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Mutants are generated with a modified version of the AjMutator tool [20], which implements a subset of operators defined in our previous work [12].
In the model, mutants are generated during cell division.
Increased cellular quiescence increases the likelihood that resistant mutants are generated during the growth phase of the cancer before therapy is initiated.
This result suggests that mutated viruses are quickly lost upon cessation of KP1461 therapy, and that new mutants are generated upon reapplication of the drug.
These problems grow more difficult if mutants are generated via random mutagenesis, since each mutant strain may contain 50 to 100 or more random mutations [10] [11], out of which perhaps only one is responsible for the phenotype.
Conventionally, herpesvirus mutants are generated by homologous recombination in infected cells with DNA fragments or plasmids carrying the mutant allele as described almost 30 years ago [21], [22], [23].
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By using FMTS a set of mutants is generated.
This means that all the possible mutants were generated.
K3036.58E MOP receptor and E2976.58K KOP receptor mutants were generated.
Initially, mutants were generated, through μJava tool (version 4), from the systems shown in Table 1.
Five affinity mutants were generated covering binding constants between 400 nM and 11.7 mM.
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