Genetic features of neuroblastic tumors associated with opsoclonus-myoclonus syndrome opens up the possibility for detection in peripheral blood

Berbegall, Ana P.; Almaraz, Ricardo López; Navarro, Samuel; Noguera, Rosa

doi:10.1586/14737175.2016.1163221

Cited by 1 publication

(3 citation statements)

References 21 publications

(34 reference statements)

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“…In OMS-associated neuroblastoma, tumors usually do not have MYCN amplification and have aneuploid DNA content, although MYCN oncogene amplification and hyperdiploid tumors have also been reported. 6,8,[13][14][15] Numerical chromosome alterations (NCA) and segmental chromosome alterations (SCA), such as the gain of chromosomes 1q, 2p, and 17q and deletion of 1p, 3p, 11q, and 14q, are usually observed in neuroblastoma. 14,[16][17][18][19] NCA is often observed in children with localized tumors and favorable outcomes, whereas SCA is more frequently observed in children with advanced stages and poorer prognoses.…”

Section: Histological and Genetic Featuresmentioning

confidence: 99%

“…Furthermore, tumor cells are typically well differentiated, 8,12 with a low mitotic karyorrhexis index. However, one study 13 . reported that 80% of OMS‐associated neuroblastomas were poorly differentiated, and this was attributed to intratumoral heterogeneity, but this did not affect general genetic findings.…”

Section: Features Of Oms‐associated Neuroblastomamentioning

confidence: 99%

“…However, one study. 13 reported that 80% of OMSassociated neuroblastomas were poorly differentiated, and this was attributed to intratumoral heterogeneity, but this did not affect general genetic findings.…”

Section: Histological and Genetic Featuresmentioning

confidence: 99%

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Opsoclonus‐myoclonus syndrome associated with neuroblastoma: Insights into antitumor immunity

Cai

2022

Pediatric Blood & Cancer

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Opsoclonus‐myoclonus syndrome (OMS) is a rare neurological disorder. Half of these cases occur in children with neuroblastoma. Neuroblastoma patients with OMS usually have better oncological outcomes than those without OMS even after stratification by tumor stage and age, indicating that factors mediating OMS may also inhibit tumor cell proliferation. Although the mechanisms underlying OMS remain undefined, the cytokines and lymphocytes alterations in the cerebrospinal fluid support the concept that it is a pattern of neuroinflammation due to an autoimmune effect. The presence of lymphoid follicles consisting of follicular dendritic cells, CD20+ B lymphocytes, CD3+ T lymphocytes, and CD68+ macrophages in the tumor microenvironment in OMS‐associated neuroblastoma support the autoimmune nature of this disorder. This review focuses on the clinical and genetic features of OMS‐associated neuroblastoma, and we update readers on immune features of neuroblastoma with or without OMS to gain insights into antitumor immunity as it relates to tumor biology and prognosis.

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