TY - JOUR
T1 - Revolutionizing pediatric neuroblastoma treatment
T2 - unraveling new molecular targets for precision interventions
AU - Zheng, Min
AU - Kumar, Ankush
AU - Sharma, Vishakha
AU - Behl, Tapan
AU - Sehgal, Aayush
AU - Wal, Pranay
AU - Shinde, Nirmala Vikram
AU - Kawaduji, Bhosale Sachin
AU - Kapoor, Anupriya
AU - Anwer, Md Khalid
AU - Gulati, Monica
AU - Shen, Bairong
AU - Singla, Rajeev K.
AU - Bungau, Simona Gabriela
N1 - Publisher Copyright:
Copyright © 2024 Zheng, Kumar, Sharma, Behl, Sehgal, Wal, Shinde, Kawaduji, Kapoor, Anwer, Gulati, Shen, Singla and Bungau.
PY - 2024
Y1 - 2024
N2 - Neuroblastoma (NB) is the most frequent solid tumor in pediatric cases, contributing to around 15% of childhood cancer-related deaths. The wide-ranging genetic, morphological, and clinical diversity within NB complicates the success of current treatment methods. Acquiring an in-depth understanding of genetic alterations implicated in the development of NB is essential for creating safer and more efficient therapies for this severe condition. Several molecular signatures are being studied as potential targets for developing new treatments for NB patients. In this article, we have examined the molecular factors and genetic irregularities, including those within insulin gene enhancer binding protein 1 (ISL1), dihydropyrimidinase-like 3 (DPYSL3), receptor tyrosine kinase-like orphan receptor 1 (ROR1) and murine double minute 2-tumor protein 53 (MDM2-P53) that play an essential role in the development of NB. A thorough summary of the molecular targeted treatments currently being studied in pre-clinical and clinical trials has been described. Recent studies of immunotherapeutic agents used in NB are also studied in this article. Moreover, we explore potential future directions to discover new targets and treatments to enhance existing therapies and ultimately improve treatment outcomes and survival rates for NB patients.
AB - Neuroblastoma (NB) is the most frequent solid tumor in pediatric cases, contributing to around 15% of childhood cancer-related deaths. The wide-ranging genetic, morphological, and clinical diversity within NB complicates the success of current treatment methods. Acquiring an in-depth understanding of genetic alterations implicated in the development of NB is essential for creating safer and more efficient therapies for this severe condition. Several molecular signatures are being studied as potential targets for developing new treatments for NB patients. In this article, we have examined the molecular factors and genetic irregularities, including those within insulin gene enhancer binding protein 1 (ISL1), dihydropyrimidinase-like 3 (DPYSL3), receptor tyrosine kinase-like orphan receptor 1 (ROR1) and murine double minute 2-tumor protein 53 (MDM2-P53) that play an essential role in the development of NB. A thorough summary of the molecular targeted treatments currently being studied in pre-clinical and clinical trials has been described. Recent studies of immunotherapeutic agents used in NB are also studied in this article. Moreover, we explore potential future directions to discover new targets and treatments to enhance existing therapies and ultimately improve treatment outcomes and survival rates for NB patients.
KW - immunotherapy
KW - molecular targets
KW - neuroblastoma
KW - precision interventions
KW - preclinical studies
UR - http://www.scopus.com/inward/record.url?scp=85189898557&partnerID=8YFLogxK
U2 - 10.3389/fcell.2024.1353860
DO - 10.3389/fcell.2024.1353860
M3 - Review article
AN - SCOPUS:85189898557
SN - 2296-634X
VL - 12
JO - Frontiers in Cell and Developmental Biology
JF - Frontiers in Cell and Developmental Biology
M1 - 1353860
ER -