Yujie Ma

108 statements · 2 topics

Neuroblastoma · guest expert

Featured statements

Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest.
quote · High-risk Neuroblastoma
KEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton.
clinical · High-risk Neuroblastoma
Gene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity.
clinical · Neuroblastoma
The CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients.
opinion · Neuroblastoma

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Yujie's statements about High-risk Neuroblastoma 54 statements

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Dr. Yujie Ma - Best of the Best in Pediatric Surgery 2025

Quotation Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. Open
Statement Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. Open
Quotation Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. Open
Statement Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. Open
Statement Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. Open
Statement Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. Open
Statement Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. Open
Statement Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. Open
Statement PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. Open
Statement PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. Open
Quotation PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. Open
Statement PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. Open
Quotation PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. Open
Statement PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. Open
Statement CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. Open
Statement The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. Open
Statement CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. Open
Statement The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. Open
Statement CAMK2G is a member of the serine/threonine protein kinase family. Open
Statement CAMK2G is a member of the serine/threonine protein kinase family. Open
Statement CAMK2G plays an important role in neuronal development and synaptic plasticity. Open
Statement CAMK2G plays an important role in neuronal development and synaptic plasticity. Open
Statement When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. Open
Statement When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. Open
Statement PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. Open
Statement PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. Open
Statement Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. Open
Statement Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. Open
Statement Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. Open
Statement Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. Open
Statement Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. Open
Statement Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. Open
Statement CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. Open
Statement CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. Open
Statement Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. Open
Statement Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. Open
Statement Gene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity. Open
Statement Gene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity. Open
Statement CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. Open
Statement CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. Open
Statement KEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton. Open
Statement KEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton. Open
Statement CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. Open
Statement CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. Open
Statement CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. Open
Statement CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. Open
Statement CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. Open
Statement CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. Open
Statement CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. Open
Statement CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. Open
Statement The CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients. Open
Quotation I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients. Open
Statement The CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients. Open
Quotation I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients. Open
Yujie's statements about Neuroblastoma 54 statements

Open the Neuroblastoma collection →

Dr. Yujie Ma - Best of the Best in Pediatric Surgery 2025

Statement Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. Open
Statement Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. Open
Quotation Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. Open
Quotation Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. Open
Statement Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. Open
Statement Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. Open
Statement Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. Open
Statement Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. Open
Statement PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. Open
Statement PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. Open
Statement PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. Open
Statement PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. Open
Quotation PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. Open
Quotation PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. Open
Statement CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. Open
Statement CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. Open
Statement The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. Open
Statement The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. Open
Statement CAMK2G is a member of the serine/threonine protein kinase family. Open
Statement CAMK2G is a member of the serine/threonine protein kinase family. Open
Statement CAMK2G plays an important role in neuronal development and synaptic plasticity. Open
Statement CAMK2G plays an important role in neuronal development and synaptic plasticity. Open
Statement When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. Open
Statement When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. Open
Statement PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. Open
Statement PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. Open
Statement Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. Open
Statement Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. Open
Statement Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. Open
Statement Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. Open
Statement Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. Open
Statement Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. Open
Statement CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. Open
Statement CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. Open
Statement Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. Open
Statement Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. Open
Statement Gene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity. Open
Statement Gene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity. Open
Statement CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. Open
Statement CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. Open
Statement KEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton. Open
Statement KEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton. Open
Statement CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. Open
Statement CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. Open
Statement CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. Open
Statement CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. Open
Statement CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. Open
Statement CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. Open
Statement CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. Open
Statement CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. Open
Quotation I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients. Open
Statement The CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients. Open
Quotation I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients. Open
Statement The CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients. Open