Academic literature on the topic 'Neuroblastoma – Genetic aspects'
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Journal articles on the topic "Neuroblastoma – Genetic aspects"
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Milovic, Ivan, Marija Scekic, Dragana Vujic, Slavisa Djuricic, and Dragomir Djokic. "The characteristics of mediastinal neuroblastoma and perspectives on surgical excision." Acta chirurgica Iugoslavica 50, no. 4 (2003): 103–7. http://dx.doi.org/10.2298/aci0304103m.
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Thoracic (mediastinal) neuroblastomas (NB) have been reported to differ from abdominal (suprarenal and retroperitoneal) NB and to be associated with better prognosis.The comparison between them is rarely published.In this retrospective study,the characteristics of thoracic NB (17 cases) are investigated and compared with abdominal NB (51 case).Regarding the diagnosis, thoracic NB presented in lower clinical stages I and II in 35,3 percent of cases, compared to 11,7 percent of abdominal NB in stages I and II (p< 0,001).The disease was initially diagnosed at less than one year of age in 7/17 (41,2 percent) of thoracic NB and in 12/51 (23,5 percent) in abdominal cases (p< 0,001).The median age at the time of initial diagnosis was 15,3 months for thoracic NB and 27,6 months for abdominal neuroblastoma (p< 0,05).The cases with an elevated vanillylmandelic acid (VMA) and homovanyillic acid (HVA) excretion were 9/17 (52,9 percent) in the mediastinal NB, and 43/51 (84,3 percent) in the abdominal NB, respectively (p< 0,05).The quantitative values of tumour markers were significantly lower in thoracic NB (0,85 vs.2,14, p<0,001).Regarding surgery, complete tumour resection was achieved in 15/17 thoracic NB (88,2 percent) compared to 36/51 (70,6 percent) radicality in abdominal NB. Surgical complications developed in 5/17 thoracic procedures (29,4 percent) without a lethal outcome.The mean tumour mass of thoracic NB was 56,5g vs. 106,3 g of abdominal neuroblastoma (p< 0,001).The incidence of ganglioneuroblastoma in mediastinal tumours was 3/17 (17,6 percent) compared to 8/51 (15,7 percent) in abdominal NB (non significant).A favorable histology based on Shimada classification was found in 37 percent of the mediastinal neuroblastoma cases and in 22 percent in the abdominal NB cases (p< 0,05).Regarding the biological properties, genetic malformations associated with NB were identified in 2 thoracic cases ( 1p deletion and poliploidy).Genetic changes were identified in 12 cases of abdominal NB (1p deletion in 4 cases, DNA plody in 6 cases, N-myc amplification in 1 case) .One additional abdominal NB had 1p deletion, DNA ploidy and N-myc amplification.This study supports results of other investigations that thoracic NB differs significantly in many aspects from abdominal NB.Important differences in favorable histology and biological properties of thoracic NB have changed the concept of surgical treratment, although unnecessry attempts of surgical radicality still lead to serious complications. Complete excision remains the mainstay of therapy of localised thoracic NB, while in most abdominal tumours the aim of an initial operation should be sampling of tumour tissue for histology and molecular biological examination, with complete excision of the mass as the second priority.
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Olivera, Gladys G., Andrea Urtasun, Luis Sendra, Salvador F. Aliño, Yania Yáñez, Vanessa Segura, Pablo Gargallo, et al. "Pharmacogenetics in Neuroblastoma: What Can Already Be Clinically Implemented and What Is Coming Next?" International Journal of Molecular Sciences 22, no. 18 (September 10, 2021): 9815. http://dx.doi.org/10.3390/ijms22189815.
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Pharmacogenetics is one of the cornerstones of Personalized Precision Medicine that needs to be implemented in the routine of our patients’ clinical management in order to tailor their therapies as much as possible, with the aim of maximizing efficacy and minimizing toxicity. This is of great importance, especially in pediatric cancer and even more in complex malignancies such as neuroblastoma, where the rates of therapeutic success are still below those of many other types of tumors. The studies are mainly focused on germline genetic variants and in the present review, state of the art is presented: which are the variants that have a level of evidence high enough to be implemented in the clinic, and how to distinguish them from the ones that still need validation to confirm their utility. Further aspects as relevant characteristics regarding ontogeny and future directions in the research will also be discussed.
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Bown, N. "Neuroblastoma tumour genetics: clinical and biological aspects." Journal of Clinical Pathology 54, no. 12 (December 1, 2001): 897–910. http://dx.doi.org/10.1136/jcp.54.12.897.
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Jain, Neha, Shaista Sattar, Sarah Inglott, Susan Burchill, Jonathan Fisher, Andrea Serban, Rebecca Thomas, et al. "Flow cytometry of bone marrow aspirates from neuroblastoma patients is a highly sensitive technique for quantification of low-level neuroblastoma." F1000Research 10 (September 21, 2021): 947. http://dx.doi.org/10.12688/f1000research.53133.1.
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Background: Bone marrow involvement is an important aspect of determining staging of disease and treatment for childhood neuroblastoma. Current standard of care relies on microscopic examination of bone marrow trephine biopsies and aspirates respectively, to define involvement. Flow cytometric analysis of disaggregated tumour cells, when using a panel of neuroblastoma specific markers, allows for potentially less subjective determination of the presence of tumour cells. Methods: A retrospective review of sequential bone marrow trephine biopsies and aspirates, performed at Great Ormond Street Hospital, London, between the years 2015 and 2018, was performed to assess whether the addition of flow cytometric analysis to these standard of care methods provided concordant or additional information. Results: There was good concurrence between all three methods for negative results 216/302 (72%). Positive results had a concordance of 52/86 (61%), comparing samples positive by flow cytometry and positive by either or both cytology and histology. Of the remaining samples, 20/86 (23%) were positive by either or both cytology and histology, but negative by flow cytometry. Whereas 14/86 (16%) of samples were positive only by flow cytometry. Conclusions: Our review highlights the ongoing importance of expert cytological and histological assessment of bone marrow results. Flow cytometry is an objective, quantitative method to assess the level of bone marrow disease in aspirates. In this study, flow cytometry identified low-level residual disease that was not detected by cytology or histology. The clinical significance of this low-level disease warrants further investigation.
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Andreeva, N. A., E. O. Bezdolnova, D. Yu Kachanov, A. B. Smirnova, M. V. Teleshova, D. T. Utalieva, I. G. Khamin, and T. V. Shamanskaya. "OPHTHALMIC TOXICITY OF ANTI-GD2 IMMUNOTHERAPY (DINUTUXIMAB BETA) IN A PATIENT WITH HIGH-RISK NEUROBLASTOMA: A CASE REPORT AND LITERATURE REVIEW." Pediatria. Journal named after G.N. Speransky 100, no. 3 (May 28, 2021): 248–57. http://dx.doi.org/10.24110/0031-403x-2021-100-3-248-257.
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Neuroblastoma (NB) is the most common extracranial solid embryonic tumor in children. The age of patient, the prevalence of the tumor process and the molecular genetic profile formed the basis of risk-adapted therapy protocols. High-risk patients receive complex treatment, including various combinations of chemotherapy drugs, surgical removal of the tumor, radiation and radioisotope therapy. Since the end of the 90s of the last century, immunotherapy has been introduced into clinical practice as a post-consolidation phase with the aim of affecting the minimal residual tumour mass. GD2-targeted drugs are used as a therapeutic agent for immunotherapy. An important aspect is the study of the early and late toxicity of this therapeutic method. The main side effects include fever, neuropathic pain, allergic reactions, and capillary leak syndrome. The article presents the analysis of literature data on toxic effects arising from immunotherapy (dinutuximab beta), as well and a description of clinical case report of rare specific pathology – ophthalmic complications, which include mydriasis and accommodation disorder up to paresis. The pathogenesis of these disorders is described in the literature as a parasympathetic deficiency, realized through exposure to anti-GD2 drugs, and is leveled after the end of treatment. Given the reversible nature of the disorders, the occurrence of ophthalmic complications does not require the abolition of immunotherapy, however, careful ophthalmological monitoring of the dynamics of pathological manifestations and timely symptomatic correction of the revealed changes are necessary. This information is very important not only for pediatric oncologists/hematologists, but also for ophthalmologists and pediatricians.
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Barrozo, Enrico R., Sanae Nakayama, Pankaj Singh, Donna M. Neumann, and David C. Bloom. "Herpes Simplex Virus 1 microRNA miR-H8 is Dispensable for Latency and Reactivation in Vivo." Journal of Virology, November 18, 2020. http://dx.doi.org/10.1128/jvi.02179-20.
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The regulatory functions of 10 individual viral miRNAs that are abundantly expressed from the Herpes Simplex Virus 1 (HSV-1) latency-associated transcript (LAT) region remain largely unknown. Here, we focus on HSV-1 miRNA miR-H8, which is within the LAT 3p exon, antisense to the first intron of ICP0, and has previously been shown to target a host GPI-anchoring pathway. However, the functions of this miRNA have not been assessed in the context of the viral genome during infection. Therefore, we constructed a recombinant virus lacking miR-H8 (17dmiR-H8) and compared it to the parental wild-type and rescue viruses to characterize phenotypic differences. In rabbit skin cells, 17dmiR-H8 exhibited only subtle reductions in viral yields. In contrast, we found significant decreases in both viral yields (8-fold) and DNA replication (9.9-fold) in murine neuroblastoma cells, while 17dmiR-H8 exhibited a 3.6 fold increase in DNA replication in differentiated human neuronal cells (LUHMES). These cell culture phenotypes suggested potential host and/or neuronal-specific roles for miR-H8 in acute viral replication. To assess whether miR-H8 plays a role in HSV latency or reactivation, we used a human in vitro reactivation model, as well as mouse and rabbit reactivation models. In the LUHMES-induced reactivation model, there was no difference in viral yields at 48 h post-reactivation. In the murine dorsal root ganglia explant and rabbit ocular adrenergic reactivation models, the deletion of miR-H8 had no detectable effect on genome load during latency, or reactivation. These results indicate that miR-H8 is dispensable for establishment of HSV-1 latency and reactivation. IMPORTANCE Herpesviruses have a remarkable ability to sustain lifelong infections by evading host immune responses, establishing a latent reservoir, and by maintaining the ability to reactivate the lytic cascade to transmit the virus to the next host. The HSV-1 latency-associated transcript region is known to regulate many aspects of HSV-1 latency and reactivation, though the mechanisms for these functions remain unknown. To this end, we characterize an HSV-1 recombinant containing a deletion of a LAT-encoded miRNA, miR-H8, and demonstrate that it plays no detectable role in the establishment of latency or reactivation in differentiated human neurons (LUHMES), mouse and rabbit models. Therefore, this study allows us to exclude miR-H8 from phenotypes previously attributed to the LAT region. Elucidating the genetic elements of HSV-1 responsible for the establishment, maintenance, and reactivation from latency may lead to novel strategies for combating persistent herpesvirus infections.
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Abbas, Adil Abdelhamed, and Alaa Mohammed Noor Samkari. "High-risk Neuroblastoma: Poor Outcomes Despite Aggressive Multimodal Therapy." Current Cancer Therapy Reviews 17 (August 5, 2021). http://dx.doi.org/10.2174/1573394717666210805114226.
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: Neuroblastoma (NBL) is a highly malignant embryonal tumor that originates from the primordial neural crest cells. NBL is the most common tumor in infants and the most common extracranial solid tumor in children. The tumor is more commonly diagnosed in children of 1-4 years of age. NBL is characterized by enigmatic clinical behavior that ranges from spontaneous regression to an aggressive clinical course leading to frequent relapses and death. Based on the likelihood of progression and relapse, the International Neuroblastoma Risk Group classification system categorized NBL into very low risk, low risk, intermediate risk, and high risk (HR) groups. HR NBL is defined based on the patient's age (> 18 months), disease metastasis, tumor histology, and MYCN gene amplification. HR NBL is diagnosed in nearly 40% of patients, mainly those > 18 months of age, and is associated with aggressive clinical behavior. Treatment strategies involve the use of intensive chemotherapy (CTR), surgical resection, high dose CTR with hematopoietic stem cell support, radiotherapy, biotherapy, and immunotherapy with Anti-ganglioside 2 monoclonal antibodies. Although HR NBL is now better characterized and aggressive multimodal therapy is applied, the outcomes of treatment are still poor, with overall survival and event-free survival of approximately 40% and 30% at 3-years, respectively. The short and long-term side effects of therapy are tremendous. HR NBL carries a high mortality rate accounting for nearly 15% of pediatric cancer deaths. However, most mortalities are attributed to the high frequency of disease relapse (50%) and disease reactiveness to therapy (20%). Newer treatment strategies are therefore urgently needed. Recent discoveries in the field of biology and molecular genetics of NBL have led to the identification of several targets that can improve the treatment results. In this review, we discuss the different aspects of the epidemiology, biology, clinical presentations, diagnosis, and treatment of HR NBL, in addition to the recent developments in the management of the disease.
Dissertations / Theses on the topic "Neuroblastoma – Genetic aspects"
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Tsoi, Lai-shan, and 蔡麗珊. "Tumor suppressive functions of Krüppel-like factor 4 (KLF 4) in neuroblastoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hdl.handle.net/10722/208425.
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Neuroblastoma is a childhood solid tumor of a unique propensity to either regress
spontaneously or grow relentlessly. Emerging evidence indicated that neuroblastoma
contains heterogeneous populations of cells, and commitment of these cells to
neuronal lineage may result in aggressive progression in patients, whereas to
fibromuscular lineage may give a favorable outcome. However, mechanism(s)
controlling the lineage commitment of neuroblastoma cells remains to be identified.
Our preliminary data suggested that Kr?ppel-Like Factor 4 (KLF4) might promote
neuroblastoma regression. KLF4 is a transcription factor regulating a variety of
cellular functions, including proliferation and cell cycle progression. Recent studies
have demonstrated that KLF4 may act as both tumor suppressor and oncogene in a
cell-context dependent manner. Importantly, our preliminary data showed that low
KLF4 expression is highly associated with poor clinical outcomes of the
neuroblastoma patients. In addition, we found that overexpression of KLF4
suppresses neuroblastoma cell growth accompanied with loss of tumorigenicity.
Morphologically, KLF4 overexpressing cells changed their morphologies to become
epithelial-like, strongly substrate-adherent and expressing smooth muscle marker.
Therefore, we hypothesized that KLF4 exerts its effects through two ways, it may (i)
function to inhibit cell growth and reduce tumorigenicity; and (ii) promote
differentiation of the neuroblastoma cells to the non-tumorigenic, fibromuscular-like
cells.
RT-PCR data revealed the differential expression of KLF4 in 11 neuroblastoma cell
lines. In particular, a modest expression was found in Be(2)C, a cell line which was
formerly demonstrated to differentiate and form tumor in mice xenograft assay. It
was therefore chosen as the study model.
To assess the effects of KLF4 knockdown on tumor growth, stable knockdown clones
from Be(2)C cells were established by lentiviral transduction of KLF4-targeting
shRNA. In parallel, clones that stably expressed non-target shRNA were used as
controls. After the transduction, two stable knockdown clones showing significant
KLF4 downregulation were isolated from single colony (monoclonal stable clones)
and a pool of cells (polyclonal stable clones) respectively. The cell proliferation and
growth rate of the stable clones were then measured by 5-bromo-2’-deoxyuridine
(BrdU) proliferation assay and growth curve assay. The results have indicated that
both monoclonal and polyclonal stable KLF4 knockdown clones grow faster than the
control clones. In order to examine the tumorigenicity in vivo, the stable clones were
xenotransplanted to severe combined immunodeficient mice. The stable KLF4
knockdown clones showed a significant higher growth rate and formed a larger
tumor. The stable clones were also treated with BrdU for four weeks for
differentiation towards fibromuscular lineage. As anticipated, the control clones
showed fibromuscular features, like more flattened and epithelial-like morphology. In
contrast, the stable KLF4 knockdown clones failed to present the fibromuscular
features after treatment. In addition, immunocytochemistry staining of SMA and
quantitative analysis of the immunocytochemistry further confirmed that only the
control clones showed higher SMA expression after BrdU treatment, while there is no
change in the SMA expression in the stable KLF4 knockdown clones. These results
demonstrated that KLF4 functioned by inhibiting neuroblastoma cell proliferation
and growth, reducing the tumorigenicity, and it was required for fibromuscular
differentiation.published_or_final_version
Surgery
Master
Master of Philosophy
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Hung, Chun-hin, and 孔進軒. "Effect of novel Chinese specific presenilin-1 V97L mutation on intracellular calcium homeostasis in human neuroblastoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193533.
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Presenilin-1 (PS1) mutations caused by the PSEN1 gene mutations are the major cause of early onset familial Alzheimer’s disease (EOFAD). Two Chinesespecific EOFAD related PS1 mutations, V97L and A136G, have been found. Studies suggested that V97L mutation lead to the overexpression of Aβ42 and tau hyperphosphorylation, which are the major hallmarks of Alzheimer’s disease (AD), while properties of A136G were unclear. Since calcium dysregulation was suggested to play an important role in AD, the research project investigated if V97L and A136G mutations also lead to altered endoplasmic reticulum (ER) 〖Ca〗^(2+) regulation. SH-SY5Y cells transduced with retrovirus carrying V97L mutant or A136 mutant PSEN1 were used as the experiment models.
In Western blotting, while the PS1 expression level was unaffected in V97L mutant, the expression level was significantly lower in A136G mutant. In carbachol (CCh) perfusion experiment, V97L mutant was found to exaggerate ER 〖Ca〗^(2+) release when stimulated by higher concentration (30, 100 and 300 μM) CCh, while A136G mutant exaggerated ER Ca2+ release when stimulated by 30 μM and 300 μM CCh, but not 100 μM CCh. In 5% fetal bovine serum (FBS) perfusion experiment, both V97L and A136G mutants were found to sensitize 〖Ca〗^(2+) oscillation, which the sensitization effect of V97L was 3 folds of A136G.
The results suggested that V97L mutation exaggerates ER 〖Ca〗^(2+) release, possibly via interaction with IP3R. However the results of A136G were inconclusive and contradicting, therefore further investigation is needed.published_or_final_version
Physiology
Master
Master of Medical Sciences
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Rajbhandari, Presha. "Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma." Thesis, 2016. https://doi.org/10.7916/D8J67H0X.
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Neuroblastoma is a heterogeneous pediatric malignancy originating from the developing sympathetic nervous system, with poor long-term survival for high-risk patients (~40%). About half of advanced neuroblastomas harbor high-level amplification of the MYCN gene, and these tumors show few, if any, additional driver lesions. Despite significant increase in the body of knowledge of genetics in neuroblastoma, all the high-risk patients follow similar therapeutic procedures and little advancement has been made on molecular target based therapies. The major challenge is to dissect the complexity and heterogeneity of these tumors to find driver genes and activated pathways that are essential for the survival of these cancer cells.
We used an integrated systems biology approach to define the core regulatory machinery responsible for maintenance of an aggressive neuroblastoma phenotypic state. In the first part of the thesis, I will discuss our computational approach to decipher the tumor heterogeneity by subtype classification, followed by identification of master regulator protein modules for three distinct molecular subtypes of high-risk neuroblastomas, which were validated in a large independent cohort of cases. We propose that such modules are responsible for integrating the effect of mutations in upstream pathways and for regulating the genetic programs and pathways necessary for tumor state implementation and maintenance.
The second part of the thesis is focused on experimental validation of putative master regulators in the subtype of neuroblastomas associated with MYCN amplification. By using RNAi screening followed by experimental and computational analyses to elucidate the interdependencies between the top master regulators, we identified TEAD4-MYCN positive feedback loop as a major tumor maintenance mechanism in this subtype. While MYCN regulates TEAD4 transcriptionally, TEAD4 regulates MYCN through transcriptional and post-translational mechanisms. Jointly, MYCN and TEAD4 regulate 90% of inferred MR proteins and causally orchestrate 70% of the subtype-specific gene expression signature. TEAD4 gene expression was associated with neuroblastoma patient survival independently of age, tumor stage and MYCN status (P=2.1e-02). In cellular assays, MYCN promoted growth and repressed differentiation, while TEAD4 activated proliferation and DNA damage repair programs, the signature hallmarks of MYCN-amplified neuroblastoma cells. Specifically, TEAD4 was shown to induce MYCN-independent proliferation by transactivating key genes implicated in high-risk neuroblastoma pathogenesis, including cyclin-dependent kinases, cyclins, E2Fs, DNA replication factors, checkpoint kinases and ubiquitin ligases. The critical role of the core master regulator module in controlling tumor cell viability, both in vitro and in vivo, and its clinical relevance as a prognostic factor highlights TEAD4 as a novel and highly effective candidate target for therapeutic intervention.
In this thesis, we demonstrate that interrogation of tumor specific regulatory networks with patient-derived gene expression signatures can effectively elucidate molecular subtypes as well as the core transcriptional machinery driving subtype specific hallmarks. This approach enables identification of oncogenic and non-oncogenic dependencies of high-risk neuroblastoma and is applicable to other tumor subtypes.
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Zhang, Shuobo. "Transcription factor activating protein 4 is synthetic lethal and a master regulator of MYCN amplified neuroblastoma." Thesis, 2015. https://doi.org/10.7916/D8VX0FPF.
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Despite the identification of MYCN amplification as an adverse prognostic marker in neuroblastoma, no drugs that target MYCN have yet been developed. Here, by combining a whole genome shRNA library screen and Master Regulator Inference Algorithm (MARINa) analysis, we identified Transcription Factor Activating Protein 4 (TFAP4) as a novel synthetic lethal interactor with MYCN amplification in neuroblastoma. Silencing TFAP4 selectively inhibits MYCN amplified neuroblastoma growth both in vitro and in xenograft mice models. TFAP4 expression is inversely correlated with patient survival in MYCN-high neuroblastoma. Mechanistically, silencing TFAP4 induces neuroblastoma differentiation, as seen by increased neurite outgrowth, and up-regulation of neuronal markers. TFAP4 regulates a downstream signature similar to the signature of the oncogene anaplastic lymphoma kinase (ALK). Taken together, our results validate TFAP4 as an important master regulator in MYCN amplified neuroblastoma and a novel synthetic interactor with MYCN amplification. Thus, TFAP4 may be a novel drug target for neuroblastoma treatment.
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Xue, Chengyuan School of Women?s & Children?s Health UNSW. "The role of p53 in the drug resistance phenotype of childhood neuroblastoma." 2007. http://handle.unsw.edu.au/1959.4/40876.
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The development of resistance to chemotherapeutic drugs is the main obstacle to the successful treatment of many cancers, including childhood neuroblastoma, the most common solid tumour of infants. One factor that may play a role in determining response of neuroblastoma tumours to therapeutic agents is the p53 tumour suppressor gene. A number of previous studies have suggested that this tumour suppressor protein is inactive in neuroblastoma due to its cytoplasmic sequestration. This thesis therefore has examined the functionality of p53 and its role in determining drug response of neuroblastoma cells. An initial study was undertaken that characterised an unusually broad multidrug resistance (MDR) phenotype of a neuroblastoma cell line (IMR/KAT100). The results demonstrated that the MDR phenotype of the IMR/KAT100 cells was associated with the acquisition of mutant p53. To explore the role of p53 in drug resistance further, p53-deficient variants in cell lines with wild-type p53 were generated by transduction of p53-suppressive constructs encoding either shRNA or a dominant-negative p53 mutant. Analysis of these cells indicated that: (i) in contrast to previous reports, wild-type p53 was fully functional in all neuroblastoma lines tested, as evidenced by its activation and nuclear translocation in response to DNA damage, transactivation of target genes and control of cell cycle checkpoints; (ii) inactivation of p53 in neuroblastoma cells resulted in establishment of an MDR phenotype; (iii) knockdown of mutant p53 did not revert the drug resistance phenotype, suggesting it is determined by loss of wild-type function rather than gain of mutant function; (iv) p53-dependent cell senescence, the primary response of S-type neuroblastoma cells to DNA damage, is replaced, after p53 inactivation, by mitotic catastrophe and subsequent apoptosis. In contrast to neuroblastoma, p53 suppression had no effect or increased drug susceptibility in several other tumour cell types, indicating the importance of tissue context for p53- mediated modulation of tumour cell sensitivity to treatment. Taken together, these data provide strong evidence for p53 having a role in mediating drug resistance in neuroblastoma and suggest that p53 status may be an important prognostic marker of treatment response in this disease.
Books on the topic "Neuroblastoma – Genetic aspects"
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1925-, Evans Audrey E., D'Angio Giulio J. 1922-, and Seeger Robert C, eds. Advances in neuroblastoma research: Proceedings of the Third Symposium on Advances in Neuroblastoma Research held in the Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, May 1984. New York: Liss, 1985.
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Human neuroblastoma: Recent advances in clinical and genetic analysis. Chur, Switzerland: Harwood Academic Publishers, 1992.
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Advances in neuroblastoma research: Proceedings of the Third Symposium on Advances in Neuroblastoma Research held in the Children's Hospital of Philadelphia, ... in clinical and biological research). Liss, 1985.
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1930-, Sluyser M., and Voûte P. A. 1906-, eds. Molecular biology and genetics of childhood cancers: Approaches to neuroblastoma. Chichester [England]: E. Horwood, 1988.
Find full textBook chapters on the topic "Neuroblastoma – Genetic aspects"
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Yamasaki, Toshiki, Kouzo Moritake, and George Klein. "Genetic Interaction Between Proto-Oncogene and Histocompatibility Antigen Gene Expressions in Cellular Differentiation of Mouse Neuroblastoma." In Biological Aspects of Brain Tumors, 386–90. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68150-2_53.
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Loreta Paun, Diana, and Alexandra Mirica. "Pheochromocytomas and Paragangliomas: Genotype-Phenotype Correlations." In Pheochromocytoma, Paraganglioma and Neuroblastoma. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95888.
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Pheochromocytomas and paragangliomas are rare neuroendocrine tumors, with genetic background in about 40% of cases, involving more than 30 susceptibility genes. The susceptibility genes can be divided into three main molecular clusters: pseudohypoxic, kinase signaling, and Wnt signaling. Biochemical characterization of these particular tumors should be integrated into the diagnostic algorithm because it can help apply personalized medicine principles and targeted therapy. These tumors can present with very different genotype-phenotype correlations, and their characterization can help the clinical practitioner make optimal clinical management decisions and prioritize genetic testing. This chapter summarizes the most important aspects of genetics and clinical characteristics, together with new genotype-phenotype correlation data.
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"Chemical Carcinogenesis and Mutagenesis." In Environmental Toxicology, edited by Sigmund F. Zakrzewski. Oxford University Press, 2002. http://dx.doi.org/10.1093/oso/9780195148114.003.0010.
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Cancer is a common name for about 200 diseases characterized by abnormal cell growth. According to Kundson (1), the causes of cancer may be classified into the following groups: 1. genetic predisposition 2. environmental factors 3. environmental factors superimposed on genetic predisposition 4. unknown factors Typical examples of the first group are childhood cancers such as retinoblastoma (a genetically predisposed malignancy of the retina), neuroblastoma (a malignancy of the brain), and Wilms’ tumor (a malignancy of the kidney). In adults, an example is polyposis of the colon, a genetic condition that frequently leads to colon cancer. The third group is represented by xeroderma pigmentosum, a genetic condition characterized by a deficient DNA excision repair mechanism (see the discussion later in this chapter). Individuals so predisposed develop skin cancer when exposed to ultraviolet light. The variable susceptibility of the population to the carcinogenic effects of cigarette smoke may also reflect genetic predisposition. Very little can be said about the fourth group because the causes of this group of cancers are not known. Groups 2 and 3 combined (i.e., cancer attributable to environmental causes, with or without genetic predisposition) probably account for 60– 90% of all cancers (2). The environment, in this context, involves not only air, water, and soil, but also food, drink, living habits, occupational exposure, drugs, and practically all aspects of human interaction with the surroundings. This definition implies that a great majority of cancers could be prevented by avoiding exposure to potential carcinogens and by changing living habits. It is therefore not surprising that the study of chemical carcinogenesis represents a major aspect of environmental toxicology. Table 5.1 gives an overview of estimated environmentally associated cancer mortality or incidence in the United States. The data presented in this table have to be considered as rough estimates only. There are great variations in the estimates, depending on the investigators and their methods of collecting the pertinent statistics. The Office of Technology Assessment report on cancer risk offers a more in-depth treatment of this subject.
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BRODEUR, GARRETT M. "Patterns and Significance of Genetic Changes in Neuroblastomas." In Biochemical and Molecular Aspects of Selected Cancers, 251–76. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-12-564498-3.50011-x.
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