Neuroblastoma

Esiashvili, Natia; Anderson, C.; Katzenstein, Howard M.

doi:10.1016/j.currproblcancer.2009.12.001

Cited by 40 publications

(34 citation statements)

References 119 publications

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“…The median age of diagnosis is 22 months. 3 Rarely does it present in adolescence and adulthood, but outcomes are much poorer in this age group. There does not appear to be an increased prevalence among races, but there is a slight predilection for males (1.2:1).…”

Section: Epidemiologymentioning

confidence: 99%

Neuroblastoma

Colon

Chung

2011

Advances in Pediatrics

161

138

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Section: Epidemiologymentioning

confidence: 99%

Neuroblastoma

Colon

Chung

2011

Advances in Pediatrics

161

138

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“…The most common primary tumor location in children is in the abdomen, predominantly in the adrenal glands. The etiology is not clearly understood; however, both familial genetic predisposition and environmental exposures have been postulated as potential causes [1][2][3]. This solid tumor usually originates in the tissue of the adrenal gland (80%) or in the mediastinum (15%) [4].…”

Section: Introductionmentioning

confidence: 98%

“…Bone marrow, bone, liver, lymph nodes, and skin are the common sites of spread. Metastatic spread can happen by both lymphatic and hematogenous routes [3].…”

Section: Introductionmentioning

confidence: 99%

Metastatic neuroblastoma of the mandible: a cytogenetic and molecular genetic study

Manor

Kapelushnik

Joshua

et al. 2011

Eur Arch Otorhinolaryngol

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Neuroblastoma (NB) jaw metastases are rare. Here, we report on cytogenetic and genetic studies on metastatic NB to the mandible. A 7-year-old boy, with an abdominal neuroblastoma, presented with a mass of the left body of the mandible. Cytogenetic analysis of the original tumor and the mandibular lesion biopsies revealed similar heterogenous subclones with 42 ~ 47,XY,+der(1)(q11 → qter),-2,del(7)(q21.1 → qter),-8,-9,-10,-11,del(11)(q13.3 → qter),-13,-14,-15,-17, + 18-18,der(18)(?),+21,+m1,+m2,+m3,+m4,+m5,+m6,+m7[cp25]. The different markers were identified by SKY analysis. Most of the cells carried 3-6 of these translocations: der(1;21), der(2;9;17), der(2;15;18), der(2;15;Y), der(8;10), der(10;17). Molecular examination using Neuroblastoma MLPA kit (MRC-Holland) revealed gain of 1q25, 1q42, 2q33, 2p23, 2p24 (N-myc), and 21q22, and loss of 11q22, 11q23, 17p13, and 17q11. FISH analysis using N-myc probe showed high amplification levels of N-myc. The cytogenetic and molecular genetic work-ups revealed that the mandibular lesion is a metastasis of the original abdominal tumor and not a second primary caused by the aggressive treatment. Clinical parameters such as : patient's age, site of primary tumor and the mandibular metastasis, together with poor prognosis genetic markers explain the patient's short-term survival.

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“…Neuroblastoma is the most common pediatric extracranial solid tumor 1 , accounting for 12% of all pediatric cancer deaths 2 . Patients over one year of age and those diagnosed with stage III or stage IV disease are considered high-risk 3,4 .…”

Section: Introductionmentioning

confidence: 99%

Examining T Cells at Vaccine Sites of Tumor-bearing Hosts Provides Insights to Dysfunctional T-Cell Immunity

Barr

Jing

Hallett

et al. 2013

Journal of Immunotherapy

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When tumor vaccines are administered as cancer immunotherapy, cellular interactions at the vaccine site are crucial to the generation anti-tumor immunity. Examining interactions at the vaccine site could provide important insights to the success or failure of vaccination. Our laboratory previously showed that while administration of a cell-based vaccine to tumor-free mice leads to productive anti-neuroblastoma immunity, vaccination of tumor-bearing mice does not. The goal of this study was to examine immune effectors at the vaccine site to identify mechanisms responsible for the generation of ineffective anti-tumor immunity in tumor-bearing mice. The results of this study show that vaccine sites of tumor-bearing mice contained significantly fewer T cells than vaccine sites of tumor-free mice. Similar migration and proliferation of T cells was observed in the vaccine sites of tumor-bearing and tumor-free mice, but T cells in the sites of tumor-bearing mice were more apoptotic. T cells at the vaccine sites of both tumor-free and tumor-bearing mice had an effector-memory phenotype and expressed activation markers. Despite the activated phenotype, T cells from tumor-bearing mice elicited defective anti-tumor immune responses. Although T cells from vaccine sites of tumor-bearing mice were capable of producing inflammatory cytokines, the T cells from tumor-bearing mice produced lower levels of cytokines compared to T cells from the tumor-free mice. Remarkably, this defect appears to be systemic, affecting distal T cells in tumor-bearing mice. This study demonstrates that the defective vaccine-induced immune response to neuroblastoma in tumor-bearing hosts originates as a result of tumor burden, resulting in poor anti-tumor immunity.

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Neuroblastoma

Cited by 40 publications

References 119 publications

Neuroblastoma

Neuroblastoma

Metastatic neuroblastoma of the mandible: a cytogenetic and molecular genetic study

Examining T Cells at Vaccine Sites of Tumor-bearing Hosts Provides Insights to Dysfunctional T-Cell Immunity

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