Successful growth of fresh retinoblastoma cells in chorioallantoic membrane

Fialho, Sílvia Ligório; Silvestrini, Bárbara R.; Vieira, J. N.; Paiva, Mayara Rodrigues Brandão de; Chahud, Fernando; Silva-Cunha, Armando; Corrêa, Zélia M.; Jorge, Rodrigo

doi:10.1186/s40942-020-00236-x

Cited by 4 publications

(1 citation statement)

References 12 publications

(20 reference statements)

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“…Utilizing recognized cell lines like WERI-Rb1 [40], Y-79, RB 383, and RB355 [27] enables the study of tumor dynamics and metastatic behaviors under controlled conditions by implanting these cells onto the CAM. RB cells derived from primary tumors can be expanded and cultured on the CAM to assess various drugs, identifying tumor sensitivity and potential responses [41]. Despite the promise of 3D cell culture models in retinoblastoma research, challenges such as sample variability, limited access to patient-derived materials, and scalability issues persist, hindering large-scale drug screening efforts.…”

Section: Retinoblastoma Pre-clinical Modelsmentioning

confidence: 99%

Histone Deacetylases in Retinoblastoma

Lisek,

Tomczak,

Swiatek

et al. 2024

IJMS

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Retinoblastoma, a pediatric ocular malignancy, presents significant challenges in comprehending its molecular underpinnings and targeted therapeutic approaches. The dysregulated activity of histone deacetylases (HDACs) has been associated with retinoblastoma pathogenesis, influencing critical cellular processes like cell cycle regulation or retinal ganglion cell apoptosis. Through their deacetylase activity, HDACs exert control over key tumor suppressors and oncogenes, influencing the delicate equilibrium between proliferation and cell death. Furthermore, the interplay between HDACs and the retinoblastoma protein pathway, a pivotal aspect of retinoblastoma etiology, reveals a complex network of interactions influencing the tumor microenvironment. The examination of HDAC inhibitors, encompassing both established and novel compounds, offers insights into potential approaches to restore acetylation balance and impede retinoblastoma progression. Moreover, the identification of specific HDAC isoforms exhibiting varying expression in retinoblastoma provides avenues for personalized therapeutic strategies, allowing for interventions tailored to individual patient profiles. This review focuses on the intricate interrelationship between HDACs and retinoblastoma, shedding light on epigenetic mechanisms that control tumor development and progression. The exploration of HDAC-targeted therapies underscores the potential for innovative treatment modalities in the pursuit of more efficacious and personalized management strategies for this disease.

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Section: Retinoblastoma Pre-clinical Modelsmentioning

confidence: 99%