The Hallmarks of Cancer

We suggest that research over the past decades has revealed a small number of molecular, biochemical, and cellular traits—acquired capabilities—shared by most and perhaps all types of human cancer

Douglas Hanahan

2004

Scholarcy highlights

  • We foresee cancer research developing into a logical science, where the complexities of the disease, described in the laboratory and clinic, will become understandable in terms of a small number of underlying principles
  • We suggest that research over the past decades has revealed a small number of molecular, biochemical, and cellular traits—acquired capabilities—shared by most and perhaps all types of human cancer
  • Several lines of evidence indicate that tumorigenesis in humans is a multistep process and that these steps reflect genetic alterations that drive the progressive transformation of normal human cells into highly malignant derivatives
  • How many distinct regulatory circuits within each type of target cell must be disrupted in order for such a cell to become cancerous? Does the same set of cellular regulatory circuits suffer disruption in the cells of the disparate neoplasms arising in the human body? Which of these circuits operate on a cell-autonomous basis, and which are coupled to the signals that cells receive from their surrounding microenvironment within a tissue? Can the large and diverse collection of cancerassociated genes be tied to the operations of a small group of regulatory circuits?
  • We suggest that the vast catalog of cancer cell genotypes is a manifestation of six essential alterations in cell physiology that collectively dictate malignant growth: self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evasion of programmed cell death, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis
  • Attempts at explaining the cell biological effects of integrins in terms of a small number of mechanistic rules have been confounded by the large number of distinct integrin genes, by the even larger number of heterodimeric receptors resulting from combinatorial expression of various ␣ and ␤ receptor subunits, and by the increasing evidence of complex signals emitted by the cytoplasmic domains of these receptors
  • Cancers do appear at substantial frequency in the human population, causing some to argue that the genomes of tumor cells must acquire increased mutability in order for the process of tumor progression to reach completion in several decades time

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