S-Y Cheng

Northwestern University

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Mark C. Willingham

University College London

Zhu Xg

National Cancer Institute

Bo Hu

Henan University

Lin Zhao

China Medical University

Wenlong Chang

Shenyang Agricultural University

Cheng Lü

Wenzhou Medical University

Jann N. Sarkaria

Mayo Clinic

A-M Zou

Air Force Medical University

W. C. Liu

National Cheng Kung University

Haizhong Feng

Harbin Medical University

Cooperative Institutions

Air Force Medical University

National Cheng Kung University

National Cancer Institute

Center for Cancer Research

University of Rochester Medical Center

Northwestern University

China Medical University

Chinese Academy of Medical Sciences & Peking Union Medical College

Shanghai Jiao Tong University

National Institutes of Health

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PTEN deficiency accelerates tumour progression in a mouse model of thyroid cancer

Oncogene (2008)

Céline J. Guigon Lin Zhao Mark C. Willingham S-Y Cheng

Tensin

Follicular thyroid cancer

10.1038/onc.2008.407

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Citations (95)

Activation of tumor cell proliferation by thyroid hormone in a mouse model of follicular thyroid carcinoma

Oncogene (2011)

Cheng Lü X Zhu Mark C. Willingham S-Y Cheng

Follicular cell

Follicular carcinoma

10.1038/onc.2011.390

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Citations (20)

EGFRvIII stimulates glioma growth and invasion through PKA-dependent serine phosphorylation of Dock180

Oncogene (2013)

Haizhong Feng Bo Hu Kristiina Vuori Jann N. Sarkaria Frank B. Furnari

10.1038/onc.2013.198

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Citations (71)

Modeling Thyroid Cancer in the Mouse

Hormone and Metabolic Research (2009)

Zhu Xg S-Y Cheng

Thyroid carcinomas, the most common endocrine tumors in humans, have an increasing incidence in the U.S. and worldwide. There are four major types of thyroid cancers: papillary, follicular, anaplastic, and medullary carcinomas. In recent years, significant progress has been made in the identification of genetic alterations in thyroid carcinomas, particularly, papillary and medullary thyroid cancers. Mouse models of thyroid cancer are valuable tools in elucidating molecular genetic changes underlying thyroid carcinogenesis and in identifying potential molecular targets for therapeutic intervention. Representative mouse models of papillary, follicular, and medullary carcinomas are reviewed here with particular emphasis on those for follicular thyroid carcinomas. Challenges for further development in the modeling of thyroid cancer will also be discussed.

Medullary Thyroid Cancer

Follicular cell

Medullary carcinoma

10.1055/s-0029-1215572

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Citations (12)

The steroid receptor coactivator-3 is a tumor promoter in a mouse model of thyroid cancer

Oncogene (2007)

Hao Ying Mark C. Willingham S-Y Cheng

Thyroid hormone receptor

Follicular thyroid cancer

Tumor progression

10.1038/sj.onc.1210680

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Citations (31)

Overexpression of VEGF121, but not VEGF165 or FGF-1, improves oxygenation in MCF-7 breast tumours

British Journal of Cancer (2004)

Bruce M. Fenton Scott F. Paoni W Liu S-Y Cheng Bo Hu

Vascular endothelial growth factor (VEGF) is an intensively studied molecule that has significant potential, both in stimulating angiogenesis and as a target for antiangiogenic approaches. We utilised MCF-7 breast cancer cells transfected with either of two of the major VEGF isoforms, VEGF121 or VEGF165, or fibroblast growth factor-1 (FGF-1) to distinguish the effects of these factors on tumour growth, vascular function, and oxygen delivery. While each transfectant demonstrated substantially increased tumorigenicity and growth rate compared to vector controls, only VEGF121 produced a combination of significantly reduced total and perfused vessel spacing, as well as a corresponding reduction in overall tumour hypoxia. Such pathophysiological effects are of potential importance, since antiangiogenic agents designed to block VEGF isoforms could in turn result in the development of therapeutically unfavourable environments. If antiangiogenic agents are also combined with conventional therapies such as irradiation or chemotherapy, microregional deficiencies in oxygenation could play a key role in ultimate therapeutic success.

MCF-7

Hypoxia

10.1038/sj.bjc.6601539

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Citations (14)

Investigation of InGaP/GaAs double-delta-doped heterojunction bipolar transistor

Semiconductor Science and Technology (1998)

W-C Wang S-Y Cheng Wenlong Chang H-J Pan Y.S. Shie

The double-delta-doped heterojunction bipolar transistor is successfully fabricated with improved current-voltage characteristics by employing the insertion of delta-doped sheets at emitter-base (E-B) and base-collector (B-C) heterojunction. Because of the use of delta-doped sheets, the potential spikes at E-B and B-C heterojunction are suppressed substantially. Thus a higher emitter injection efficiency (current gain) and a lower knee voltage are obtained. From experimental results, it is shown that the studied device is a good candidate for high-speed and high-power circuit applications.

Heterostructure-emitter bipolar transistor

Heterojunction bipolar transistor

10.1088/0268-1242/13/6/015

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Citations (9)

Silencing Livin gene expression to inhibit proliferation and enhance chemosensitivity in tumor cells

Cancer Gene Therapy (2008)

Rongquan Wang Lin Fang Xiuchao Wang Peng Gao Ke Dong

10.1038/cgt.2008.16

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Citations (38)

Thyroid hormone receptors are tumor suppressors in a mouse model of metastatic follicular thyroid carcinoma