Yujia Xiong

Beijing Institute of Neurosurgery

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Jiwei Bai

Beijing Tian Tan Hospital

Yutao Shen

Beijing Institute of Neurosurgery

Chuzhong Li

Beijing Institute of Neurosurgery

Tianshun Ma

Beijing Institute of Neurosurgery

Xiaohong R. Yang

Division of Cancer Epidemiology and Genetics

Mingxuan Li

Beijing Institute of Neurosurgery

Songbai Gui

Beijing Tian Tan Hospital

Hela Koka

Division of Cancer Epidemiology and Genetics

Difei Wang

Leidos (United States)

Dilys M. Parry

Research Network (United States)

Cooperative Institutions

National Institutes of Health

National Cancer Institute

Capital Medical University

Division of Cancer Epidemiology and Genetics

Chinese Academy of Sciences

Beijing Institute of Genomics

Beijing Institute of Neurosurgery

Shanghai Center For Bioinformation Technology

United States Department of Health and Human Services

University of Chinese Academy of Sciences

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Supplementary fig 5 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Figure S5. SNAI1, SNAI3, and TWIST expression in CC1 and CC2 tumors.

Profiling (computer programming)

Chordoma

10.1158/1078-0432.22489379.v1

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Supplementary Legend 1 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Supplementary Legend

Legend

Profiling (computer programming)

Chordoma

10.1158/1078-0432.22489397

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Table S1-S5 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Table S1. Genes included in the targeted DNA panel sequencing. Table S2. Differences in clinical characteristics by molecular subtype. Table S3. Distributions of mutation status in PBRM1 and SETD2 by molecular subtype in RNASeq and Nanostring datasets. Table S4. Differentially expressed genes among molecular subtypes. Table S5. GSEA results for up- and down-regulated gene sets comparing CC2 to CC1.

Table (database)

10.1158/1078-0432.22489376.v1

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Trends of incidence and prognosis of gastric neuroendocrine neoplasms: a study based on SEER and our multicenter research

Gastric Cancer (2020)

Ping Hu Jian’an Bai Min Liu Jingwen Xue Tiaotiao Chen

To investigate the recent epidemiological trends of gastric neuroendocrine neoplasms (GNENs) and establish a new tool to estimate the prognosis of gastric neuroendocrine carcinoma (GNEC) and gastric neuroendocrine tumor (GNET).Nomograms were established based on a retrospective study on patients diagnosed with GNENs from 1975 to 2016 in Surveillance, Epidemiology and End Results database. External validation was performed among 246 GNENs patients in Jiangsu province to verify the discrimination and calibration of the nomograms.The age-adjusted incidence of GNENs has increased from 0.309 to 6.149 per 1,000,000 persons in the past 4 decades. Multivariate analysis indicated independent prognostic factors for both GNEC and GNET including age, distant metastasis and surgical intervention (P < 0.05). In addition, T, N staging and grade were significantly associated with survival of GNEC, while size was a predictor for GNET (P < 0.05). The C-indexes of the nomograms were 0.840 for GNEC and 0.718 for GNET, which were higher than those of the 8th AJCC staging system (0.773 and 0.599). Excellent discrimination was observed in the validation cohorts (C-index of nomogram vs AJCC staging for GNEC: 0.743 vs 0.714; GNET: 0.945 vs 0.927). Survival rates predicted by nomograms were close to the actual survival rates in the calibration plots in both training and validation sets.The incidence of the GNENs is increasing steadily in the past 40 years. We established more excellent nomograms to predict the prognosis of GNENs than traditional staging system, helping clinicians to make tailored decisions.

Surgical oncology

10.1007/s10120-020-01046-8

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Supplementary fig 5 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Figure S5. SNAI1, SNAI3, and TWIST expression in CC1 and CC2 tumors.

SNAI1

Profiling (computer programming)

10.1158/1078-0432.22489379

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Supplementary fig 4 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Figure S4. Expression of selected markers in relation to overall survival (left) and recurrence-free survival (right) in Chinese chordoma patients with long-term follow-up data. A. CLDN11; B. GLI1; C. EPHA3; D. LEF1.

Chordoma

10.1158/1078-0432.22489382.v1

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PALB2 as a factor to predict the prognosis of patients with skull base chordoma

Frontiers in Oncology (2022)

Yujia Xiong Mingxuan Li Yutao Shen Tianshun Ma Jiwei Bai

This study aimed to study the role of PALB2 on the prognosis of skull base chordoma patients and the proliferation, migration, and invasion of chordoma cells.187 patients with primary skull base chordoma were involved in the study. Immunohistochemical analysis was used to measure the PALB2 protein expression. Kaplan-Meier analysis, univariate and multivariate Cox analysis were used to evaluate the impact of PALB2 on patient prognosis. A nomogram was established for predicting the progression free survival of chordoma patients. Cell counting kit-8, colony formation, transwell migration, and invasion assays were used to assess the proliferation, migration, and invasion of chordoma cells with PALB2 knockdown. TIMER 2.0 was used to explore the expression and prognostic role of PALB2 in cancers.High PALB2 expression indicated an adverse prognosis in chordoma. A nomogram involved PALB2, degree of resection, pathology, and Al-mefty classification could accurately predict the progression free survival of chordoma patients. The proliferation, migration, and invasion of chordoma cells significantly decreased after PALB2 knockdown. Additionally, PALB2 showed high expression in various cancers and was associated with a poor prognosis.In summary, our results reveal that high PALB2 expression indicates a poor prognosis of chordoma patients and promotes the malignant phenotypes of chordoma cells in vitro.

Chordoma

10.3389/fonc.2022.996892

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Loss of SMARCB1 promotes autophagy and facilitates tumour progression in chordoma by transcriptionally activating ATG5

Cell Proliferation (2021)

Mingxuan Li Yutao Shen Yujia Xiong Shuai Wang Chuzhong Li

SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1) loss is associated with a poor prognosis in chordoma, while the mechanism remains largely unclear. Here, we aim to explore the function and regulatory mechanisms of SMARCB1 in chordoma.The effect of SMARCB1 on chordoma cells was investigated in vitro and in vivo. Chromatin immunoprecipitation (ChIP) sequencing was used to investigate the mechanisms of SMARCB1 in chordoma. The association between SMARCB1 and autophagy was validated by Western blot, immunofluorescence and transmission electron microscopy. In addition, the ATG5 expression in chordoma tissue was assessed using immunohistochemistry and correlated with patient survival.SMARCB1 inhibited the malignant phenotype of chordoma cells in vitro and in vivo, supporting a tumour suppressor role of SMARCB1 in chordoma. ATG5-mediated autophagy was identified as a potential downstream pathway of SMARCB1. Mechanistically, SMARCB1 bound directly to the ATG5 promoter and epigenetically inhibited its transcription, which decreased ATG5 expression and impaired autophagy. Additionally, autophagy inhibitor chloroquine had a potential anti-cancer effect on chordoma cells in vitro. Moreover, high ATG5 expression was observed in recurrent chordoma patients, which independently correlated with adverse outcomes.Taken together, our results revealed that the SMARCB1/ATG5 axis is a promising therapeutic target for chordoma and autophagy inhibitors may be effective agents for chordoma treatment.

SMARCB1

Chordoma

10.1111/cpr.13136

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Supplementary fig 2 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Figure S2. A. Contributions of small indel (ID) signatures (A and E) between CC1 and CC2; B. Number of mutations in small indel (ID) signatures (A and E) between CC1 and CC2.

Indel

Profiling (computer programming)

10.1158/1078-0432.22489391.v1

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Loss of INI1 inhibits the expression of SIDT1 and promotes tumor progression in skull base chordoma by regulating EZH2-mediated H3K27me3

Research Square (Research Square) (2022)

Yazhuo Zhang Yutao Shen Mingxuan Li Yujia Xiong Tianshun Ma

Abstract Integrase interactor 1 (INI1) loss is associated with a poor prognosis of skull base chordoma, while the molecular mechanism remains generally unclear. Hence, we herein explored the regulatory mechanism underlying INI1 action in skull base chordoma. We exploited transcriptomic sequencing of 48 skull base chordomas to analyze the INI1 -correlated genes, and we found that EZH2 was negatively correlated with INI1 . As EZH2 regulated the expression of the repressive histone mark H3K27me3, we applied chromatin immunoprecipitation (ChIP) sequencing of H3K27me3 to investigate the downstream molecules involved. ChIP sequencing and ChIP-qPCR revealed that H3K27me3 directly bound to the SIDT1 promoter, and qRT-PCR verified that H3K27me3 suppressed the transcription of SIDT1 . The expression of SIDT1 in skull base chordoma was assessed using immunohistochemical staining and its low expression was associated with a poor prognosis in chordoma patients. When the potential tumor-suppressive effects ofSIDT1 were further investigatedby cytologic experiments, our results verified that SIDT1 played a tumor-suppressive role in chordoma both in vitro and in vivo. In conclusion, these findings suggested the INI1-EZH2-H3K27me3-SIDT1 axis as a possible novel therapeutic target in skull base chordoma.

Chordoma

Chromatin immunoprecipitation

10.21203/rs.3.rs-1995178/v1

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