pediatric center for further evaluation. Our investigation found a mass in the mediastinum with lung involvement. This patient is a rare case of neuroblastoma that occurred earlier in the age of onset with uncommon respiratory manifestation, unresponsive to outpatient treatment.
ConclusionsWe presented a neuroblastoma case with persistent respiratory manifestations that repeatedly received outpatient treatment for respiratory diseases, but his condition did not improve. Physicians should always suspect this condition in addition to other differential diagnoses, especially in patients unresponsive to outpatient treatment, with abnormal chest X-rays and respiratory symptoms.
Keywords: Neuroblastoma, Pediatrics, Oncology, Malignant Tumor -
Asia Oceania Journal of Nuclear Medicine & Biology, Volume:11 Issue: 1, Winter and Spring 2023, PP 93 -96
A 2-year-old girl started to wobble without any specific triggers, so the patient was admitted to our hospital's pediatric department. The entire cerebellum showed severe atrophy on MRI and much lower uptake than that in the cerebral cortex on perfusion SPECT. The diagnosis of opsoclonus-myoclonus syndrome (OMS) was suspected. MRI visualized a small mass behind the inferior vena cava. Although its uptake on I-123 MIBG scintigraphy was inconclusive, the mass was surgically removed, and the diagnosis of neuroblastoma was pathologically confirmed. OMS is one of the paraneoplastic neurological syndromes with cerebellar ataxia, myoclonus of the trunk and extremities, and opsoclonus as its main symptoms. Approximately 50% of children cases with OMS are associated with neuroblastoma. The prognosis for neuroblastoma itself with OMS is relatively good, but the neurological prognosis is very poor. If there is decreased blood flow in the cerebellum of an infant, it may be necessary to search for neuroblastoma.
Keywords: opsoclonus-myoclonus syndrome, Neuroblastoma, Brain Perfusion SPECT -
Environmental Health Engineering and Management Journal, Volume:9 Issue: 4, Autumn 2022, PP 365 -374Background
Titanium dioxide (TiO2) nanoparticles (NPs) are among the most important and usable photocatalysts. Recently, the biological properties of these NPs, particularly, its anticancer activity, have been considered. Glioblastoma and neuroblastoma are two fatal brain tumors with a high mortality rate in humans, the hope for treatment of which is weak by the common methods.
MethodsIn this study, the cytotoxicity effects of TiO2 alone and in combination with ultraviolet A (UVA) irradiation on two different cell lines, neuroblastoma (SH-SY5Y) and glioblastoma U87, were investigated. After administration of 10, 50, 100, and 500 μg/mL TiO2, 0.043 and 1.4 mW/cm2 UVA irradiation, cell viability was investigated after 4, 24, and 48 hours by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay.
ResultsMTT assay and light microscope demonstrated that the effect of TiO2 NPs varied based on the dose of the substance, the impact time, the cell type, and the amount of radiation. In this study, for NPs alone, both toxicity and non-toxicity of the substance were observed. For NPs in the presence of UV, based on the comparison with its status alone and the difference in the viability assay of the two groups, both the photocatalytic and the coating effect of the NPs were observed.
ConclusionAccording to the results, different concentrations of TiO2 can be used for different purposes. Low concentrations of TiO2 can be used to increase the efficiency of photodynamic therapy and high concentrations of TiO2 can be used to protect the normal cell. This strategy improves the photodynamic therapy and reduces the harmful effects.
Keywords: Titanium, Nanoparticles, UV radiation, Neuroblastoma, Glioblastoma -
Background
Neuroblastoma (NB), a malignant sympathetic nervous system cancer, is the second most common type of pediatric tumor. Increasing the number of NB death emerges to design a new strategy for NB treatment. Nowadays, the development of natural compounds has gradually increased due to their ability to apoptosis induction. Tea catechin, a flavonoid compound, is one of the natural combinations which inhibit tumor growth and enhance tumor cell apoptosis. In the current study, the effects of pure catechin, doxorubicin (DOX), and their combination on a cellular model of NB [BE(2)C cells] are perused. (NB) a malignant sympathetic nervous system cancer is the second most common type of pediatric tumor. Increasing the number of NB death emerges to design a new strategy for NB treatment. Nowadays, the development of natural compounds has gradually increased due to their ability to apoptosis induction. Tea catechin, a flavonoid compound, is one of the natural combinations which inhibit tumor growth and enhance tumor cell apoptosis.
ObjectivesIn the current study, the effects of pure catechin, doxorubicin (DOX), and their combination on a cellular model of NB [BE(2)C cells] are perused.
MethodsThe 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was done to assess a response dose for each drug. Fluorescent Microscopic and cell cycle analyses were performed for apoptosis detection. Finally, Colony formation was performed to examine cell migration and invasion.
ResultsThe MTT assay showed that catechin and DOX treatment inhibited the viability of the cells while the combination of their ineffective doses had more cytotoxic effects. However, these treatments could not inhibit the cell growth of the normal human fibroblast. Moreover, this combination reduced cell attachment, chromatin fragmentation, and G/S arrest in the cell cycle. The clonogenic assay demonstrated that colony size and numbers obviously reduced after ten days; therefore, Catchin and its combination with DOX suppressed cell capacities of clone formation and migration.
ConclusionsThese results suggest that catechin, DOX, and their combination may inhibit the proliferation, invasion, and migration of BE(2)C Neuroblastoma cells in vitro while inducing cell apoptosis by arresting the cell cycle.
Keywords: BE(2)C Cells, Cancer, Catechin, Cytotoxicity, Doxorubicin, Neuroblastoma -
Journal of Advances in Medical and Biomedical Research, Volume:30 Issue: 143, Nov-Dec 2022, PP 553 -560Background and Objective
Rheum turkestanicum (R. turkestanicum) has been known to reduce inflammation and has antioxidant properties such as protective effect in neurons. This study aimed to determine the effects of R. turkestanicum on neuronal toxicity induced by the pro-parkinsonian neurotoxin 6-hydroxydopamine (6-OHDA) in neuroblastoma SH-SY5Y cells.
Materials and MethodsMTT and DNA fragmentation by PI staining (sub-G1 peak) assays were used to determine cell viability and induction of apoptosis, respectively. Fluorimetry methods measured lipid peroxidation malondialdehyde (MDA) and reactive oxygen species (ROS) levels. The amount of glutathione (GSH) and the activity of superoxide dismutase (SOD) were measured by DTNB (5, 5′-Dithiobis(2-nitrobenzoic acid) and pyrogallol respectively.
ResultsPretreatment with 12.5 to 100 μg/mL of R. turkestanicum extract for 24 hours attenuated 6-OHDA (final concentration 42.5 μg/mL)-induced cytotoxicity. Also, the pretreatment of SH-SY5Y cells with R. turkestanicum inhibited 6-OHDA-stimulated apoptosis in a dose-dependent manner. Additionally, R. turkestanicum extract repressed 6-OHDA-induced oxidative stress as measured by the MDA, ROS, GSH, and SOD levels.
ConclusionThe findings suggest that R. turkestanicum extract has neuroprotective activity on 6-OHDA-induced neuronal toxicity of neuroblastoma cells.
Keywords: Rheum turkestanicum, Oxidative stress, 6-Hydroxydopamine, Neuroblastoma, Apoptosis -
Neuroblastoma (NB) is considered one of the malignant tumors of the nervous system which originates from primordial neural crest cell and is known as the most common extra-cranial solid tumor in childhood. This tumor which is often intra-abdominal, metastases in various sites including the skull, long bones, liver, bone marrow and lymph nodes, but lung metastasis at initial diagnosis is rare (0.2-3.7%). Here, the authors reported a two-year-old boy who referred to Imam Hussein Children's Hospital affiliated to Isfahan University of Medical Sciences, Iran in April 2017 with complaint of abdominal pain and distension along with diarrhea, vomiting and fever. In physical examination, a palpable mass was observed at the right side of the abdomen, that in further studies, NB with lung metastasis along with poorly differentiated, low MKI, positive MYCN amplification was reported. This is the first documented case report of NB with lung metastasis from Iran. In conclusion, although lung is considered as an unfavorable metastatic site for NB, in high grade and poor prognosis cases, this organ should also be examined in metastatic site examinations. Therefore, lung High-resolution computed tomography (HRCT) is introduced as the gold standard modality for this work.
Keywords: Lung, Metastasis, MYCN Protein, Neuroblastoma -
International Journal of Hematology-Oncology and Stem Cell Research, Volume:15 Issue: 4, Oct 2021, PP 221 -229Background
The protein kinase B/mammalian target of the rapamycin (Akt/mTOR) pathway is one of the most potent prosurvival signaling cascades that is constitutively active in neuroblastoma. The eukaryotic translation elongation factor-1, alpha-2 (eEF1A2) protein has been found to activate the Akt/mTOR pathway. However, there is a lack of data on the role of eEF1A2 in neuroblastoma. The present study investigated the effect of eEF1A2 silencing on the viability of neuroblastoma cells and its possible signaling.
Materials and MethodsHuman SH-SY5Y neuroblastoma cells were transfected with small interfering RNA (siRNA) against eEF1A2. After 48 h of transfection, cell viability was assessed using an MTT assay. The mRNA expression of p53, Bax, Bcl-2, caspase-3 and members of the phosphoinositide 3-kinases (PI3K)/Akt/mTOR pathway was determined using quantitative real-time RT-PCR (qRT-PCR). The protein expression of Akt and mTOR was measured using Western blot analysis.
ResultseEF1A2 knockdown significantly decreased the viability of neuroblastoma cells. No significant changes were observed on the expression of p53, Bax/Bcl-2 ratio, and caspase-3 mRNAs; however, the upregulated trends were noted for the p53 and Bax/Bcl-2 ratio. eEF1A2 knockdown significantly inhibited the phosphorylation of both Akt and mTOR. Almost, all of the class I (PIK3CA, PIK3CB, and PIK3CD) and all of the class II PI3K genes were slightly increased in tumor cells with eEF1A2 knockdown. In addition, a slightly decreased expression of the Akt2, mTORC1, and mTORC2 was observed.
ConclusioneEF1A2 knockdown induced neuroblastoma cell death, in part through the inhibition of Akt and mTOR, suggesting a potential role of eEF1A2 as a molecular target for neuroblastoma therapy.
Keywords: Eukaryotic translation elongation factor-1, alpha-2 (eEF1A2), Neuroblastoma, Small interfering RNA (siRNA), SH-SY5Y cells, Phosphoinositide 3-kinases (PI3K), Akt, mTOR, p53 -
Objective(s)The use of mesenchymal stem cells in malignancies has attracted much attention due to their ability to deliver anticancer agents to tumors, including cytokines, chemokines, etc. This study aimed to investigate the effect of MSCs on the neuroblastoma SH-SY5Y cells through proliferation/apoptosis, senescence assessment, telomere length, and telomerase activity in vitro. BAX and BCL2 were also examined as potential signaling pathways in this process.Materials and MethodsFor this reason, two cell populations (MSCs and SH-SY5Y cells) were co-cultured on trans-well plates for 7 days. In a subsequent step, SH-SY5Y cells were harvested from both control and experimental groups and subjected to flow cytometry, ELISA, real-time PCR, PCR-ELISA TRAP assay, and Western blotting assay for Ki67/Caspase3 investigation, β-Galactosidase assessment, telomere length, and telomerase activity assay. Also, expression of genes and proteins through real-time PCR and Western blotting demonstrated the involvement of the aforementioned signaling pathways in this process.ResultsIt was found that MSCs contributed significantly to decrease and increase of Ki-67 and Caspase-3, respectively. Also, MSCs dramatically reduced the length of telomere and telomerase activity and increased the β-Galactosidase activity in a significant manner. In addition, significant increase and decrease were also seen in BAX and BCL2 gene and protein expressions, respectively.ConclusionThese findings revealed that close interaction between MSCs and neuroblastoma cells causes inhibition of the SH-SY5Y cell proliferation and promotes cell senescence via BAX and caspase-3 cascade pathways.Keywords: Caspase3, Mesenchymal stem cells, Neuroblastoma, Signaling pathways, Telomerase, Telomere
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سابقه و هدف
نوروبلاستوم یکی از شایع ترین سرطان های کودکان است که هنوز برخی از موارد آن به درمان های رایج پاسخ نمی دهند و کاندیدای مناسبی جهت ایمنی درمانی توسط سلول های کشنده ذاتی است. در این پژوهش، به تکثیر و فعا ل سازی سلول های NK با استفاده از مجموعه ای از سایتوکاین ها پرداخته شد و نتیجه این فعال سازی در بررسی های برون تنی و درون تنی بررسی گردید.
مواد و روش هاجداسازی سلول ها از خون محیطی با استفاده از شاخص CD56 توسط جداکننده MACS صورت گرفت و از سایتوکاین های IL-2 و IL-15 در تکثیر و IL-21 جهت فعال سازی سلول ها استفاده گردید. مدل نوروبلاستومی با استفاده از رده SK-N-SH در موش های نیود ایجاد شد. تاثیر سلول های NK فعال شده، بر 2 رده سلول سرطانی نوروبلاستومایی پس از تایید فعال سازی توسط فلوسایتومتری سنجیده شد.
نتایجنتایج نشان داد که سلول های NK فعال شده با اینترلوکین 21 در نسبت 1:10 قادرند 94% از سلول های رده SK-N-SH و 91% از سلول های رده سلول های CHLA-255 را از بین ببرند (P<0.05)؛ در حالی که در مورد سلول های فعال نشده میزان کشندگی برای این رده ها به ترتیب 40% و 38% بود (P<0.05). سلول های NK فعال شده با اینترلوکین 21 قادر به از بین بردن تومور در 70% از موش های نیود. مدل زنوگرافت نوروبلاستوم بودند.
نتیجه گیریپژوهش حاضر نشان داد که استفاده از سلول های NK فعال شده با اینترلوکین 21 در درمان نوروبلاستوم مفید و برای استفاده در مطالعات کارآزمایی بالینی آتی بسیار موثر خواهد بود.
کلید واژگان: ایمنی درمانی, اینترلوکین, پیش بالین, سلول کشنده ذاتی, نوروبلاستومFeyz, Volume:25 Issue: 3, 2021, PP 1009 -1019BackgroundNeuroblastoma (NB) is one of the most prevalent childrenchr('39')s neoplasm and some of which still do not respond to common treatments and is an ideal candidate for NK cell immune therapy. In this research, we have performed cytokine activation of NKs by using proper interleukins to obtain more cytolysis which was evaluated in vitro and in vivo.
Materials and MethodsIsolation of NKs from human peripheral blood was performed using CD56 marker via magnetic activated cell sorter (MACS). The IL-2 and IL-15 cytokines were used for proliferation, and IL-21 for activation of cells. The neuroblastoma model was developed using the SK-N-SH cell line in Nude mice. The in vitro effect of the NKs on the two neuroblastoma lines were assessed after activation and via flow cytometry confirmation.
ResultsThe results showed that at the ratio of 1:10 the IL-21 activated NKs lysed 94% of the SK-N-SH and 91% of the CHLA-255 cell lines (P<0.05), in spite of the only 40% and 38% of lysis for these cell lines without activation (P<0.05), respectively. The NKs activated by IL-21 were able to eliminate 70% (P<0.05) of the xenograft neuroblastoma tumors in nude mice.
ConclusionThe present investigation was showed that the activation of NK cells using IL-21 can be useful in the treatment of neuroblastoma and could be applied in future clinical trials.
Keywords: Immune therapy, Interleukin, Natural killer cell, Neuroblastoma, Preclinical -
Background
Neonatal sepsis is a leading cause of mortality and morbidity in the first month of life. The underlying risk factors for early-onset infection (in the first 3 days of life) are prematurity, low birth weight, maternal history of infection, difficult delivery, male gender, twin pregnancy, and congenital malformations. Acinetobacter is a nosocomial infection and rarely caused the early-onset-sepsis and meningitis. The most common neonatal tumor is neuroblastoma; however, it is not defined as a risk factor for early-onset sepsis.
Case report:
A 13-day-old newborn female was referred to our hospital due to ventriculitis, persistent meningitis, and an abdominal mass. She was a term neonate delivered by cesarean section from a mother with a nearly normal pregnancy with no complications, such as chorioamnionitis, prolonged rupture of membrane, urinary tract infection, preeclampsia, and diabetes. A fetal abdominal mass was detected on the left kidney in prenatal sonography. The patient was admitted to the Neonatal Intensive Care Unit in the first minutes of life because of respiratory distress and cyanosis. Subsequently, mechanical ventilation, endotracheal surfactant instillation, and antibiotic therapy were prescribed. Due to the deterioration of the general condition, fever, seizure, and hematuria on the third day, sepsis workup and changing the antibiotics were performed. Blood culture and cerebrospinal fluid (CSF) were positive for Acinetobacter baumannii. Persistent positive CSF culture led to the diagnosis of ventriculitis which was confirmed by brain computed tomography scan (CTS) and ventricular tap. The condition of the patient got better after intraventricular amikacin injection in addition to intravenous colistin and piperacillin. Postnatal sonography and CTS confirmed the abdominal neuroblastoma. Chemotherapy was initiated after the complete treatment of sepsis, meningitis, and ventriculitis. This case report presents a term and female neonate with early-onset neonatal sepsis and meningitis, caused by an unusual microorganism, and a prenatal history of abdominal neuroblastoma.
ConclusionBy this case report, the clinicians are suggested to consider the Acinetobacter baumannii as the cause of fulminant sepsis and meningitis in a term neonate with no underlying risk factors for infection. Keywords
Keywords: Meningitis, Neonatal sepsis, Neuroblastoma, Ventriculitis -
Objective
Neuroblastoma (NB) is one of the frequently observed malignant solid tumors of childhood and infancy, accounting for 15% of pediatric cancer deaths. Recently, the approach of differentiation therapy has shown considerable promise in effective treatment of NB patients. MiR-124 belongs to the nervous system-specific miRNAs that is increased during neuronal differentiation and may be one of the potential therapeutic targets for the treatment of NB. However, despite its well-established therapeutic potential, its efficient delivery to the targeted tumor cells is a challenging task. Mesenchymal stem cells (MSCs) are multipotent adult progenitor cells that have antitumor properties, and they can migrate to cancer cells and tumors. This study aimed to assess whether human adipose tissue-derived MSCs (hADMSCs) have the potential to deliver exogenous miRNAs to NB cells to induce differentiation and decrease proliferation of cancer cells.
Materials and MethodsIn this experimental study, hAD-MSCs were isolated, cultured, and differentiated. The M17 human NB cell line were also cultured. A specific type of miRNAs, i.e., miR-124 was successfully delivered to M17 NB cells with the aid of hAD-MSCs using the direct or indirect (exosome-based) contacts.
ResultsIt was shown that indirect delivery of miR-124 considerably decreased the proliferation of NB cells and induced their differentiation.
ConclusionThe results suggest the use of delivered exogenous miRNAs by the derived exosomes from hAD-MSCs as a novel cell-free stem cell-based therapy for NB cancer.
Keywords: Differentiation, Exosome, Mesenchymal Stem Cells, MiR-124, Neuroblastoma -
Neuroblastoma is an extracranial solid tumor that is most commonly observed in children, yet it is rare to have brain metastasis in neuroblastoma during primary involvement or relapse. In this article, we report a successful treatment of high risk neuroblastoma with primary leptomeningeal metastasis based on developing countries facilities and explain combination chemotherapy (a classic regimen with salvage regimen based on temozolamid and methotroxate intratechal chemotherapy and localized radiation therapy) as a multimodal therapy.
Keywords: Neuroblastoma, Brain metastasis, Leptomeningeal metastasis -
BackgroundNeuroblastoma, oneof themostprevalent infant malignancies, is heterogeneousandeasily spreads into other organs causing life-threatening consequences. Different characters of organs (such as the germ layers where the organs derived from) exert different growth microenvironments and potentially influence the behavior of metastatic neuroblastoma cells and the prognosis of patients. However, limited information is been known about this in neuroblastoma.ObjectivesTo compare characteristics of neuroblastoma, primarily originating from the same germ layer (the seeds), in different tissues (microenvironment) derived from different germ layers.MethodsWe performed retrospective analysis of SEER (Surveillance, Epidemiology, and End Results) data (1973 - 2014), patients with malignant neuroblastoma were grouped basedonthe primary lesion site (mesoderm-, ectoderm- or endoderm-derived tissue). Baseline demographic and clinical characteristics were compared between groups. Due to difficulties of processing incomplete SEER data, therapeutic method and survival rates were analyzed using cases from another SEER database (2000 - 2014).ResultsThe analysis included 3701 patients: 1970 (53.2%) in themesodermgroup, 1017 (27.5%) in the ectoderm groupand714 (19.3%) in the endoderm group. Tumor histology differed between groups (P < 0.01): the ectoderm group had mostly neuroblastoma (79.2%), as did the mesoderm group (71.1%), whereas the endoderm group contained mainly olfactory neuroblastoma (94.7%). The tumors (mean size: 69.14 58.37 mm) were most commonly poorly differentiated with local extension, although lymph node invasion and distant metastasis occurred in a minority of cases. Compared with the other groups, the endoderm group had smaller (43.89 20.84 mm) and better-differentiated tumors and a lower prevalence of lymph node invasion and metastasis (P < 0.05). Despite this, overall survival was poorest for the endoderm group (P < 0.05). Radiotherapy improved overall survival in the endoderm and ectoderm groups but worsened overall survival in the mesoderm group (P < 0.05).ConclusionsMalignant neuroblastoma characteristics may be influenced by the tumor microenvironment. In the youngest patients, decision-making regarding the best choice of therapy should be delayed until accurate risk stratification is possible.Keywords: Neuroblastoma, Tumorigenesis, Germ Layers, Mesoderm, Ectoderm, Endoderm
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IntroductionRecently, studies of diketocarotenoids such as astaxanthin (Ax) and canthaxanthin (Cx) with powerful antioxidant have focused on numerous biological mechanisms such as singlet oxygen quenching, radical scavenging, anti-diabetic, anti-carcinogenesis, anti-inflammatory, anti-obesity and anti-melanogenesis activities. There is evidence demonstrating that diketocarotenoid confers neuroprotective effects in experimental models of chronic neurodegenerative disorders and neurological diseases. This study used Ax and Cx to detect its role on senescence of SHSY-5Y Cells.MethodsIn this study, the sample included the cell control group (SH-SY5Y cell line) that did not receive Ax and Cx, , and the experimental group that received Ax and Cx (20 mM). Ax and Cx were treated with SH-SY5Y cell line at 48 hours. To measure the expression of BAX, Bcl-2 and PPARγ different groups were compared by real‑time PCR analysis. The cell senescence effects of Ax and Cx, a β-galactosidase (SA-β-gal) senescence assay was evaluated. The results were analyzed by the one-way analysis of variance (ANOVA) using Prism version 6.0 software.ResultsThe results showed that treatment with Ax and Cx (20 mM) for 48h induced apoptosis and senescence. The BAX and Bcl-2 gene expression analysis revealed a significant impact of Ax and Cx in apoptosis induction (P<0.05). The measuring of cell senescence also indicated that Ax and Cx exhibited a senescence inductive activity as determined by an increase in β-galactosidase activity and PPARγ gene expression (P<0.05).ConclusionIt appears that Ax and Cx have therapeutic properties in SH-SY5Y cells and can cause the proliferation of these cells to cease. The results suggest that Ax and Cx treatment may be beneficial for therapy of neuroblastoma and neurodegenerative disorders.Keywords: Astaxanthin, Canthaxanthin, Apoptosis, Senescence, Neuroblastoma, SHSY-5Y Cells
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BackgroundThe true incidence of peripheral neuroblastic tumors (PNTs) in children is unknown. This study aims to review and analyze clinical data on the diagnosis and management of pediatric PNTs.MethodsBetween 2007 and 2016, a total of 43 pediatric patients admitted to our institute with PNTs were reviewed.ResultsThe series comprised of 23 males and 20 females with a median age of 1.2 years old. Among the 43 PNTs, 26 tumors originated from the abdomen, 13 from the thorax and four from other primary sites. A total of 16 tumors were identified in routine examinations. Abdominal pain and distension were the main clinical manifestations of abdominal PNTs, while coughing was the most frequent presenting symptom of thoracic PNTs. Elevated vanillylmandelic acid level in the urine over 24 hours was observed in 18 neuroblastoma cases and three ganglioneuroblastoma cases. Neuroblastoma was the most common type of PNT that was reported in 30 (69.8%) patients, followed by ganglioneuroblastoma, which was diagnosed in 11 (25.6%) patients. Only 2 (4.6%) patients were diagnosed with ganglioneuroma. A total of 12 cases were stage, six cases were stage II, three cases were stage III, 18 cases were stage IV, and four cases were stage IVs. The overall two year survival rate was 62.9%, which was related to pathological type, Shimada classification, stage, and primary site.ConclusionsPediatric PNTs have different clinical characteristics and outcomes. Imaging and laboratory data may be useful for the differentiation of PNTs. This study will help pediatric surgeons be aware of the possible manifestations of PNTs in children.Keywords: Children, Peripheral Neuroblastic Tumors, Neuroblastoma, Ganglioneuroblastoma
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