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Turning up the heat on colorectal cancer

Nature Medicine volume 17, pages 1186–1188 (2011)Cite this article

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Mutations in the microsatellite of the chaperone heat shock protein 110 (HSP110) yield a mutant protein that counteracts oncogenic potential, enhances responsiveness to chemotherapy and associates with increased survival in individuals with colorectal cancers that arise through defective DNA mismatch repair (pages 1283–1289).

The advent of molecularly targeted therapy for individuals with cancer has been a spectacular achievement, a product of decades of work in unraveling the molecular basis of many tumors. Colorectal cancer (CRC), as one of the early successes of this effort, was arguably the first solid tumor in which molecularly distinct entities arising from completely unique pathogenic mechanisms—chromosomal or microsatellite instability (MSI)—were clearly characterized1. Surprisingly, we have not yet been able to fully exploit this understanding of CRC's molecular heterogeneity to develop robust prognostic biomarkers or treatment strategies tailored for these defined subtypes.

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Figure 1: Model for the interaction of HSP110 and HSP110ΔE9 in colorectal cancers.

Marina Corral

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Authors and Affiliations

  1. Andrew T. Chan is in the Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.,

    Andrew T Chan

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  1. Andrew T Chan
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Correspondence to Andrew T Chan.

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Competing interests

A.T.C. has served as a consult to Bayer HealthCare and Millennium Pharmaceuticals.

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Chan, A. Turning up the heat on colorectal cancer. Nat Med 17, 1186–1188 (2011). https://doi.org/10.1038/nm.2500

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