Farting around I looked up childhood cancers and CCR5.
Came across an interesting genetic pathway to neuroblastomas in kids. From 2020. Nothing very new here, but just thought to think about Leronlimab for kids.
CCR5 and CXCL12 allelic variants: Possible association with childhood neuroblastoma susceptibility?
https://www.sciencedirect.com/science/article...2819302322
“Abstract
Neuroblastoma (NB) is a heterogeneous and particularly malignant childhood neoplasm in its higher stages, prone to form metastasis in selected organs and for which there is still no efficient treatment available beyond surgery. Evidence indicates that chemokines and their receptors present involvement as mediators of neuroinflammation and have a neurophysiological role. In the present study, we aimed to verify if CCR5 (rs333) and CXCL12 (rs1801157) allelic variants were associated with NB. For CCR5 (rs333) D32 carriers (OR: 5.96, IC: 2.21–16.06) and for CXCL12 genotype 3′A/3′A (OR:26.18, IC:6.15–111.4) there were statistically significant differences as well to allelic frequency (OR:4.20, IC: 2.19–8.03). Although no correlation was verified regarding prognostic parameters for both CCR5 and CXCL12 polymorphic variants, these polymorphisms may be associated with NB susceptibility which deserve attention for future investigations.”
“Introduction
Neuroblastomas (NB) are tumors originated from undifferentiated nerve cells of the neural crest, which gives origin to the medular adrenal gland and all the sympathetic ganglia and plexuses, that can justify not only the preferential site for localized disease but also its wide distribution through the body in the disseminated form. NB may be viewed as neural tissue derived from the neural crest that remains or becomes undifferentiated after reaching its peripheral location (Grosfeld, 1998). It is more prevalent in children younger than 4 years (85%), falling to 8% in children up to 9 years and 1.5% after 15 years old (Navalkele et al., 2011). Approximately 45% of cases are classified as high risk, being metastatic when diagnosed (London et al., 2005).”
“Therefore, given the involvement of these chemokine receptors in nervous system development and cancer, the known contribution of gentic predisposition in NB onset and the functional implications of these genetic variants in chemokine/chemokine receptor biology, the aim of the present study was to verify if these polymorphisms in CCR5 (rs333) and CXCL12 (rs1801157) genes are associated with NB susceptibility and/or prognosis.”
“Results
Mean age for NB patients was 4 years (ranging from 1 month to 13 years) and for control group was 10 years (1–18 years) (p > 0.05).
CCR5 (rs333) and CXCL12 (rs1801157) were genotyped in NB patients and in control group. Eletrophoretic profiles for CCR5-Δ32 (rs333) and CXCL12 (rs1801157) are shown in Fig. 1, Fig. 2, respectively.
CCR5 (rs333) polymorphism was genotyped in 28 NB patients and in 80 control individuals and genotype and allelic frequencies were evaluated (Table 1).D32 allele was not
Discussion
This work evaluated CCR5 and CXCL12 gene polymorphisms in NB regarding susceptibility and/or prognosis. Although there was no difference in prognosis regarding these genetic variants, for the first time, it was verified that there is an association between genetic polymorphisms in CCR5 and CXCL12 with NB susceptibility.
NB is an embryonal malignant tumor of neural crest origin that most commonly arises in the adrenal gland. In children with localized disease or before 1 year of age, the disease”
Came across an interesting genetic pathway to neuroblastomas in kids. From 2020. Nothing very new here, but just thought to think about Leronlimab for kids.
CCR5 and CXCL12 allelic variants: Possible association with childhood neuroblastoma susceptibility?
https://www.sciencedirect.com/science/article...2819302322
“Abstract
Neuroblastoma (NB) is a heterogeneous and particularly malignant childhood neoplasm in its higher stages, prone to form metastasis in selected organs and for which there is still no efficient treatment available beyond surgery. Evidence indicates that chemokines and their receptors present involvement as mediators of neuroinflammation and have a neurophysiological role. In the present study, we aimed to verify if CCR5 (rs333) and CXCL12 (rs1801157) allelic variants were associated with NB. For CCR5 (rs333) D32 carriers (OR: 5.96, IC: 2.21–16.06) and for CXCL12 genotype 3′A/3′A (OR:26.18, IC:6.15–111.4) there were statistically significant differences as well to allelic frequency (OR:4.20, IC: 2.19–8.03). Although no correlation was verified regarding prognostic parameters for both CCR5 and CXCL12 polymorphic variants, these polymorphisms may be associated with NB susceptibility which deserve attention for future investigations.”
“Introduction
Neuroblastomas (NB) are tumors originated from undifferentiated nerve cells of the neural crest, which gives origin to the medular adrenal gland and all the sympathetic ganglia and plexuses, that can justify not only the preferential site for localized disease but also its wide distribution through the body in the disseminated form. NB may be viewed as neural tissue derived from the neural crest that remains or becomes undifferentiated after reaching its peripheral location (Grosfeld, 1998). It is more prevalent in children younger than 4 years (85%), falling to 8% in children up to 9 years and 1.5% after 15 years old (Navalkele et al., 2011). Approximately 45% of cases are classified as high risk, being metastatic when diagnosed (London et al., 2005).”
“Therefore, given the involvement of these chemokine receptors in nervous system development and cancer, the known contribution of gentic predisposition in NB onset and the functional implications of these genetic variants in chemokine/chemokine receptor biology, the aim of the present study was to verify if these polymorphisms in CCR5 (rs333) and CXCL12 (rs1801157) genes are associated with NB susceptibility and/or prognosis.”
“Results
Mean age for NB patients was 4 years (ranging from 1 month to 13 years) and for control group was 10 years (1–18 years) (p > 0.05).
CCR5 (rs333) and CXCL12 (rs1801157) were genotyped in NB patients and in control group. Eletrophoretic profiles for CCR5-Δ32 (rs333) and CXCL12 (rs1801157) are shown in Fig. 1, Fig. 2, respectively.
CCR5 (rs333) polymorphism was genotyped in 28 NB patients and in 80 control individuals and genotype and allelic frequencies were evaluated (Table 1).D32 allele was not
Discussion
This work evaluated CCR5 and CXCL12 gene polymorphisms in NB regarding susceptibility and/or prognosis. Although there was no difference in prognosis regarding these genetic variants, for the first time, it was verified that there is an association between genetic polymorphisms in CCR5 and CXCL12 with NB susceptibility.
NB is an embryonal malignant tumor of neural crest origin that most commonly arises in the adrenal gland. In children with localized disease or before 1 year of age, the disease”
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