Biomedical Engineering Reference
In-Depth Information
[50]
Munzenmaier, A. et al., A secreted/shed product of H. pylori activates transcription
factor NF-κB, J. Immunol ., 159, 6140, 1997.
[51]
Ishihara, S. et al., Essential role of MD2 in TLR4-dependent signaling during H.
pylori -associated gastritis, J. Immunol ., 173, 1406, 2004.
[52]
Viala, J. et al., Nod1 responds to peptidoglycan delivery by H. pylori cag pathoge-
nicity island, Nat. Immunol ., 5, 1166, 2004.
[53]
Mokdad, A.H. et al., Prevalence of obesity, diabetes, and obesity-related health risk
factors, JAMA, 289, 76, 2003.
[54]
Hotamisligil, G.S., Inflammatory pathways and insulin action, Int. J. Obes. Relat.
Metab. Disord., 27, S53, 2003.
[55]
Hanahan, D. and Weinberg, R., The hallmarks of cancer, Cell, 100, 57, 2000.
[56]
Campbell, P.M. and Der, C.J., Oncogenic Ras and its role in tumor cell invasion and
metastasis, Semin. Cancer Biol ., 14, 105, 2004.
[57]
Evan, G. and Vousden, K., Proliferation, cell cycle and apoptosis in cancer, Nature,
411, 342, 2001.
[58]
Shay, J.W. and Bacchetti, S., A survey of telomerase activity in human cancer, Eur.
J. Cancer, 33, 787, 1997.
[59]
Johnsen, M. et al., Cancer invasion and tissue remodeling: Common themes in
proteolytic matrix degradation, Curr. Opin. Cell Biol ., 10, 667, 1998.
[60]
Hay, E.D., An overview of epithelio-mesenchymal transformation, Acta Anat ., 154,
8, 1995.
[61]
Thiery, J.P., Epithelial-mesenchymal transitions in tumor progression, Nat. Rev. Can-
cer, 2, 442, 2003.
[62]
Coussens, L. and Werb, Z., Inflammation and cancer, Nature, 420, 860, 2002.
[63]
Turini, M.E. and Dubois, R.N., Cyclooxygenase-2: A therapeutic target, Ann. Rev.
Med ., 53, 35, 2002.
[64]
Greten, F.R. et al., IKKβ links inflammation and tumorigenesis in a mouse model of
colitis-associated cancer, Cell, 118, 285, 2004.
[65]
Pikarsky, E. et al., NF-κB functions as a tumor promoter in inflammation-associated
cancer, Nature, 353, 180, 2004.
[66]
Clevers, H., At the crossroads of inflammation and cancer, Cell, 118, 671, 2004.
[67]
Rutter, M. et al., Severity of inflammation is a risk for colorectal neoplasia in
ulcerative colitis, Gastroenterology, 126, 451, 2004.
[68]
Bissell, M. and Radisky, D., Putting tumors in context, Nat. Rev. Cancer, 1, 46, 2001.
[69]
Balkwill, F., Charles, K., and Mantovani, A., Smoldering and polarized inflammation
in the initiation and promotion of malignant disease, Cancer Cell, 7, 211, 2005.
[70]
Sparmann, A. and Bar-Sagi, D., Ras-induced IL-8 expression plays a critical role in
tumor growth and angiogenesis, Cancer Cell, 6, 447, 2004.
[71]
Alcamo et al., Targeted mutation of the TNF receptor 1 rescues the RelA-deficient
mouse and reveals a critical role for NF-κB in leukocyte recruitment, J. Immunol .,
167, 1592, 2001.
[72]
Grigoriadis, G. et al., The Rel subunit of NF-κB-like transcription factors is a positive
and negative regulator of macrophage gene expression: Distinct roles for Rel in
different macrophage populations, Embo J ., 15, 7099, 1996.
[73]
Grossmann, M. et al., The combined absence of the transcription factor Rel and RelA
leads to multiple hemopoietic cell defects, Proc. Nat. Acad. Sci. USA, 96, 11848,
1999.
[74]
Lawrence, T. et al., Possible new role for NF-κB in the resolution of inflammation,
Nat. Med ., 7, 1291, 2001.
 
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