The loss of gene function would be expected to be close to random initially, but the cancer specific effects would occur because of hits on tumor suppressor genes. There are of course notable examples of gain of gene function too, that are selected for, but I am asking about the big picture here
I agree with the Alkhatib. While the loss and gain of tumor suppressor and oncogenes respectively plays key role in the cancer progression , there are several incidences where epigenetic events could surrogate for oncogenic (genetic) lesions. For instance, Retinoblastoma was originally proposed to arise by homozygous loss of tumor suppressor gene retinoblastoma (rb). However, there are cases where loss of heterozygosity is not found in the retinoblastoma, instead the second rb allele is found to be silenced by DNA methylation.
You may refer to the excellent review by Andy Feinberg et al for the details:
"The epigenetic progenitor origin of human cancer"
Pubmed ID: 16369569
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