Defining the Cancer Master Switch

Overview

Journal World J Surg

Publisher Wiley

Specialty General Surgery

Date 2011 Feb 3

PMID 21286716

Citations 1

Authors

Courtney J Balentine

David H Berger

Shi-He Liu

Changyi Chen

John Nemunaitis

F Charles Brunicardi

Affiliations

Soon will be listed here.

Abstract

Background: Recent research has focused on signaling cascades and their interactions yielding considerable insight into which genetic pathways are targeted and how they tend to be altered in tumors. Therapeutic interventions now can be designed based on the knowledge of pathways vital to tumor growth and survival. These critical targets for intervention, master switches for cancer, are termed so because the tumor attempts to "flip the switch" in a way that promotes its survival, whereas molecular therapy aims to "switch off" signals important for tumor-related processes.

Methods: Literature review.

Conclusions: Defining useful targets for therapy depends on identifying pathways that are crucial for tumor growth, survival, and metastasis. Because not all signaling cascades are created equal, selecting master switches or targets for intervention needs to be done in a systematic fashion. This discussion proposes a set of criteria to define what it means to be a cancer master switch and provides examples to illustrate their application.

Citing Articles

The role of Rhox homeobox factors in tumorigenesis.

MacLean 2nd J Front Biosci (Landmark Ed). 2013; 18(2):474-92.

PMID: 23276937 PMC: 7768896. DOI: 10.2741/4115.

References

Yarden Y, Sliwkowski M . Untangling the ErbB signalling network. Nat Rev Mol Cell Biol. 2001; 2(2):127-37. DOI: 10.1038/35052073. View

Sjoblom T, Jones S, Wood L, Parsons D, Lin J, Barber T . The consensus coding sequences of human breast and colorectal cancers. Science. 2006; 314(5797):268-74. DOI: 10.1126/science.1133427. View

Herbst R, Shin D . Monoclonal antibodies to target epidermal growth factor receptor-positive tumors: a new paradigm for cancer therapy. Cancer. 2002; 94(5):1593-611. DOI: 10.1002/cncr.10372. View

Suzuki H, Watkins D, Jair K, Schuebel K, Markowitz S, Chen W . Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer. Nat Genet. 2004; 36(4):417-22. DOI: 10.1038/ng1330. View

Wood L, Parsons D, Jones S, Lin J, Sjoblom T, Leary R . The genomic landscapes of human breast and colorectal cancers. Science. 2007; 318(5853):1108-13. DOI: 10.1126/science.1145720. View

Lee J, Kang M, Jang S, Qian T, Kim H, Kim C . Id-1 activates Akt-mediated Wnt signaling and p27(Kip1) phosphorylation through PTEN inhibition. Oncogene. 2008; 28(6):824-31. DOI: 10.1038/onc.2008.451. View

Marsh V, Winton D, Williams G, Dubois N, Trumpp A, Sansom O . Epithelial Pten is dispensable for intestinal homeostasis but suppresses adenoma development and progression after Apc mutation. Nat Genet. 2008; 40(12):1436-44. DOI: 10.1038/ng.256. View

Hussein S, Duff E, Sirard C . Smad4 and beta-catenin co-activators functionally interact with lymphoid-enhancing factor to regulate graded expression of Msx2. J Biol Chem. 2003; 278(49):48805-14. DOI: 10.1074/jbc.M305472200. View

Kinzler K, Vogelstein B . Lessons from hereditary colorectal cancer. Cell. 1996; 87(2):159-70. DOI: 10.1016/s0092-8674(00)81333-1. View

10.

Jonmarker S, Glaessgen A, Culp W, Pisa P, Lewensohn R, Ekman P . Expression of PDX-1 in prostate cancer, prostatic intraepithelial neoplasia and benign prostatic tissue. APMIS. 2008; 116(6):491-8. DOI: 10.1111/j.1600-0463.2008.01020.x. View

11.

Wang H, Maechler P, Ritz-Laser B, Hagenfeldt K, Ishihara H, Philippe J . Pdx1 level defines pancreatic gene expression pattern and cell lineage differentiation. J Biol Chem. 2001; 276(27):25279-86. DOI: 10.1074/jbc.M101233200. View

12.

Issa J . CpG island methylator phenotype in cancer. Nat Rev Cancer. 2004; 4(12):988-93. DOI: 10.1038/nrc1507. View

13.

Molenaar M, van de Wetering M, Oosterwegel M, Peterson-Maduro J, Godsave S, Korinek V . XTcf-3 transcription factor mediates beta-catenin-induced axis formation in Xenopus embryos. Cell. 1996; 86(3):391-9. DOI: 10.1016/s0092-8674(00)80112-9. View

14.

Moscatello D, Godwin A, Ramirez G, Gunn G, Zoltick P, Biegel J . Frequent expression of a mutant epidermal growth factor receptor in multiple human tumors. Cancer Res. 1995; 55(23):5536-9. View

15.

Clevers H . Wnt/beta-catenin signaling in development and disease. Cell. 2006; 127(3):469-80. DOI: 10.1016/j.cell.2006.10.018. View

16.

Delesque N, Buscail L, Esteve J, Saint-Laurent N, Muller C, Weckbecker G . sst2 somatostatin receptor expression reverses tumorigenicity of human pancreatic cancer cells. Cancer Res. 1997; 57(5):956-62. View

17.

Wheeler D, Srinivasan M, Egholm M, Shen Y, Chen L, McGuire A . The complete genome of an individual by massively parallel DNA sequencing. Nature. 2008; 452(7189):872-6. DOI: 10.1038/nature06884. View

18.

Nicholson R, Gee J, Harper M . EGFR and cancer prognosis. Eur J Cancer. 2001; 37 Suppl 4:S9-15. DOI: 10.1016/s0959-8049(01)00231-3. View

19.

Murtaugh L, Stanger B, Kwan K, Melton D . Notch signaling controls multiple steps of pancreatic differentiation. Proc Natl Acad Sci U S A. 2003; 100(25):14920-5. PMC: 299853. DOI: 10.1073/pnas.2436557100. View

20.

Miyatsuka T, Kaneto H, Shiraiwa T, Matsuoka T, Yamamoto K, Kato K . Persistent expression of PDX-1 in the pancreas causes acinar-to-ductal metaplasia through Stat3 activation. Genes Dev. 2006; 20(11):1435-40. PMC: 1475756. DOI: 10.1101/gad.1412806. View