\name{allFitnessEffects}
\alias{allFitnessEffects}
\title{Create fitness effects specification from restrictions,
epistasis, and order effects.
}
\description{
Given one or more of a set of poset restrictions, epistatic
interactions, order effects, and genes without interactions, as well
as, optionally, a mapping of genes to modules, return the complete
fitness specification.
The output of this function is not intended for user consumption, but
as a way of preparing data to be sent to the C++ code. }
\usage{
allFitnessEffects(rT = NULL, epistasis = NULL, orderEffects = NULL,
noIntGenes = NULL, geneToModule = NULL, drvNames = NULL, keepInput =
TRUE) }
\arguments{
\item{rT}{A restriction table that is an extended version of a poset
(see \code{\link{poset}} ).
A restriction table is a data frame where each row shows one edge
between a parent and a child. A restriction table contains exactly these
columns, in this order:
\describe{
\item{parent}{The identifiers of the parent nodes, in a
parent-child relationship. There must be at least on entry with the
name "Root".}
\item{child}{The identifiers of the child nodes.}
\item{s}{A numeric vector with the fitness effect that applies
if the relationship is satisfied.}
\item{sh}{A numeric vector with the fitness effect that applies if
the relationship is not satisfied. This provides a way of
explicitly modeling deviatons from the restrictions in the graph,
and is discussed in Diaz-Uriarte, 2015. }
\item{typeDep}{The type of dependency. Three possible types of
relationship exist:
\describe{
\item{AND, monotonic, or CMPN}{Like in the CBN model, all parent nodes
must be present for a relationship to be satisfied. Specify it
as "AND" or "MN" or "monotone".}
\item{OR, semimonotonic, or DMPN}{A single parent node is enough
for a relationship to be satisfied. Specify it as "OR" or
"SM" or "semimonotone".}
\item{XOR or XMPN}{Exactly one parent node must be mutated for a
relationship to be satisfied. Specify it as "XOR" or "xmpn" or
"XMPN".}
}
In addition, for the nodes that depend only on the root node, you
can use "--" or "-" if you want (though using any of the other
three would have the same effects if a node that connects to root
only connects to root).}
}
}
\item{epistasis}{
A named numeric vector. The names identify the relationship, and the
numeric value is the fitness effect. For the names, each of the
genes or modules involved is separated by a ":". A negative sign
denotes the absence of that term.
}
\item{orderEffects}{
A named numeric vector, as for \code{epistasis}. A ">" separates the
names of the genes of modules of a relationship, so that "U > Z" means
that the relationship is satisfied when mutation U has happened before
mutation Z.
}
\item{noIntGenes}{
A numeric vector (optionally named) with the fitness coefficients of genes
(only genes, not modules) that show no interactions.
}
\item{geneToModule}{
A named character vector that allows to match genes and modules. The
names are the modules, and each of the values is a character vector
with the gene names, separated by a comma, that correspond to a
module. Note that modules cannot share genes. There is no need for
modules to contain more than one gene. If you specify a geneToModule
argument, it must necessarily contain "Root".
}
\item{drvNames}{The names of genes that are considered drivers. This is
only used for: a) deciding when to stop the simulations, in case you
use number of drivers as a simulation stopping criterion (see
\code{\link{oncoSimulIndiv}}); b) for summarization purposes (e.g.,
how many drivers are mutated); c) in figures. But you need not
specifiy anything if you do not want to, and you can pass an empty
vector (as \code{character(0)}). The default is to assume that all
genes that are not in the \code{noIntGenes} are drivers.}
\item{keepInput}{
If TRUE, whether to keep the original input. This is only useful for
human consumption of the output. It is useful because it is easier to
decode, say, the restriction table from the data frame than from the
internal representation. But if you want, you can set it to FALSE and
the object will be a little bit smaller.}
}
\details{
This function is used for extremely flexible specification of fitness
effects, including posets, XOR relationships, synthetic mortality and
synthetic viability, arbitrary forms of epistatis, arbitrary forms of
order effects, etc. Please, see the vignette for detailed and
commented examples.
}
\value{
An object of class "fitnessEffects". This is just a list, but it is not
intended for human consumption. The components are:
\item{long.rt}{The restriction table in "long format", so as to be
easy to parse by the C++ code.}
\item{long.epistasis}{Ditto, but for the epistasis specification.}
\item{long.orderEffects}{Ditto for the order effects.}
\item{long.geneNoInt}{Ditto for the non-interaction genes.}
\item{geneModule}{Similar, for the gene-module correspondence.}
\item{graph}{An \code{igraph} object that shows the restrictions,
epistasis and order effects, and is useful for plotting.}
\item{drv}{The numeric identifiers of the drivers. The numbers
correspond to the internal numeric coding of the genes.}
\item{rT}{If \code{keepInput} is TRUE, the original restriction
table.}
\item{epistasis}{If \code{keepInput} is TRUE, the original epistasis
vector.}
\item{orderEffects}{If \code{keepInput} is TRUE, the original order
effects vector.}
\item{noIntGenes}{If \code{keepInput} is TRUE, the original
noIntGenes.}
}
\references{
Diaz-Uriarte, R. (2015). Identifying restrictions in the order of
accumulation of mutations during tumor progression: effects of
passengers, evolutionary models, and sampling
\url{http://www.biomedcentral.com/1471-2105/16/41/abstract}
McFarland, C.~D. et al. (2013). Impact of deleterious passenger
mutations on cancer progression. \emph{Proceedings of the National
Academy of Sciences of the United States of America\/}, \bold{110}(8),
2910--5.
}
\note{Please, note that the meaning of the fitness effects in the
McFarland model is not the same as in the original paper; the fitness
coefficients are transformed to allow for a simpler fitness function
as a product of terms. This differs with respect to v.1. See the
vignette for details.}
\author{ Ramon Diaz-Uriarte
}
\seealso{
\code{\link{evalGenotype}}, \code{\link{oncoSimulIndiv}}, \code{\link{plot.fitnessEffects}}
}
\examples{
## A simple poset or CBN-like example
cs <- data.frame(parent = c(rep("Root", 4), "a", "b", "d", "e", "c"),
child = c("a", "b", "d", "e", "c", "c", rep("g", 3)),
s = 0.1,
sh = -0.9,
typeDep = "MN")
cbn1 <- allFitnessEffects(cs)
plot(cbn1)
## A more complex example, that includes a restriction table
## order effects, epistasis, genes without interactions, and moduels
p4 <- data.frame(parent = c(rep("Root", 4), "A", "B", "D", "E", "C", "F"),
child = c("A", "B", "D", "E", "C", "C", "F", "F", "G", "G"),
s = c(0.01, 0.02, 0.03, 0.04, 0.1, 0.1, 0.2, 0.2, 0.3, 0.3),
sh = c(rep(0, 4), c(-.9, -.9), c(-.95, -.95), c(-.99, -.99)),
typeDep = c(rep("--", 4),
"XMPN", "XMPN", "MN", "MN", "SM", "SM"))
oe <- c("C > F" = -0.1, "H > I" = 0.12)
sm <- c("I:J" = -1)
sv <- c("-K:M" = -.5, "K:-M" = -.5)
epist <- c(sm, sv)
modules <- c("Root" = "Root", "A" = "a1",
"B" = "b1, b2", "C" = "c1",
"D" = "d1, d2", "E" = "e1",
"F" = "f1, f2", "G" = "g1",
"H" = "h1, h2", "I" = "i1",
"J" = "j1, j2", "K" = "k1, k2", "M" = "m1")
set.seed(1) ## for repeatability
noint <- rexp(5, 10)
names(noint) <- paste0("n", 1:5)
fea <- allFitnessEffects(rT = p4, epistasis = epist, orderEffects = oe,
noIntGenes = noint, geneToModule = modules)
plot(fea)
}
\keyword{ manip }
\keyword{ list }
