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48 results on '"Yu, Jindan"'

7. Genotypic and phenotypic features of 39 Chinese patients with glycogen storage diseases type I, VI, and IX.

Author

Yu, Jindan, Ling, Xiuxin, Chen, Lingli, Fang, Youhong, Lin, Haihua, Lou, Jingan, Ren, Yanqi, and Chen, Jie

Subjects
*GLYCOGEN storage disease, *PROTEIN deficiency, *GENETIC mutation, *CHINESE people, *HEARING disorders
Abstract

Glycogen storage diseases (GSDs) are abnormally inherited glycogen metabolism mainly affecting the liver, muscles, and heart. Deficiency of proteins involved in glycogen metabolism caused by genetic mutations are responsible for different subtype of GSDs. However, there are still some challenges in diagnosing GSD. This study includes 39 suspected GSDs patients from unrelated families in China. Next‐generation sequencing (NGS) was used to investigate the reason for their diseases at the genetic level. Finally, all 39 patients were diagnosed with GSDs, including 20 GSD‐Ia, 4 GSD‐VI, and 15 GSD IX (12 GSD‐IXa patients and 3 GSD‐IXb patients). Thirty‐two mutations in G6PC1, PYGL, PHKA2, and PHKB genes were identified, with 14 of them being novel variants. The pathogenicity of novel variants was classified according to ACMG guildlines and predicted by in slico algorithms. Mutations p.L216L and p.R83H in G6PC1 gene may be the hot spot mutation in Chinese. Hearing impairment is a rare clinical feature of GSD Ia, which has also been observed in our cohort. The severity of GSD VI and IX was indicated by our patients. Close follow‐up should be applied to GSD VI and IX patients. Our findings provided evidence for building the phenotype–genotype of GSDs and expanded the mutation spectrum of related genes. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Ferroptosis: the vulnerability within a cancer monster

Author

Xie, Wanqing, Agarwal, Shivani, and Yu, Jindan

Subjects
Health care industry
Abstract

Treatment-resistant cancer, such as neuroendocrine prostate cancer (NEPC), is a lethal disease with limited therapeutic options. RB1 is a tumor suppressor gene that is lost in a majority of NEPC tumors. In this issue of the JCI, Wang and colleagues examined how RB1 loss may sensitize cancer cells to ferroptosis inducers through elevation of ACSL4, a key enzyme that promotes lipid peroxidation and triggers ferroptosis. We discuss a high potential of RBI-deficient cells to undergo ferroptosis due to the elevation of ACSL4. This is normally kept in check by abundant expression of GPX4, an antioxidant enzyme, in cancer cells. This balance, however, is tilted by GPX4 inhibitors, leading to massive ferroptosis. We highlight possible therapeutic strategies that exploit this inherent vulnerability for targeting RBI-deficient, treatment-resistant cancer., Emerging roles of ferroptosis in cancer and treatment resistance Ferroptosis is a recently identified, iron-dependent form of programmed cell death that is distinct from other cell death pathways, such as [...]

Published
2023
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10. MYO5B gene mutations may promote the occurrence of very early onset inflammatory bowel disease: a case report.

Author

Lou, Yue, Lv, Yao, Yu, Jindan, Gu, Weizhong, Jiang, Ming, and Chen, Jie

Subjects
INFLAMMATORY bowel diseases, GENETIC mutation, POLYMERASE chain reaction, MISSENSE mutation, TIGHT junctions, VAGINAL discharge
Abstract

Background: With recent advances in gene sequencing technology, more than 60 genetic mutations associated with very early onset inflammatory bowel disease (VEO-IBD) have been reported. Most of the genes are associated with immune deficiencies. The Myosin 5B (MYO5B) gene is primarily involved in cell motility and material transport which is associated with congenital intractable diarrhea and cholestasis. No studies have examined the relationship between the MYO5B gene and VEO-IBD. We report a case of a child with a mutation in the MYO5B gene who was diagnosed with VEO-IBD, then we investigated the association between the MYO5B gene and VEO-IBD. Case presentation: A 7-month-old baby girl with a chief complaint of "blood in the stool for more than 4 months and vaginal pus and blood discharge for 3 weeks" was diagnosed with VEO-IBD, and her symptoms improved after treatment with mesalazine. The whole-exome sequencing was performed with peripheral blood. Immunohistochemistry was performed on the terminal ileal tissue. Western blotting, quantitative polymerase chain reaction (Q-PCR) and immunofluorescence were performed with cultured organoid tissue from the terminal ileum. Whole-exome sequencing identified heterozygous missense of MYO5B variant of unknown significance (p. [I769N]; [T1546M]). Immunohistochemistry revealed a significant decrease in the expression of MYO5B protein in the terminal ileum of the child with MYO5B mutation; Q-PCR revealed a decrease in the mRNA levels of occludin and ZO-1 and both the mRNA levels and protein levels of MYO5B was downregulated in the patient. Immunofluorescence images showed that MYO5B gene mutation disrupted the apical delivery of transporters SGLT1, NHE3 and AQP7. Conclusions: MYO5B gene mutation leading to the downregulation of MYO5B protein may promote the occurrence of VEO-IBD by decreasing mRNA and protein levels of intestinal tight junction genes and dislocating the apical transporters. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Myeloid differentiation factor-2/LY96, a potential predictive biomarker of metastasis and poor outcomes in prostate cancer: clinical implications as a potential therapeutic target

Author

Ferrari, Marina G., primary, Jimenez-Uribe, Alexis P., additional, Wang, Li, additional, Hoeppner, Luke H., additional, Murugan, Paari, additional, Hahm, Eunsil, additional, Yu, Jindan, additional, Kuzel, Timothy M., additional, Gradilone, Sergio A., additional, and Mansini, Adrian P., additional

Published
2023
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13. Chemokine receptor CXCR7 activates Aurora Kinase A and promotes neuroendocrine prostate cancer growth

Author

Gritsina, Galina, primary, Fong, Ka-wing, additional, Lu, Xiaodong, additional, Lin, Zhuoyuan, additional, Xie, Wanqing, additional, Agarwal, Shivani, additional, Lin, Dong, additional, Schiltz, Gary E., additional, Beltran, Himisha, additional, Corey, Eva, additional, Morrissey, Colm, additional, Wang, Yuzhuo, additional, Zhao, Jonathan C., additional, Hussain, Maha, additional, and Yu, Jindan, additional

Published
2023
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16. Data from Activation of MAPK Signaling by CXCR7 Leads to Enzalutamide Resistance in Prostate Cancer

Author

Li, Shangze, primary, Fong, Ka-wing, primary, Gritsina, Galina, primary, Zhang, Ali, primary, Zhao, Jonathan C., primary, Kim, Jung, primary, Sharp, Adam, primary, Yuan, Wei, primary, Aversa, Caterina, primary, Yang, Ximing J., primary, Nelson, Peter S., primary, Feng, Felix Y., primary, Chinnaiyan, Arul M., primary, de Bono, Johann S., primary, Morrissey, Colm, primary, Rettig, Matthew B., primary, and Yu, Jindan, primary

Published
2023
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17. Supplementary Table from A Genome-Wide CRISPR Activation Screen Identifies PRRX2 as a Regulator of Enzalutamide Resistance in Prostate Cancer

Author

Rodríguez, Yara, primary, Unno, Kenji, primary, Truica, Mihai I., primary, Chalmers, Zachary R., primary, Yoo, Young A., primary, Vatapalli, Rajita, primary, Sagar, Vinay, primary, Yu, Jindan, primary, Lysy, Barbara, primary, Hussain, Maha, primary, Han, Huiying, primary, and Abdulkadir, Sarki A., primary

Published
2023
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18. Supplementary Data from Activation of MAPK Signaling by CXCR7 Leads to Enzalutamide Resistance in Prostate Cancer

Author

Li, Shangze, primary, Fong, Ka-wing, primary, Gritsina, Galina, primary, Zhang, Ali, primary, Zhao, Jonathan C., primary, Kim, Jung, primary, Sharp, Adam, primary, Yuan, Wei, primary, Aversa, Caterina, primary, Yang, Ximing J., primary, Nelson, Peter S., primary, Feng, Felix Y., primary, Chinnaiyan, Arul M., primary, de Bono, Johann S., primary, Morrissey, Colm, primary, Rettig, Matthew B., primary, and Yu, Jindan, primary

Published
2023
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20. Supplementary Data from A Genome-Wide CRISPR Activation Screen Identifies PRRX2 as a Regulator of Enzalutamide Resistance in Prostate Cancer

Author

Rodríguez, Yara, primary, Unno, Kenji, primary, Truica, Mihai I., primary, Chalmers, Zachary R., primary, Yoo, Young A., primary, Vatapalli, Rajita, primary, Sagar, Vinay, primary, Yu, Jindan, primary, Lysy, Barbara, primary, Hussain, Maha, primary, Han, Huiying, primary, and Abdulkadir, Sarki A., primary

Published
2023
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21. Supplementary Table 5 from Autoantibody Profiles Reveal Ubiquilin 1 as a Humoral Immune Response Target in Lung Adenocarcinoma

Author

Chen, Guoan, primary, Wang, Xiaoju, primary, Yu, Jianjun, primary, Varambally, Sooryanarayana, primary, Yu, Jindan, primary, Thomas, Dafydd G., primary, Lin, Mu-Yen, primary, Vishnu, Prakash, primary, Wang, Zhuwen, primary, Wang, Rui, primary, Fielhauer, Jeff, primary, Ghosh, Debashis, primary, Giordano, Thomas J., primary, Giacherio, Donald, primary, Chang, Andrew C., primary, Orringer, Mark B., primary, El-Hefnawy, Talal, primary, Bigbee, William L., primary, Beer, David G., primary, and Chinnaiyan, Arul M., primary

Published
2023
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24. Supplementary Data, Methods, Figures 1-5, Tables 1-5 from A Polycomb Repression Signature in Metastatic Prostate Cancer Predicts Cancer Outcome

Author

Yu, Jindan, primary, Yu, Jianjun, primary, Rhodes, Daniel R., primary, Tomlins, Scott A., primary, Cao, Xuhong, primary, Chen, Guoan, primary, Mehra, Rohit, primary, Wang, Xiaoju, primary, Ghosh, Debashis, primary, Shah, Rajal B., primary, Varambally, Sooryanarayana, primary, Pienta, Kenneth J., primary, and Chinnaiyan, Arul M., primary

Published
2023
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25. Supplementary Data from Autoantibody Profiles Reveal Ubiquilin 1 as a Humoral Immune Response Target in Lung Adenocarcinoma

Author

Chen, Guoan, primary, Wang, Xiaoju, primary, Yu, Jianjun, primary, Varambally, Sooryanarayana, primary, Yu, Jindan, primary, Thomas, Dafydd G., primary, Lin, Mu-Yen, primary, Vishnu, Prakash, primary, Wang, Zhuwen, primary, Wang, Rui, primary, Fielhauer, Jeff, primary, Ghosh, Debashis, primary, Giordano, Thomas J., primary, Giacherio, Donald, primary, Chang, Andrew C., primary, Orringer, Mark B., primary, El-Hefnawy, Talal, primary, Bigbee, William L., primary, Beer, David G., primary, and Chinnaiyan, Arul M., primary

Published
2023
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26. Data from A Fluorescence In situ Hybridization Screen for E26 Transformation–Specific Aberrations: Identification of DDX5-ETV4 Fusion Protein in Prostate Cancer

Author

Han, Bo, primary, Mehra, Rohit, primary, Dhanasekaran, Saravana M., primary, Yu, Jindan, primary, Menon, Anjana, primary, Lonigro, Robert J., primary, Wang, Xiaosong, primary, Gong, Yusong, primary, Wang, Lei, primary, Shankar, Sunita, primary, Laxman, Bharathi, primary, Shah, Rajal B., primary, Varambally, Sooryanarayana, primary, Palanisamy, Nallasivam, primary, Tomlins, Scott A., primary, Kumar-Sinha, Chandan, primary, and Chinnaiyan, Arul M., primary

Published
2023
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28. Supplementary Table 1, Figures 1-3 from A Fluorescence In situ Hybridization Screen for E26 Transformation–Specific Aberrations: Identification of DDX5-ETV4 Fusion Protein in Prostate Cancer

Author

Han, Bo, primary, Mehra, Rohit, primary, Dhanasekaran, Saravana M., primary, Yu, Jindan, primary, Menon, Anjana, primary, Lonigro, Robert J., primary, Wang, Xiaosong, primary, Gong, Yusong, primary, Wang, Lei, primary, Shankar, Sunita, primary, Laxman, Bharathi, primary, Shah, Rajal B., primary, Varambally, Sooryanarayana, primary, Palanisamy, Nallasivam, primary, Tomlins, Scott A., primary, Kumar-Sinha, Chandan, primary, and Chinnaiyan, Arul M., primary

Published
2023
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31. Supplementary Methods, Tables 1-2, Figures 1-6 from Definition of a FoxA1 Cistrome That Is Crucial for G1 to S-Phase Cell-Cycle Transit in Castration-Resistant Prostate Cancer

Author

Zhang, Chunpeng, primary, Wang, Liguo, primary, Wu, Dayong, primary, Chen, Hongyan, primary, Chen, Zhong, primary, Thomas-Ahner, Jennifer M., primary, Zynger, Debra L., primary, Eeckhoute, Jérôme, primary, Yu, Jindan, primary, Luo, Jun, primary, Brown, Myles, primary, Clinton, Steven K., primary, Nephew, Kenneth P., primary, Huang, Tim H.-M., primary, Li, Wei, primary, and Wang, Qianben, primary

Published
2023
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37. Data from Autoantibody Profiles Reveal Ubiquilin 1 as a Humoral Immune Response Target in Lung Adenocarcinoma

Author

Chen, Guoan, primary, Wang, Xiaoju, primary, Yu, Jianjun, primary, Varambally, Sooryanarayana, primary, Yu, Jindan, primary, Thomas, Dafydd G., primary, Lin, Mu-Yen, primary, Vishnu, Prakash, primary, Wang, Zhuwen, primary, Wang, Rui, primary, Fielhauer, Jeff, primary, Ghosh, Debashis, primary, Giordano, Thomas J., primary, Giacherio, Donald, primary, Chang, Andrew C., primary, Orringer, Mark B., primary, El-Hefnawy, Talal, primary, Bigbee, William L., primary, Beer, David G., primary, and Chinnaiyan, Arul M., primary

Published
2023
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38. Data from Definition of a FoxA1 Cistrome That Is Crucial for G1 to S-Phase Cell-Cycle Transit in Castration-Resistant Prostate Cancer

Author

Zhang, Chunpeng, primary, Wang, Liguo, primary, Wu, Dayong, primary, Chen, Hongyan, primary, Chen, Zhong, primary, Thomas-Ahner, Jennifer M., primary, Zynger, Debra L., primary, Eeckhoute, Jérôme, primary, Yu, Jindan, primary, Luo, Jun, primary, Brown, Myles, primary, Clinton, Steven K., primary, Nephew, Kenneth P., primary, Huang, Tim H.-M., primary, Li, Wei, primary, and Wang, Qianben, primary

Published
2023
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39. The impact of exclusive enteral nutrition on the gut microbiome and bile acid metabolism in pediatric Crohn's disease

Author

Lv, Yao, primary, Lou, Yue, additional, Liu, Ana, additional, Cheng, Qi, additional, Yang, Gan, additional, Xu, Cuifang, additional, Luo, Youyou, additional, Lou, Jingan, additional, Yu, Jindan, additional, Fang, Youhong, additional, Zhao, Hong, additional, Peng, Kerong, additional, Ni, Yan, additional, and Chen, Jie, additional

Published
2023
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46. A Genome-Wide CRISPR Activation Screen Identifies PRRX2 as a Regulator of Enzalutamide Resistance in Prostate Cancer

Author

Rodríguez, Yara, primary, Unno, Kenji, additional, Truica, Mihai I., additional, Chalmers, Zachary R., additional, Yoo, Young A., additional, Vatapalli, Rajita, additional, Sagar, Vinay, additional, Yu, Jindan, additional, Lysy, Barbara, additional, Hussain, Maha, additional, Han, Huiying, additional, and Abdulkadir, Sarki A., additional

Published
2022
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47. Profiles and interactions of gut microbiome and intestinal microRNAs in pediatric Crohn's disease.

Author

Lv Y, Zhen C, Liu A, Hu Y, Yang G, Xu C, Lou Y, Cheng Q, Luo Y, Yu J, Fang Y, Zhao H, Peng K, Yu Y, Lou J, Chen J, and Ni Y

Subjects
Humans, Child, Male, Female, Adolescent, Feces microbiology, Dysbiosis genetics, Dysbiosis microbiology, Intestines microbiology, Bacteria genetics, Bacteria isolation & purification, Intestinal Mucosa microbiology, Intestinal Mucosa metabolism, MicroRNAs genetics, MicroRNAs metabolism, Crohn Disease microbiology, Crohn Disease genetics, Crohn Disease metabolism, Gastrointestinal Microbiome
Abstract

Gut dysbiosis is closely related to dysregulated microRNAs (miRNAs) in the intestinal epithelial cells, which plays an important role in the pathogenesis of Crohn's disease (CD). We investigated the relationship between fecal gut microbiome (GM) and intestinal tissue miRNAs in different stages of pediatric CD. Metagenomic analysis and miRNA sequencing were conducted to examine the GM and intestinal miRNA profiles of CD patients before and after clinical induction therapy and the controls. Twenty-seven newly diagnosed, therapy-naïve pediatric patients with active CD and 11 non-inflammatory bowel disease (IBD) controls were recruited in this study. Among CD patients, 11 patients completed induction treatment and reached clinical remission. Both GM and miRNA profiles were significantly changed between CD patients and controls. Seven key bacteria were identified at species level including Defluviitalea raffinosedens , Thermotalea metallivorans , Roseburia intestinalis , Dorea sp. AGR2135, Escherichia coli , Shigella sonnei , and Salmonella enterica , the exact proportions of which were further validated by real-time quantitative PCR analysis. Eight key miRNAs were also identified including hsa-miR-215-5p, hsa-miR-194-5p, hsa-miR-12135, hsa-miR-509-3-5p, hsa-miR-212-5p, hsa-miR-4448, hsa-miR-501-3p, and hsa-miR-503-5p. The functional enrichment analysis of differential miRNAs indicated the significantly altered cyclin protein, cyclin-dependent protein, and cell cycle pathway. The close interactions between seven key bacteria and eight key miRNAs were further investigated by miRNA target prediction. The association between specific miRNA expressions and key gut bacteria at different stages of CD supported their important roles as potential molecular biomarkers. Understanding the relationship between them will help us to explore the molecular mechanisms of CD., Importance: Since previous studies have focused on the change of the fecal gut microbiome and intestinal tissue miRNA in pediatric Crohn's disease (CD), the relationship between them in different stages is still not clear. This is the first study to explore the gut microbiota and miRNA and their correlations with the Pediatric Crohn's Disease Activity Index (PCDAI). Crohn's Disease Endoscopic Index of Severity (CDEIS), and calprotectin, by applying two omics approach in three different groups (active CD, CD in remission with exclusive enteral nutrition or infliximab induction therapy, and the healthy controls). Both gut microbiome structure and the miRNA profiles were significantly changed in the different stage of CD. Seven key gut microbiome at species and eight key miRNAs were found, and their close interactions were further fully investigated by miRNA target prediction., Competing Interests: The authors declare no conflict of interest.

Published
2024
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48. Myeloid differentiation factor-2/LY96, a new predictive biomarker of metastasis in prostate cancer: Clinical implications as a potential therapeutic target.

Author

Ferrari M, Wang L, Hoeppner L, Hahm E, Yu J, Kuzel T, and Mansini A

Abstract

Relapsed prostate cancer (CaP), usually treated with androgen deprivation therapy, acquires resistance to develop into lethal metastatic castration-resistant CaP. The cause of resistance remains elusive, and the lack of biomarkers predictive of castration-resistance emergence is a stumbling block in managing the disease. We provide strong evidence that Myeloid differentiation factor-2 (MD2) plays a critical role in metastasis and CaP progression. Analysis of tumor genomic data and IHC of tumors showed a high frequency of MD2 amplification and association with poor overall survival in patients. The Decipher-genomic test validated the potential of MD2 in predicting metastasis. In vitro studies demonstrated that MD2 confers invasiveness by activating MAPK and NF-kB signaling pathways. Furthermore, we show that metastatic cells release MD2 (sMD2). We measured serum-sMD2 in patients and found that the level is correlated to disease extent. We determined the significance of MD2 as a therapeutic target and found that targeting MD2 significantly inhibited metastasis in a murine model. We conclude that MD2 predicts metastatic behavior and serum-MD2 is a non-invasive biomarker for tumor burden, whereas MD2 presence on prostate biopsy predicts adverse disease outcome. We suggest MD2-targeted therapies could be developed as potential treatments for aggressive metastatic disease., Competing Interests: No conflict statement: All authors have approved this version. The authors declare no potential conflicts of interest.

Published
2023
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