Yujie Ma

135 timestamped statements across 3 topics — auto-found in recorded discussions, each timestamp jumps to the exact moment.

Neuroblastoma · guest expert

Featured statements

▶ Ep 3 · 0:45
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
▶ Ep 3 · 1:38
PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase.
quote · High-risk Neuroblastoma
▶ Ep 18 · 3:58
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
▶ Ep 18 · 7:33
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
▶ Ep 555 · 0:45
Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest.
epidemiological · Pediatric Oncology
▶ Ep 555 · 1:38
PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase.
clinical · Pediatric Oncology

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Yujie's statements about High-risk Neuroblastoma 54 statements

Open the High-risk Neuroblastoma collection →

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

▶ Ep 3 · 0:45
quote Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. ↗
▶ Ep 3 · 0:45
epidemiological Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. ↗
▶ Ep 3 · 0:45
quote Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. ↗
▶ Ep 3 · 0:45
epidemiological Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. ↗
▶ Ep 3 · 0:56
clinical Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. ↗
▶ Ep 3 · 0:56
clinical Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. ↗
▶ Ep 3 · 1:03
clinical Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. ↗
▶ Ep 3 · 1:03
clinical Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. ↗
▶ Ep 3 · 1:19
clinical PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. ↗
▶ Ep 3 · 1:19
clinical PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. ↗
▶ Ep 3 · 1:38
quote PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. ↗
▶ Ep 3 · 1:38
clinical PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. ↗
▶ Ep 3 · 1:38
quote PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. ↗
▶ Ep 3 · 1:38
clinical PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. ↗
▶ Ep 3 · 1:49
clinical The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. ↗
▶ Ep 3 · 1:49
clinical CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. ↗
▶ Ep 3 · 1:49
clinical The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. ↗
▶ Ep 3 · 1:49
clinical CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. ↗
▶ Ep 3 · 2:06
clinical CAMK2G is a member of the serine/threonine protein kinase family. ↗
▶ Ep 3 · 2:06
clinical CAMK2G is a member of the serine/threonine protein kinase family. ↗
▶ Ep 3 · 2:10
clinical CAMK2G plays an important role in neuronal development and synaptic plasticity. ↗
▶ Ep 3 · 2:10
clinical CAMK2G plays an important role in neuronal development and synaptic plasticity. ↗
▶ Ep 3 · 2:24
clinical When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. ↗
▶ Ep 3 · 2:24
clinical When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. ↗
▶ Ep 3 · 2:33
clinical PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. ↗
▶ Ep 3 · 2:33
clinical PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. ↗
▶ Ep 3 · 3:02
clinical Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. ↗
▶ Ep 3 · 3:02
clinical Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. ↗
▶ Ep 3 · 3:02
clinical Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. ↗
▶ Ep 3 · 3:02
clinical Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. ↗
▶ Ep 3 · 3:14
clinical Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. ↗
▶ Ep 3 · 3:14
clinical Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. ↗
▶ Ep 3 · 3:30
clinical CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. ↗
▶ Ep 3 · 3:30
clinical CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. ↗
▶ Ep 3 · 3:44
clinical Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. ↗
▶ Ep 3 · 3:44
clinical Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. ↗
▶ Ep 3 · 3:58
clinical 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. ↗
▶ Ep 3 · 3:58
clinical 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. ↗
▶ Ep 3 · 4:13
clinical CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. ↗
▶ Ep 3 · 4:13
clinical CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. ↗
▶ Ep 3 · 4:21
clinical 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. ↗
▶ Ep 3 · 4:21
clinical 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. ↗
▶ Ep 3 · 6:20
clinical CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. ↗
▶ Ep 3 · 6:20
clinical CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. ↗
▶ Ep 3 · 6:33
clinical CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. ↗
▶ Ep 3 · 6:33
clinical CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 3 · 6:33
clinical CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. ↗
▶ Ep 3 · 6:33
clinical CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 3 · 7:11
clinical CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 3 · 7:11
clinical CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 3 · 7:33
opinion 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. ↗
▶ Ep 3 · 7:33
opinion 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. ↗
▶ Ep 3 · 7:33
quote 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. ↗
▶ Ep 3 · 7:33
quote 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. ↗
Yujie's statements about Neuroblastoma 54 statements

Open the Neuroblastoma collection →

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

▶ Ep 18 · 0:45
quote Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. ↗
▶ Ep 18 · 0:45
epidemiological Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. ↗
▶ Ep 18 · 0:45
epidemiological Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. ↗
▶ Ep 18 · 0:45
quote Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. ↗
▶ Ep 18 · 0:56
clinical Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. ↗
▶ Ep 18 · 0:56
clinical Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. ↗
▶ Ep 18 · 1:03
clinical Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. ↗
▶ Ep 18 · 1:03
clinical Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. ↗
▶ Ep 18 · 1:19
clinical PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. ↗
▶ Ep 18 · 1:19
clinical PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. ↗
▶ Ep 18 · 1:38
quote PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. ↗
▶ Ep 18 · 1:38
clinical PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. ↗
▶ Ep 18 · 1:38
quote PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. ↗
▶ Ep 18 · 1:38
clinical PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. ↗
▶ Ep 18 · 1:49
clinical The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. ↗
▶ Ep 18 · 1:49
clinical CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. ↗
▶ Ep 18 · 1:49
clinical The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. ↗
▶ Ep 18 · 1:49
clinical CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. ↗
▶ Ep 18 · 2:06
clinical CAMK2G is a member of the serine/threonine protein kinase family. ↗
▶ Ep 18 · 2:06
clinical CAMK2G is a member of the serine/threonine protein kinase family. ↗
▶ Ep 18 · 2:10
clinical CAMK2G plays an important role in neuronal development and synaptic plasticity. ↗
▶ Ep 18 · 2:10
clinical CAMK2G plays an important role in neuronal development and synaptic plasticity. ↗
▶ Ep 18 · 2:24
clinical When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. ↗
▶ Ep 18 · 2:24
clinical When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. ↗
▶ Ep 18 · 2:33
clinical PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. ↗
▶ Ep 18 · 2:33
clinical PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. ↗
▶ Ep 18 · 3:02
clinical Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. ↗
▶ Ep 18 · 3:02
clinical Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. ↗
▶ Ep 18 · 3:02
clinical Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. ↗
▶ Ep 18 · 3:02
clinical Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. ↗
▶ Ep 18 · 3:14
clinical Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. ↗
▶ Ep 18 · 3:14
clinical Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. ↗
▶ Ep 18 · 3:30
clinical CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. ↗
▶ Ep 18 · 3:30
clinical CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. ↗
▶ Ep 18 · 3:44
clinical Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. ↗
▶ Ep 18 · 3:44
clinical Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. ↗
▶ Ep 18 · 3:58
clinical 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. ↗
▶ Ep 18 · 3:58
clinical 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. ↗
▶ Ep 18 · 4:13
clinical CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. ↗
▶ Ep 18 · 4:13
clinical CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. ↗
▶ Ep 18 · 4:21
clinical 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. ↗
▶ Ep 18 · 4:21
clinical 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. ↗
▶ Ep 18 · 6:20
clinical CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. ↗
▶ Ep 18 · 6:20
clinical CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. ↗
▶ Ep 18 · 6:33
clinical CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. ↗
▶ Ep 18 · 6:33
clinical CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 18 · 6:33
clinical CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. ↗
▶ Ep 18 · 6:33
clinical CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 18 · 7:11
clinical CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 18 · 7:11
clinical CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 18 · 7:33
opinion 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. ↗
▶ Ep 18 · 7:33
quote 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. ↗
▶ Ep 18 · 7:33
opinion 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. ↗
▶ Ep 18 · 7:33
quote 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. ↗
Yujie's statements about Pediatric Oncology 27 statements

Open the Pediatric Oncology collection →

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

▶ Ep 555 · 0:45
quote Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest. ↗
▶ Ep 555 · 0:45
epidemiological Neuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest. ↗
▶ Ep 555 · 0:56
clinical Retinoic acid is used to induce differentiation in treatment of high risk neuroblastoma. ↗
▶ Ep 555 · 1:03
clinical Retinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma. ↗
▶ Ep 555 · 1:19
clinical PCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication. ↗
▶ Ep 555 · 1:38
clinical PCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase. ↗
▶ Ep 555 · 1:38
quote PCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase. ↗
▶ Ep 555 · 1:49
clinical CAMK2G was identified as a target kinase of calmodulin using mass spectrometry. ↗
▶ Ep 555 · 1:49
clinical The binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation. ↗
▶ Ep 555 · 2:06
clinical CAMK2G is a member of the serine/threonine protein kinase family. ↗
▶ Ep 555 · 2:10
clinical CAMK2G plays an important role in neuronal development and synaptic plasticity. ↗
▶ Ep 555 · 2:24
clinical When CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287. ↗
▶ Ep 555 · 2:33
clinical PCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells. ↗
▶ Ep 555 · 3:02
clinical Low CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients. ↗
▶ Ep 555 · 3:02
clinical Low CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma. ↗
▶ Ep 555 · 3:14
clinical Low CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma. ↗
▶ Ep 555 · 3:30
clinical CAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction. ↗
▶ Ep 555 · 3:44
clinical Expression of neuronal differentiation markers were downregulated following CAMK2G knockdown. ↗
▶ Ep 555 · 3:58
clinical 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. ↗
▶ Ep 555 · 4:13
clinical CAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays. ↗
▶ Ep 555 · 4:21
clinical 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. ↗
▶ Ep 555 · 6:20
clinical CAMK2G is expressed at low levels in SKNSH neuroblastoma cell line. ↗
▶ Ep 555 · 6:33
clinical CAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines. ↗
▶ Ep 555 · 6:33
clinical CAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 555 · 7:11
clinical CAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines. ↗
▶ Ep 555 · 7:33
opinion 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. ↗
▶ Ep 555 · 7:33
quote 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. ↗