Printzlau and Andersen, 2004).

The prevalence of PRS is the

same in both sexes (Printzlau and Andersen, 2004).
Some factors point to a genetic etiology of PRS. Patients
with PRS often have other family members with cleft lip or
palate (13.0%27.7%) (Bixler and Christian, 1971; Williams
et al., 1981; Marques et al., 1998; Holder-Espinasse et al.,
2001), and PRS is often present in other syndromes such as
Stickler syndrome, Velocardiofacial syndrome, Marshall syndrome,
Treacher Collins syndrome, Catel-Mancke syndrome,
Kabuki syndrome, Nager syndrome, teratogene syndromes,
and many more (Sheffield et al., 1987; Shprintzen, 1988;
Marques et al., 1998; Cohen, 1999; Holder-Espinasse et al.,
2001). The most common (12.0%16.3%) underlying syndrome
is Stickler syndrome (Sheffield et al., 1987; Marques et
al., 1998; Printzlau and Andersen, 2004). When PRS is not
associated with other malformations, it is referred to as nonsyndromic
PRS.
To be able to identify candidate genes for PRS, a search of
Medline, the Mendelian Cytogenetics Network database
(MCNdb), and two reviews of the Human Cytogenetics Database
(HCDB) (Brewer et al., 1998, 1999) was performed.
SEARCHING FOR PRS GENES
Examining CL/P subgroups may provide us with knowledge
that can be extended to the general CL/P population. An example
is Zucchero et al. (2004), who found the IRF6 gene
causing Van der Woude syndrome. Subsequently, they tested
for linkage and transmission disequilibrium in a total of 1968
CL/P families and found that a polymorphism in IRF6 is responsible
for 12% of the genetic contribution in CL/P.
Searching Medline (http://www4.ncbi