Neuroblastoma

Piskareva, Olga; Stallings, Raymond L.

doi:10.1016/b978-0-12-800206-3.00013-6

Cited by 2 publications

(1 citation statement)

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“…Changes in gene expression ultimately affect all cell processes, so drugs targeting epigenetic modifications might affect cellular response to RA treatment [ 55 ]. Thus, treating SH-SY5Y cells with ATRA and HDAC inhibitors trichostatin A, sodium butyrate, and suberoylanilide hydroxamic acid resulted in a robust dose-dependent decrease of cell viability and proliferation [ 56 ].…”

Section: Resultsmentioning

confidence: 99%

Differentiating Neuroblastoma: A Systematic Review of the Retinoic Acid, Its Derivatives, and Synergistic Interactions

Bayeva¹,

Coll²,

Piskareva

2021

JPM

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A neuroblastoma (NB) is a solid paediatric tumour arising from undifferentiated neuronal cells. Despite the recent advances in disease management and treatment, it remains one of the leading causes of childhood cancer deaths, thereby necessitating the development of new therapeutic agents and regimens. Retinoic acid (RA), a vitamin A derivative, is a promising agent that can induce differentiation in NB cells. Its isoform, 13-cis RA or isotretinoin, is used in NB therapy; however, its effectiveness is limited to treating a minimal residual disease as maintenance therapy. As such, research focuses on RA derivatives that might increase the anti-NB action or explores the potential synergy between RA and other classes of drugs, such as cellular processes mediators, epigenetic modifiers, and immune modulators. This review summarises the in vitro, in vivo, and clinical data of RA, its derivatives, and synergising compounds, thereby establishing the most promising RA derivatives and combinations of RA for further investigation.

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Section: Resultsmentioning

confidence: 99%

Differentiating Neuroblastoma: A Systematic Review of the Retinoic Acid, Its Derivatives, and Synergistic Interactions

Bayeva¹,

Coll²,

Piskareva

2021

JPM

Self Cite

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The Ups and Downs of STAT Inhibition in Acute Myeloid Leukemia

Moser¹,

Edtmayer²,

Witalisz-Siepracka³

et al. 2021

Biomedicines

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Aberrant Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling is implicated in the pathogenesis of acute myeloid leukemia (AML), a highly heterogeneous hematopoietic malignancy. The management of AML is complex and despite impressive efforts into better understanding its underlying molecular mechanisms, survival rates in the elderly have not shown a substantial improvement over the past decades. This is particularly due to the heterogeneity of AML and the need for personalized approaches. Due to the crucial role of the deregulated JAK-STAT signaling in AML, selective targeting of the JAK-STAT pathway, particularly constitutively activated STAT3 and STAT5 and their associated upstream JAKs, is of great interest. This strategy has shown promising results in vitro and in vivo with several compounds having reached clinical trials. Here, we summarize recent FDA approvals and current potential clinically relevant inhibitors for AML patients targeting JAK and STAT proteins. This review underlines the need for detailed cytogenetic analysis and additional assessment of JAK-STAT pathway activation. It highlights the ongoing development of new JAK-STAT inhibitors with better disease specificity, which opens up new avenues for improved disease management.

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Neuroblastoma

Cited by 2 publications

References 100 publications

Differentiating Neuroblastoma: A Systematic Review of the Retinoic Acid, Its Derivatives, and Synergistic Interactions

Differentiating Neuroblastoma: A Systematic Review of the Retinoic Acid, Its Derivatives, and Synergistic Interactions

The Ups and Downs of STAT Inhibition in Acute Myeloid Leukemia

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