1. Articles in category: Cancer Cell

    1-24 of 160 1 2 3 4 5 6 7 »
    1. High-Affinity GD2-Specific Car T Cells Induce Fatal Encephalitis in a Preclinical Neuroblastoma Model

      High-Affinity GD2-Specific Car T Cells Induce Fatal Encephalitis in a Preclinical Neuroblastoma Model

      The GD2 ganglioside, which is abundant on the surface of neuroblastoma cells, is targeted by an FDA-approved therapeutic monoclonal antibody and is an attractive tumor-associated antigen for cellular immunotherapy. Chimeric antigen receptor (CAR)–modified T cells can have potent antitumor activity in B-cell malignancies, and trials to harness this cytolytic activity toward GD2 in neuroblastoma are under way.

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    2. The State of Cellular Adoptive Immunotherapy for Neuroblastoma and Other Pediatric Solid Tumors.

      The State of Cellular Adoptive Immunotherapy for Neuroblastoma and Other Pediatric Solid Tumors.

      Front Immunol. 2017;8:1640

      Authors: Le TP, Thai TH

      Abstract Research on adult cancer immunotherapy is proceeding at a rapid pace resulting in an impressive success rate exemplified by a few high profile cases. However, this momentum is not readily extended to pediatric immunotherapy, and it is not for lack of trying.

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      Mentions: Immunotherapy
    3. Structure-based design and biological characterization of selective histone deacetylase 8 (HDAC8) inhibitors with anti-neuroblastoma activity.

      Structure-based design and biological characterization of selective histone deacetylase 8 (HDAC8) inhibitors with anti-neuroblastoma activity.

      J Med Chem. 2017 Nov 30;:

      Authors: Heimburg T, Kolbinger FR, Zeyen P, Ghazy E, Herp D, Schmidtkunz K, Melesina J, Shaik TB, Erdmann F, Schmidt M, Romier C, Robaa D, Witt O, Oehme I, Jung M, Sippl W

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    4. MYCN Amplification Is Associated with Repressed Cellular Immunity in Neuroblastoma: An In Silico Immunological Analysis of TARGET Database.

      MYCN Amplification Is Associated with Repressed Cellular Immunity in Neuroblastoma: An In Silico Immunological Analysis of TARGET Database.

      Front Immunol. 2017;8:1473

      Authors: Zhang P, Wu X, Basu M, Dong C, Zheng P, Liu Y, Sandler AD

      Abstract Purpose: RNA and DNA sequencing data are traditionally used to discern intrinsic cellular pathways in cancer pathogenesis, their utility for investigating the tumor microenvironment (TME) has not been fully explored.

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      Mentions: MYCN
    5. Surface marker profiling of SH-SY5Y cells enables small molecule screens identifying BMP4 as a modulator of neuroblastoma differentiation.

      Surface marker profiling of SH-SY5Y cells enables small molecule screens identifying BMP4 as a modulator of neuroblastoma differentiation.

      Sci Rep. 2017 Oct 19;7(1):13612

      Authors: Ferlemann FC, Menon V, Condurat AL, Rößler J, Pruszak J

      Abstract Neuroblastoma is the most common extra-cranial solid tumor in children. Its broad spectrum of clinical outcomes reflects the underlying inherent cellular heterogeneity.

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    6. Heterogeneity of MYCN Amplification in Neuroblastoma at Diagnosis, Treatment, Relapse and Metastasis.

      "Nineteen cases (63%) showed diffuse MYCN amplification in all samples tested. Nine cases (30%) showed a reduction in MYCN copy number: five cases with diffuse amplification subsequently showed focal amplification, one case with diffuse MYCN amplification showed MYCN gain after treatment, and three focally amplified cases were non-amplified in later specimens. In two cases (7%), focal amplification became diffuse in subsequent samples. Histology was not predictive of the temporal or spatial pattern of MYCN amplification for a particular tumour. If extent of amplification (focal vs. diffuse) is not considered, 26/30 (87%) of cases were consistently MYCN-amplified. However, our data ...

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    7. MYCN promotes neuroblastoma malignancy by establishing a regulatory circuit with transcription factor AP4.

      "We show for the first time that high expression of TFAP4 in primary neuroblastoma patients is associated with poor clinical outcome. siRNA-mediated suppression of TFAP4 in MYCN-expressing neuroblastoma cells led to inhibition of cell proliferation and migration. Chromatin immunoprecipitation assay demonstrated that TFAP4 expression is positively regulated by MYCN. Microarray analysis identified genes regulated by both MYCN and TFAP4 in neuroblastoma cells, including Phosphoribosyl-pyrophosphate synthetase-2 (PRPS2) and Syndecan-1 (SDC1), which are involved in cancer cell proliferation and metastasis. Overall this study suggests a regulatory circuit in which MYCN by elevating TFAP4 expression, cooperates with it to control a specific set ...

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      Mentions: MYCN
    8. Loss of a microRNA family, let-7, found key in neuroblastoma

      Loss of a microRNA family, let-7, found key in neuroblastoma

      "The let-7 family of microRNAs (bits of genetic code that regulate genes) is known to be involved in both stem-cell differentiation and tumor suppression. Recent research had implicated LIN28B, a protein that inhibits let-7 maturation, in neuroblastoma. But the new study, through work on neuroblastoma cells and analysis of patient data, found that LIN28B is only one of several cancer mechanisms that involve let-7 suppression.  "We're showing that let-7 inhibition is central to the development of this disease," Powers says. "So critical in fact that neuroblastoma uses at least three distinct ways of eliminating it."  Powers and colleagues first ...

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      Mentions: MYCN Chemotherapy
    9. The Relationship Between Apoptotic Activity and Prognostic Factors in Neuroblastomas.

      The Relationship Between Apoptotic Activity and Prognostic Factors in Neuroblastomas.

      Turk Patoloji Derg. 2016;32(2):99-104

      Authors: Ekmekci S, Olgun N, Özer E

      Abstract OBJECTIVE: Prognostic parameters in determining risk groups for treatment in neuroblastoma are cellular differentiation, mitosis karyorrhexis index (MKI), N-myc amplification and age. However, additional prognosticators are still needed because patients can show unpredictable biological behavior.

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    10. An Optimized GD2-Targeting Retroviral Cassette for More Potent and Safer Cellular Therapy of Neuroblastoma and Other Cancers.

      "Neuroblastoma is the commonest extra cranial solid cancer of childhood. Despite escalation of treatment regimens, a significant minority of patients die of their disease. Disialoganglioside (GD2) is consistently expressed at high-levels in neuroblastoma tumors, which have been targeted with some success using therapeutic monoclonal antibodies. GD2 is also expressed in a range of other cancer but with the exception of some peripheral nerves is largely absent from non-transformed tissues. Chimeric Antigen Receptors (CARs) are artificial type I proteins which graft the specificity of a monoclonal antibody onto a T-cell. Clinical data with early CAR designs directed against GD2 have shown ...

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      Mentions: Treatment
    11. News digest – Cancer’s ‘Achilles heel’, e-cigs, vegan diets and… condoms cause cancer?

      News digest – Cancer’s ‘Achilles heel’, e-cigs, vegan diets and… condoms cause cancer?
      • Our scientists uncovered a potential ‘Achilles heel’ on the surface of cancer cells, which helps give us important clues that could one day lead to personalised treatments using patients’ own immune systems. The BBC, Guardian, Financial Times and many more covered this story. And here’s our press release and blog post for the full scoop on the story.
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    12. Cell Proliferation in Neuroblastoma.

      Cell Proliferation in Neuroblastoma.

      Cancers (Basel). 2016;8(1)

      Authors: Stafman LL, Beierle EA

      Abstract Neuroblastoma, the most common extracranial solid tumor of childhood, continues to carry a dismal prognosis for children diagnosed with advanced stage or relapsed disease. This review focuses upon factors responsible for cell proliferation in neuroblastoma including transcription factors, kinases, and regulators of the cell cycle.

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    13. How cell death shapes cancer.

      "However, over the years, a number of studies pointed out that a model in which cell death resistance unambiguously acts as a barrier against malignant disease might be too simple. This is based on paradoxical observations made in tumor patients as well as mouse models indicating that apoptosis can indeed drive tumor formation, at least under certain circumstances. One possible explanation for this phenomenon is that apoptosis can promote proliferation critically needed to compensate for cell loss, for example, upon therapy, and to restore tissue homeostasis. However, this, at the same time, can promote tumor development by allowing expansion of ...

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    14. Novel pharmacodynamic biomarkers for MYCN protein and PI3K/AKT/mTOR pathway signaling in children with neuroblastoma.

      "We have addressed the issue of limited access to tumor biopsies for quantitative detection of protein biomarkers by optimizing a three-color fluorescence activated cell sorting (FACS) method to purify CD45-/GD2+/CD56+ neuroblastoma cells from bone marrow. We then developed a novel quantitative measurement of MYCN protein in these isolated neuroblastoma cells, providing the potential to demonstrate proof of concept for drugs that inhibit PI3K/AKT/mTOR signaling in this disease. In addition we have established quantitative detection of three biomarkers for AKT pathway activity (phosphorylated and total AKT, GSK3β and P70S6K) in surrogate platelet-rich plasma (PRP) from pediatric patients ...

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      Mentions: MYCN
    15. MYCN controls an alternative RNA splicing program in high-risk metastatic neuroblastoma.

      "Six splicing factors displayed unique differential expression patterns in MYCN-amplified tumors and cell lines, and the binding motifs for some of these splicing factors are significantly enriched in differentially-spliced genes. Direct binding of MYCN to promoter regions of the splicing factors PTBP1 and HNRNPA1 detected by ChIP-seq demonstrates that MYCN controls the splicing pattern by direct regulation of the expression of these key splicing factors. Furthermore, high expression of PTBP1 and HNRNPA1 was significantly associated with poor overall survival of stage4 NBL patients (p ≤ 0.05). Knocking down PTBP1, HNRNPA1 and their downstream target PKM2, an isoform of pro-tumor-growth, result ...

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      Mentions: MYCN
    16. Transcription factor activating protein 2 beta (TFAP2B) mediates noradrenergic neuronal differentiation in neuroblastoma.

      "Microarray analyses of primary neuroblastomas (n = 649) demonstrated that low TFAP2B expression was significantly associated with unfavorable prognostic markers as well as adverse patient outcome. We also found that low TFAP2B expression was strongly associated with CpG methylation of the TFAP2B locus in primary neuroblastomas (n = 105) and demethylation with 5-aza-2'-deoxycytidine resulted in induction of TFAP2B expression in vitro, suggesting that TFAP2B is silenced by genomic methylation. Tetracycline inducible re-expression of TFAP2B in IMR-32 and SH-EP neuroblastoma cells significantly impaired proliferation and cell cycle progression. In IMR-32 cells, TFAP2B induced neuronal differentiation, which was accompanied by up-regulation of the ...

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      Mentions: MYCN
    17. Differential role of RIP1 in Smac mimetic-mediated chemosensitization of neuroblastoma cells.

      "Mechanistic studies reveal that Receptor-interacting protein (RIP)1 is required for DOX/BV6-, but not for VCR/BV6-induced apoptosis, since transient or stable knockdown of RIP1 or the pharmacological RIP1 inhibitor necrostatin-1 significantly reduce apoptosis. By comparison, VCR/BV6-mediated apoptosis critically depends on the mitochondrial pathway. VCR/BV6 cotreatment causes phosphorylation of BCL-2 during mitotic arrest, enhanced activation of BAX and BAK and loss of mitochondrial membrane potential (MMP). Additionally, overexpression of BCL-2 profoundly suppresses VCR/BV6-induced apoptosis. Thus, BV6 sensitizes NB cells to chemotherapy-induced apoptosis via distinct initial signaling mechanisms depending on the chemotherapeutic drug. These findings provide novel ...

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    18. Change in a Single DNA Base Drives a Childhood Cancer -- Chop Researchers Detail how a Super-Enhancer Gene Causes High-Risk Neuroblastoma --

      Change in a Single DNA Base Drives a Childhood Cancer -- Chop Researchers Detail how a Super-Enhancer Gene Causes High-Risk Neuroblastoma --

      PHILADELPHIA, Nov. 11, 2015 /PRNewswire-USNewswire/ -- Pediatric oncology researchers have pinpointed a crucial change in a single DNA base that both predisposes children to an aggressive form of the childhood cancer neuroblastoma and makes the disease progress once tumors form. The change in the LMO1 gene results in a "super-enhancer," driving abnormally increased biological activity in the gene, resulting in tumor formation and progression.

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    1-24 of 160 1 2 3 4 5 6 7 »
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