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Tumor Discovery Choroid plexus tumors: Benign to malignant

glycoprotein, showed significant upregulation in CPTs loss in chromosome 13 (which included the loss of tumor
compared to other brain tumors [6,157] . In distinguishing suppressor genes RB1 and BRCA2) . Thomas et al.
[35]
between CPT subtypes, higher aCPPs expressed found that copy-number alterations mainly represented
significantly more S-100(+)/Vim(+)/Syn(+) compared to whole-chromosomal alterations with subgroup-specific
their regular counterpart . In canine models, E-cadherin enrichments (gains of chromosomes 1, 2, and 21q in the
[68]
was expressed in all CPT grades, independent of tumor “pediatric B” group and gains of chromosomes 5 and 9 and
invasion. N-cadherin immunolabeling was expressed loss of chromosome 21q in the “adult” group) [172] . Among
more in grade I than in high-grade CPTs, whereas the frequently reported genome defects were germline
doublecortin expression was not detected in CPTs [158] . TP53 mutations or Li-Fraumeni syndrome, which tend to
Further investigation into these biomarkers is warranted be associated with a poorer prognosis and poor response
to develop treatments and diagnostic approaches with to radiation therapy [34,35,171,173] .
superior specificity and efficacy.
Epigenetic profiling of CPTs can be used for the
4.3.6. Gene therapy and epigenetic modulators identification of patients at risk of recurrence and is

Gene therapy and epigenetic modulators offer another expected to play a role in treatment stratification and
potential avenue in the treatment of CPTs. Although patient management in future clinical trials. Several
current and past clinical trials have yet to include studies have explored the methylation patterns that
patients with CPTs, there are several trials focusing on characterize CPTs, distinguishing the three subtypes
using virotherapy to treat brain tumors. Notably, the from one another and categorizing them based on
trial NCT04105374 is investigating the addition of anti- aggressiveness [174-176] . In a more recent comprehensive
cancer viral gene therapy using Toca 511 and Toca FC for review, Thomas et al. used DNA methylation profiling
newly diagnosed glioblastomas [159] . Virotherapy has also to classify CPTs into three distinct epigenetic subgroups:
been explored for pediatric brain tumors, using herpes supratentorial pediatric low-risk CPTs (CPP and aCPP),
simplex virus (G207), reovirus (pelareorep/Reolysin), infratentorial adult low-risk CPTs (CPP and aCPP), and
measles virus (MV-NIS), poliovirus (PVSRIPO), and supratentorial pediatric high-risk CPTs (CPP and aCPP
adenovirus (DNX-2401, AloCELYVIR) to treat gliomas and CPC) [174] . Once a complete picture of CPT epigenetic
and meduloblastomas [160,161] . Another approach to gene traits is obtained, DNA methylation inhibitors, histone
therapy involves the therapeutic use of microRNA deacetylase inhibitors, and other such regulators can be
(miRNA). In glioblastoma, miRNAs play a major role administered, as this approach has shown some modest
in the transcriptional control, growth, and proliferation success in some studies [177,178] .
of numerous tumor genes, in addition to performing a
number of important roles in carcinogenesis, the expression 4.3.7. Nanomedicine
of cancer-related genes, glioma stem cell development, Nanomedicine, an umbrella term encompassing all
and regulatory pathways [162-166] . Furthermore, chromatin technologies on the nanoscale, has made significant
remodeling, another method with therapeutic potential progress within the realm of oncology in recent years.
in gliomas, may also find future applications in treating Although clinical literature on nanomedicine’s direct
CPTs [167-169] . While no clinical trials have been conducted application to CPTs is scarce, a growing body of research
specifically for treating CPTs, a growing body of literature demonstrates its potential in the treatment of tumors.
reports target genes and epigenetic mechanisms specific Emerging nanomedicine approaches have been used to
to choroid neoplasms, paving the way for more tailored enhance chemotherapy, phototherapy, immunotherapy,
treatments, diagnostic indicators, and prognostic and gene therapy, with several of these technologies
indicators in the future. currently under evaluation in clinical trials [125,179-183] .

Several chromosomal imbalances have been reported Nanomedicine also holds considerable promise in
in association with CPTs. These chromosomal imbalances emerging drug delivery mechanisms, such as carrier-
play a factor in as much as 94% of CPPs and 100% of free nanomedicines. These nanomedicine exhibit longer
CPCs, according to Rickert et al. [170] . de Oliveira Garcia blood half-life, better tumor selectivity, enhanced tumor
et al. reported gains on chromosomes 12, 18, and 20, as accumulation, and significantly improved antitumor
well as copy-number losses on chromosomes 13q and 22q efficacy compared to free drugs, as demonstrated in vivo
(BRD1 locus) in an aCPP [171] . Yankelevich et al. analyzed studies [184-186] . It is only a matter of time before these
the molecular changes in the malignant transformation of emerging technologies find their way into neuro-oncology,
a CPP into carcinoma and found significant aneuploidy as there is already speculation about their possible role in
with mostly gains present in the papilloma and significant the treatment of CNS disorders [187] .

Volume 2 Issue 2 (2023) 9 https://doi.org/10.36922/td.1057