Abstract
This review describes the recent advances in the molecular events involved in pancreatic cancer initiation, progression, and metastasis. Additionally, the importance of deregulated cellular signaling elements as potential targets for developing novel therapeutic strategies against incurable forms of pancreatic cancer is reported. The emphasis is on the critical functions gained by numerous growth factors and their receptors, such as epidermal growth factor receptor, hedgehog signaling, and proangiogenic agents such as vascular endothelial factor and interleukin-8 for the sustained growth, survival, and metastasis of pancreatic cancer cells. The molecular mechanisms associated with antitumoral properties and the clinical benefits of gemcitabine alone or in combination with other cytotoxic agents for the treatment of pancreatic cancer are discussed.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Apoptosis
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Biomarkers, Tumor / analysis
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Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
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Deoxycytidine / analogs & derivatives
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Deoxycytidine / therapeutic use
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ErbB Receptors / antagonists & inhibitors
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ErbB Receptors / physiology
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Gemcitabine
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Gene Expression Profiling
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Hedgehog Proteins
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Humans
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Mucin-1 / physiology
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Mucin-4
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Mucins / physiology
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NF-kappa B / physiology
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Pancreatic Neoplasms / diagnosis
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Pancreatic Neoplasms / etiology*
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Pancreatic Neoplasms / genetics
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Pancreatic Neoplasms / therapy*
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Phosphatidylinositol 3-Kinases / physiology
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Proto-Oncogene Proteins c-akt / physiology
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Receptors, Notch / physiology
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Signal Transduction
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Trans-Activators / physiology
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Wnt Proteins / physiology
Substances
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Biomarkers, Tumor
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Hedgehog Proteins
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MUC4 protein, human
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Mucin-1
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Mucin-4
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Mucins
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NF-kappa B
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Receptors, Notch
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Trans-Activators
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Wnt Proteins
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Deoxycytidine
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Phosphatidylinositol 3-Kinases
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ErbB Receptors
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Proto-Oncogene Proteins c-akt
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Cyclic AMP-Dependent Protein Kinases
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Gemcitabine