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11. Oral Pathobiont Activates Anti-Apoptotic Pathway, Promoting both Immune Suppression and Oncogenic Cell Proliferation

Author

Arjunan, Pachiappan, Meghil, Mohamed M., Pi, Wenhu, Xu, Jinxian, Lang, Liwei, El-Awady, Ahmed, Sullivan, William, Rajendran, Mythilypriya, Rabelo, Mariana Sousa, Wang, Tong, Tawfik, Omnia K., Kunde-Ramamoorthy, Govindarajan, Singh, Nagendra, Muthusamy, Thangaraju, Susin, Cristiano, Teng, Yong, Arce, Roger M., and Cutler, Christopher W.

Published
2018
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16. Genetic Variations in the Transforming Growth Factor-β1 Pathway May Improve Predictive Power for Overall Survival in Non-small Cell Lung Cancer

Author

Pi Wenhu, Weili Wang, J.Y. Jin, Fengchong Kong, Hong Zhang, Monica Cheng, Li Yang, Feng-Ming Spring Kong, Tim Lautenschlaeger, Colleen DesRosiers, Nan Bi, and Shruti Jolly

Subjects
0301 basic medicine, Oncology, Cancer Research, medicine.medical_specialty, medicine.medical_treatment, overall survival, Single-nucleotide polymorphism, single nuclear polymorphism, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, TGF-β1, medicine, SNP, Stage (cooking), Lung cancer, non-small cell lung cancer, RC254-282, Original Research, business.industry, Proportional hazards model, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, Radiation therapy, Clinical trial, 030104 developmental biology, machine learning, Tumor progression, 030220 oncology & carcinogenesis, business
Abstract

Purpose:Transforming growth factor-β1 (TGF-β1), a known immune suppressor, plays an important role in tumor progression and overall survival (OS) in many types of cancers. We hypothesized that genetic variations of single nucleotide polymorphisms (SNPs) in the TGF-β1 pathway can predict survival in patients with non-small cell lung cancer (NSCLC) after radiation therapy.Materials and Methods:Fourteen functional SNPs in the TGF-β1 pathway were measured in 166 patients with NSCLC enrolled in a multi-center clinical trial. Clinical factors, including age, gender, ethnicity, smoking status, stage group, histology, Karnofsky Performance Status, equivalent dose at 2 Gy fractions (EQD2), and the use of chemotherapy, were first tested under the univariate Cox's proportional hazards model. All significant clinical predictors were combined as a group of predictors named “Clinical.” The significant SNPs under the Cox proportional hazards model were combined as a group of predictors named “SNP.” The predictive powers of models using Clinical and Clinical + SNP were compared with the cross-validation concordance index (C-index) of random forest models.Results:Age, gender, stage group, smoking, histology, and EQD2 were identified as significant clinical predictors: Clinical. Among 14 SNPs, BMP2:rs235756 (HR = 0.63; 95% CI:0.42–0.93;p= 0.022), SMAD9:rs7333607 (HR = 2.79; 95% CI 1.22–6.41;p= 0.015), SMAD3:rs12102171 (HR = 0.68; 95% CI: 0.46–1.00;p= 0.050), and SMAD4: rs12456284 (HR = 0.63; 95% CI: 0.43–0.92;p= 0.016) were identified as powerful predictors of SNP. After adding SNP, the C-index of the model increased from 84.1 to 87.6% at 24 months and from 79.4 to 84.4% at 36 months.Conclusion:Genetic variations in the TGF-β1 pathway have the potential to improve the prediction accuracy for OS in patients with NSCLC.

Published
2021
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17. Genetic Variations in the Transforming Growth Factor-β1 Pathway May Improve Predictive Power for Overall Survival in Non-small Cell Lung Cancer

Author

Zhang, Hong, primary, Wang, Weili, additional, Pi, Wenhu, additional, Bi, Nan, additional, DesRosiers, Colleen, additional, Kong, Fengchong, additional, Cheng, Monica, additional, Yang, Li, additional, Lautenschlaeger, Tim, additional, Jolly, Shruti, additional, Jin, Jianyue, additional, and Kong, Feng-Ming (Spring), additional

Published
2021
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24. The effect of thoracic radiation on overall survival and their association with systemic immune therapy in stage IV NSCLC: Findings from the National Cancer Database.

Author

Kong, Feng-Ming Spring, primary, Wang, Weili, additional, Durm, Gerg, additional, Wan, Jun, additional, Jin, Jianyue, additional, Pi, Wenhu, additional, Hu, Chen, additional, Langer, Mark P, additional, Lautenschlaeger, Tim, additional, Paczesny, Sophie, additional, Birdas, Thomas J, additional, and Hanna, Nasser H., additional

Published
2018
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26. Hydroxyurea differentially modulates activator and repressors of γ-globin gene in erythroblasts of responsive and non-responsive patients with sickle cell disease in correlation with Index of Hydroxyurea Responsiveness

Author

Zhu, Xingguo, primary, Hu, Tianxiang, additional, Ho, Meng Hsuan, additional, Wang, Yongchao, additional, Yu, Miao, additional, Patel, Niren, additional, Pi, Wenhu, additional, Choi, Jeong-Hyeon, additional, Xu, Hongyan, additional, Ganapathy, Vadivel, additional, Kutlar, Ferdane, additional, Kutlar, Abdullah, additional, and Tuan, Dorothy, additional

Published
2017
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27. Principal component analysis identifies patterns of cytokine expression in non-small cell lung cancer patients undergoing definitive radiation therapy

Author

Ellsworth, Susannah G., primary, Rabatic, Bryan M., additional, Chen, Jie, additional, Zhao, Jing, additional, Campbell, Jeffrey, additional, Wang, Weili, additional, Pi, Wenhu, additional, Stanton, Paul, additional, Matuszak, Martha, additional, Jolly, Shruti, additional, Miller, Amy, additional, and Kong, Feng-Ming, additional

Published
2017
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30. Stereotactic body radiation therapy to generate comparable survival to surgery in treating hepatocellular carcinoma (HCC): Results of 756 patients.

Author

Kong, Feng Ming, primary, Zang, Yong, additional, Pi, Wenhu, additional, Long, David, additional, Ellsworth, Susannah, additional, Saito, Naoyuki, additional, Ghabril, Marwan, additional, Lacerda, Marco A, additional, Agarwal, David M, additional, O’Neil, Bert, additional, Tann, Mark, additional, Zellars, Richard C., additional, and Maluccio, Mary A., additional

Published
2017
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36. IL-7 signaling imparts polyfunctionality and stemness potential to CD4+ T cells

Author

Ding, Zhi-Chun, primary, Liu, Chufeng, additional, Cao, Yang, additional, Habtetsion, Tsadik, additional, Kuczma, Michal, additional, Pi, Wenhu, additional, Kong, Heng, additional, Cacan, Ercan, additional, Greer, Susanna F., additional, Cui, Yan, additional, Blazar, Bruce R., additional, Munn, David H., additional, and Zhou, Gang, additional

Published
2016
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37. UFBP1, a Key Component of the Ufm1 Conjugation System, Is Essential for Ufmylation-Mediated Regulation of Erythroid Development

Author

Cai, Yafei, primary, Pi, Wenhu, additional, Sivaprakasam, Satish, additional, Zhu, Xiaobin, additional, Zhang, Mingsheng, additional, Chen, Jijun, additional, Makala, Levi, additional, Lu, Chunwan, additional, Wu, Jianchu, additional, Teng, Yong, additional, Pace, Betty, additional, Tuan, Dorothy, additional, Singh, Nagendra, additional, and Li, Honglin, additional

Published
2015
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46. Stable and unstable transgene integration sites in the human genome: extinction of the Green Fluorescent Protein transgene in K562 cells

Author

Migliaccio, Anna Rita, primary, Bengra, Chikh, additional, Ling, Jianhua, additional, Pi, Wenhu, additional, Li, Chunhua, additional, Zeng, Shan, additional, Keskintepe, Meral, additional, Whitney, Barry, additional, Sanchez, Massimo, additional, Migliaccio, Giovanni, additional, and Tuan, Dorothy, additional

Published
2000
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47. Principal component analysis identifies patterns of cytokine expression in non-small cell lung cancer patients undergoing definitive radiation therapy

Author

Stanton, Paul, Ellsworth, Susannah G., Jolly, Shruti, Pi, Wenhu, Wang, Weili, Miller, Amy, Matuszak, Martha, Chen, Jie, Campbell, Jeffrey, Zhao, Jing, Kong, Feng-Ming, and Rabatic, Bryan M.

Subjects
3. Good health
Abstract

Radiation treatment (RT) stimulates the release of many immunohumoral factors, complicating the identification of clinically significant cytokine expression patterns. This study used principal component analysis (PCA) to analyze cytokines in non-small cell lung cancer (NSCLC) patients undergoing RT and explore differences in changes after hypofractionated stereotactic body radiation therapy (SBRT) and conventionally fractionated RT (CFRT) without or with chemotherapy.

48. IL-7 signaling imparts polyfunctionality and stemness potential to CD4+T cells

Author

Ding, Zhi-Chun, Liu, Chufeng, Cao, Yang, Habtetsion, Tsadik, Kuczma, Michal, Pi, Wenhu, Kong, Heng, Cacan, Ercan, Greer, Susanna F., Cui, Yan, Blazar, Bruce R., Munn, David H., and Zhou, Gang

Abstract

ABSTRACTThe functional status of CD4+T cells is a critical determinant of antitumor immunity. Polyfunctional CD4+T cells possess the ability to concomitantly produce multiple Th1-type cytokines, exhibiting a functional attribute desirable for cancer immunotherapy. However, the mechanisms by which these cells are induced are neither defined nor it is clear if these cells can be used therapeutically to treat cancer. Here, we report that CD4+T cells exposed to exogenous IL-7 during antigenic stimulation can acquire a polyfunctional phenotype, characterized by their ability to simultaneously express IFNγ, IL-2, TNFα and granzyme B. This IL-7-driven polyfunctional phenotype was associated with increased histone acetylation in the promoters of the effector genes, indicative of increased chromatin accessibility. Moreover, forced expression of a constitutively active (CA) form of STAT5 recapitulated IL-7 in inducing CD4+T-cell polyfunctionality. Conversely, the expression of a dominant negative (DN) form of STAT5 abolished the ability of IL-7 to induce polyfunctional CD4+T cells. These in-vitro-generated polyfunctional CD4+T cells can traffic to tumor and expand intratumorally in response to immunization. Importantly, adoptive transfer of polyfunctional CD4+T cells following lymphodepletive chemotherapy was able to eradicate large established tumors. This beneficial outcome was associated with the occurrence of antigen epitope spreading, activation of the endogenous CD8+T cells and persistence of donor CD4+T cells exhibiting memory stem cell attributes. These findings indicate that IL-7 signaling can impart polyfunctionality and stemness potential to CD4+T cells, revealing a previously unknown property of IL-7 that can be exploited in adoptive T-cell immunotherapy.

Published
2016
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49. A Facilitated Tracking and Transcription Mechanism of the HS2 Enhancer in the ß-Globin Locus Control Region.

Author

Tuan, Dorothy, Zhu, Xingguo, Ling, Jianhua, Zhang, Ling, Pi, Wenhu, and Wu, Min

Abstract

The 100 kb human ß-globin gene locus contains the embryonic e-, the fetal G?- and A?-, and the adult d- and ß-globin genes arranged in the transcriptional order of 5' e-G?-A?-d-ß 3'. The ß-globin Locus Control Region (LCR), defined by DNase I hypersensitive sites HS1, 2, 3, 4 and 5 located far upstream of the globin genes, is absolutely required for transcriptional activation of the globin genes in erythroid cells. The HS2 site, located respectively 11 and 55 kb upstream of the e- and ß-globin genes, possesses prominent enhancer activity and is able to activate transcription of the globin genes over the long distance. How the HS2 enhancer acts over the long distance is not fully understood. Three mechanisms have been proposed to explain long-range enhancer function: The looping model, the protein tracking/linking model and the facilitated tracking model. We have shown earlier that a transcription mechanism of the RNA polymerase II (pol II)-complex assembled by the HS2 enhancer mediates long-range HS2 enhancer function. In the present study, we used the chicken HS4 insulator to further study the mechanism of long-range HS2 enhancer function. We created the LCR(+I) and LCR(-I) lines in human erythroid K562 cells using Cre-loxP mediated in situ recombination and in zebrafish. The integrated LCR(+I) and LCR(-I) plasmids spanned the natural 11 kb human e-globin gene locus either with or without the chicken HS4 insulator inserted between the LCR HS2 enhancer and the e-globin promoter. Analysis of enhancer function in the integrated plasmids and the endogenous e-globin gene locus provided evidence for a novel facilitated tracking and transcription mechanism of long-range enhancer function: The HS2 enhancer complex containing both the enhancer DNA and the associated pol II tracked and transcribed through the 10 kb intervening DNA to loop with and activate the e-globin promoter. The interposed insulator interrupted this facilitated tracking and transcription mechanism of the enhancer complex through the intervening DNA, thereby blocking long-range enhancer function.

Published
2006
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50. IGF2BP3 Triggers STAT3 Pathway by Stabilizing SRC RNA in an m6A-Dependent Manner to Promote Lymphatic Metastasis in LUAD.

Author

Ding J, Wang X, Yang H, Zhang L, Ying Y, Pi W, Deng G, and Zhu Y

Abstract

Lymph node metastasis significantly affects the NSCLC patients' staging, treatment strategy, and prognosis. Studies have shown that IGF2BP3, an oncofetal protein and an m6A reader, overexpresses and correlates to lymph node metastasis and worse overall survival in histopathological studies including NSCLC, but its mechanism needs further study. This study explored IGF2BP3's function and mechanism in LUAD lymphatic metastasis using public databases, a human LUAD tissue microarray, human LUAD cells, and a lymphatic metastasis model in male BALB/c nude mice. Firstly, we proved that IGF2BP3 overexpression was positively correlated to patients' lymph node metastasis and worse overall survival in bioinformatics and a human LUAD tissue microarray analysis. IGF2BP3 was knocked out or overexpressed in human LUAD cell lines. Functionally, IGF2BP3 facilitated NCI-H1299, NCI-H358, and A549 cell growth, migration, invasion, and EMT in vitro, and promoted tumorigenesis, lymphangiogenesis, and lymphatic metastasis of NCI-H1299 cells in BALB/c nude mice. Mechanically, RIP, RNA pull-down assay, MeRIP, mRNA stability assays, rescue experiments, and immunohistochemical assays were conducted. IGF2BP3 was demonstrated to bind to the m6A site of the 3'UTR region of SRC, stabilizing its mRNA and activating the downstream STAT3 signaling pathway and lymphatic growth factors such as VEGF-C, therefore affecting lymphatic metastasis. The cell migration and EMT function of IGF2BP3 were partially rescued by utilizing SRC siRNA or AZD0530, an SRC inhibitor. This study demonstrated that IGF2BP3 promotes lymphatic metastasis in LUAD via activating the m6A-SRC-STAT3-VEGFC signaling axis, indicating that IGF2BP3 is a potential therapeutic target to overcome metastasis in LUAD patients., (© 2025 The Author(s). Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.)

Published
2025
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