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Editor’s note iNature is China’s largest academic public account.
It is jointly created by a team of doctors from Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature talent public account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNature craniopharyngioma (CP) is a rare histologically benign but clinically challenging tumor because it is closely related to the key structures of the central brain
.
CP can be divided into two main histological subtypes: diamond tumor type CP (ACP) and papillary CP (PCP)
.
Although some genetic aberrations of these two types have been revealed in previous studies, the complete genetic change spectrum of the tumor is still unknown
.
On December 18, 2021, Peng Yong, Zhu Xiaofeng, and Zhou Liangxue of Sichuan University published an online research paper entitled "Characterization of novel CTNNB1 mutation in Craniopharyngioma by whole-genome sequencing" in Molecular Cancer (IF=27).
Twenty-six CPs (including 16 ACPs and 10 PCPs) and their matched blood samples were subjected to Whole Genome Sequencing (WGS)
.
The study found that compared with malignant tumors, CP exhibits lower complexity and fewer somatic mutations
.
In addition, CTNNB1 (68.
75% of ACP) and BRAF V600E (70.
00% of PCP) mutations are mutually exclusive in ACP and PCP, consolidating the driving role of these two genes in ACP and PCP, respectively
.
A new mutation in exon 3 of CTNNB1 was discovered in ACP
.
Experiments have confirmed that the mutation enhances the stability of β-catenin by inhibiting ubiquitination, thereby activating the Wnt signaling pathway and promoting cell proliferation
.
In summary, WGS analysis revealed the genome-wide landscape of CP and identified a new mutation in exon 3 of CTNNB1
.
This new mutation activates the Wnt signaling pathway by increasing the stability of β-catenin
.
The results of this study provide a more comprehensive understanding of the genetic alteration spectrum of CP
.
Craniopharyngioma (CP) is a rare primary benign brain tumor with an incidence rate of 0.
16/100,000
.
CP occurs in the sella area adjacent to many important functional structures, such as the optic nerve, optic chiasm, pituitary stalk, hypothalamus, and internal carotid artery
.
Surgical resection is currently the main treatment for CP
.
Total resection of CP (GTR) has always been the treatment of choice, but the incidence of optic nerve and endocrine damage is high, and patients undergoing subtotal resection (STR) are usually at risk of recurrence
.
In general, CP is characterized as "the most terrifying of intracranial tumors", with a high disability rate, resulting in poor quality of life and increased mortality in long-term follow-up
.
The two histological subtypes of CP, diamond tumor type (ACP) and papillary type (PCP), have different age distributions, pathological characteristics and mechanisms
.
ACP is the more common subtype that affects all age groups, while PCP is mainly limited to adults
.
ACP is mainly cystic and shows typical obvious calcification, while typical PCP is more commonly non-calcified and "solid"
.
Through target sequencing or whole exome sequencing, recent studies have shown that these two subtypes have different molecular pathogenesis
.
ACP is driven by somatic mutations in the CTNNB1 gene (encoding β-catenin).
Most of these mutations are point mutations in exon 3, which affect the stability of β-catenin proteins
.
The mutant β-catenin cannot be effectively degraded, leading to its nuclear accumulation and activation of the Wnt signaling pathway, which is essential for tumor development
.
For PCP, apart from somatic BRAF V600E, no other recurrent mutations or genomic aberrations were found
.
This mutation has been observed in most PCPs to activate MAP kinase/ERK signaling to promote tumor progression
.
The entire content of the somatic changes in the coding region of the CP sample (picture from Molecular Cancer) Because target sequencing or whole exome sequencing may miss key insights into some important genomic regions, the complete genetic change spectrum of CP has not yet been determined
.
In this study, in order to better understand the genomic changes of CP, the study performed Whole Genome Sequencing (WGS) on 26 CPs, including 16 ACPs and 10 PCPs, and their matched normal blood samples
.
The study found that compared with other malignant counterparts, there are fewer somatic mutations in the CP genome
.
In addition, the study confirmed that CTNNB1 and BRAF V600E mutations are mutually exclusive in ACP and PCP, respectively
.
Interestingly, this study discovered a new mutation in the CTNNB1 gene in ACP and experimentally characterized its carcinogenic function in vitro
.
Therefore, this study provides a more comprehensive understanding of the genetic profile in CP
.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021-01468-7
It is jointly created by a team of doctors from Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature talent public account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNature craniopharyngioma (CP) is a rare histologically benign but clinically challenging tumor because it is closely related to the key structures of the central brain
.
CP can be divided into two main histological subtypes: diamond tumor type CP (ACP) and papillary CP (PCP)
.
Although some genetic aberrations of these two types have been revealed in previous studies, the complete genetic change spectrum of the tumor is still unknown
.
On December 18, 2021, Peng Yong, Zhu Xiaofeng, and Zhou Liangxue of Sichuan University published an online research paper entitled "Characterization of novel CTNNB1 mutation in Craniopharyngioma by whole-genome sequencing" in Molecular Cancer (IF=27).
Twenty-six CPs (including 16 ACPs and 10 PCPs) and their matched blood samples were subjected to Whole Genome Sequencing (WGS)
.
The study found that compared with malignant tumors, CP exhibits lower complexity and fewer somatic mutations
.
In addition, CTNNB1 (68.
75% of ACP) and BRAF V600E (70.
00% of PCP) mutations are mutually exclusive in ACP and PCP, consolidating the driving role of these two genes in ACP and PCP, respectively
.
A new mutation in exon 3 of CTNNB1 was discovered in ACP
.
Experiments have confirmed that the mutation enhances the stability of β-catenin by inhibiting ubiquitination, thereby activating the Wnt signaling pathway and promoting cell proliferation
.
In summary, WGS analysis revealed the genome-wide landscape of CP and identified a new mutation in exon 3 of CTNNB1
.
This new mutation activates the Wnt signaling pathway by increasing the stability of β-catenin
.
The results of this study provide a more comprehensive understanding of the genetic alteration spectrum of CP
.
Craniopharyngioma (CP) is a rare primary benign brain tumor with an incidence rate of 0.
16/100,000
.
CP occurs in the sella area adjacent to many important functional structures, such as the optic nerve, optic chiasm, pituitary stalk, hypothalamus, and internal carotid artery
.
Surgical resection is currently the main treatment for CP
.
Total resection of CP (GTR) has always been the treatment of choice, but the incidence of optic nerve and endocrine damage is high, and patients undergoing subtotal resection (STR) are usually at risk of recurrence
.
In general, CP is characterized as "the most terrifying of intracranial tumors", with a high disability rate, resulting in poor quality of life and increased mortality in long-term follow-up
.
The two histological subtypes of CP, diamond tumor type (ACP) and papillary type (PCP), have different age distributions, pathological characteristics and mechanisms
.
ACP is the more common subtype that affects all age groups, while PCP is mainly limited to adults
.
ACP is mainly cystic and shows typical obvious calcification, while typical PCP is more commonly non-calcified and "solid"
.
Through target sequencing or whole exome sequencing, recent studies have shown that these two subtypes have different molecular pathogenesis
.
ACP is driven by somatic mutations in the CTNNB1 gene (encoding β-catenin).
Most of these mutations are point mutations in exon 3, which affect the stability of β-catenin proteins
.
The mutant β-catenin cannot be effectively degraded, leading to its nuclear accumulation and activation of the Wnt signaling pathway, which is essential for tumor development
.
For PCP, apart from somatic BRAF V600E, no other recurrent mutations or genomic aberrations were found
.
This mutation has been observed in most PCPs to activate MAP kinase/ERK signaling to promote tumor progression
.
The entire content of the somatic changes in the coding region of the CP sample (picture from Molecular Cancer) Because target sequencing or whole exome sequencing may miss key insights into some important genomic regions, the complete genetic change spectrum of CP has not yet been determined
.
In this study, in order to better understand the genomic changes of CP, the study performed Whole Genome Sequencing (WGS) on 26 CPs, including 16 ACPs and 10 PCPs, and their matched normal blood samples
.
The study found that compared with other malignant counterparts, there are fewer somatic mutations in the CP genome
.
In addition, the study confirmed that CTNNB1 and BRAF V600E mutations are mutually exclusive in ACP and PCP, respectively
.
Interestingly, this study discovered a new mutation in the CTNNB1 gene in ACP and experimentally characterized its carcinogenic function in vitro
.
Therefore, this study provides a more comprehensive understanding of the genetic profile in CP
.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021-01468-7
