Caenorhabditis elegans is a small (1 to 1.

5 mm), free-living nematode that thrives in many parts

of the world feeding on microorganisms primarily bacteria (Gershon and Gershon, 2002; Wood,
1998). C. elegans was the first metazoan that had its genome sequenced which made it easy to
manipulate and use as a model organism (Hengartner and Kalleta, 2006; Kirienko et al., 2010).
There are several characteristics present in C. elegans that made it a viable model for cancer
research. First, phenotypes that damage normal proliferation and patterning can be assessed
because the worm has completely characterized and essentially invariant somatic cell lineage
(Sulston and Horvitz, 1977; Sulston et al., 1983). Second, the transparency of C. elegans
throughout its stages of development enables direct visualization of all cells, including their
divisions and movements, with the use of fluorescence markers (Hengartner and Kalleta, 2006).
Third, comprehensive analysis of genetic pathways and protein functions are feasible because C.
elegans has an established forward and reverse genetics (Kirienko et al., 2010). Lastly, biological
processes including apoptosis, cell signaling, cell cycle, cell polarity, metabolism and aging are
conserved between C. elegans and mammals and C. elegans homologous gene have been
determined for 60–80% of human genes (Harris et al., 2004).
In humans, ras activation is closely linked to 33% of cancers, making it one of the most frequent
oncogenic mutations (Karnoub and Weinberg, 2008). In C. elegans, the Ras protein is encoded
by the let-60 gene, which regulates formation of vulva, which worms use to lay eggs (Beitel et al.,
1990). The wild-type strains of C. elegans develop only a single vulva, but loss-of-function (lf)
mutations in the gene results in an organism with no vulva, known as Vulvaless or Vul phenotype,
while the gain-of-function (gf) generate extra vulval tissue, which is also called Multivulva or Muv
phenotype (Han et al., 1990). The let-60(n1046gf) allele in C. elegans that produces a LET-60
protein with the mutation Glycerine-13 to Glutamine-13, mimics the mutation present in Ras
tumors in human cancer cells (Hara and Han, 1995).

References:
Gershon H, Gershon D. Caenorhabditis elegans--A paradigm for aging research: Advantages and
limitations. Mech Ageing Develop. 2002;123:261–274.
Harris TW, Chen N, Cunningham F, Tello-Ruiz M, Antoshechkin I, Bastiani C, Bieri T, Blasiar D,
Bradnam K, Chan J. et al. WormBase: a multi-species resource for nematode biology and
genomics. Nucleic Acids Res 2004; 32:D411-7; PMID:14681445;
http://dx.doi.org/10.1093/nar/gkh066
Kirienko, N. V., Mani, K., & Fay, D. S. (2010). Cancer models inCaenorhabditis
elegans. Developmental Dynamics. doi:10.1002/dvdy.22247
Wood WB. The Nematode Caenorhabditis elegans. Cold Spring Harbor Laboratory Press;
Plainview, NY: 1988.