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Hidalgo reports receiving grant support from Roche and Daichi; being the principal investigator and receiving grant support for clinical studies of nanoparticle albumin-bound paclitaxel from American Biosciences, of erlotinib from Roche, of AGS-1C4D4 from Agensys, and of MORAb-009 from Eisai; and receiving consulting fees from American Biosciences, OSI–Genentech, Merck, and Agensys. No other potential conflict of interest relevant to this article was reported. This article (10.1056/NEJMra0901557) was updated on July 14, 2010, at NEJM.org. I thank Wells Messersmith and Anirban Maitra for critical comments on an earlier version of the manuscript and Sofia Perea for editorial assistance.

Figure 1 Components of Pancreatic Cancer. Pancreatic cancers are composed of several distinct elements, including pancreatic-cancer cells, pancreatic-cancer stem cells, and the tumor stroma. A recent analysis of 24 pancreatic cancers suggested that the mature pancreatic-cancer cell carries on average 63 genetic alterations per cancer; these alterations can be grouped in 12 core signaling pathways. These results, if confirmed in larger studies, would indicate that pancreatic cancer is genetically very complex and heterogeneous. Thus, effective treatments will probably need to attack several targets (with combination regimens) and may require individualized therapy. A small group of cells (≤5%) appear to have cancer stem-cell features that render them capable of asymmetric division, enabling them to generate mature cells as well as cancer stem cells.

These stem cells may be identified by the expression of specific membrane markers and can regenerate into full tumors on implantation in immunodeficient animals. Pancreatic-cancer stem cells are resistant to conventional treatment, but they have alterations in developmental pathways such as Notch, hedgehog, and wingless in drosophila (Wnt)–β-catenin that may result in new therapeutic targets.