Are sporadic cancers more likely to be a dominant or a recessive trait and why?

I know after a google search that hereditary (inherited genes from parents) cancers are more likely to be caused by dominant inheritance but why?

However, I also dont know if sporadic (caused by mutation in somatic cells) cancers are more likely to be a dominant or a recessive trait and why?

Is there actually an answer to this or is more research required?

Furthermore, it's interesting how familial cancers (cancers caused by a combination of genetic and environmental factors) come to exist. Someone may inherit the gene for cancer but never gets the cancer due to other genes being expressed which block the expression of the cancer gene, otherwise known as incomplete penetrance. Is there actually a difference between epistasis and incomplete penetrance? I think with epistasis, the expression of a gene for a certain trait will ALWAYS be blocked by other genes OR a gene for a certain trait will ALWAYS block the expression of another gene. As for incomplete penetrance, you have the gene for a disease, so say hereditary cancer, but only some people which inherit this particular gene get cancer,...others don't develop the cancer because they have other genes blocking expression of this cancer gene. This also shows how all humans have the same genes but different alleles of these genes and different expression of these genes... so there is a chance that the different expression of these genes can influence whether someone gets cancer.
I also think incomplete penetrance always refers to diseases and cancer, but epistasis can be for anything like hair colour.

This thread is rather confusing but it's just my view about about certain things and helps me keep on track the things I know and not forget them lol and also the things which I dont understand and are bothering me. Also, would love to hear from other TSR users about whether I am wrong, right, anything haha

It depends on the type of mutation. If the mutation is a gain-of-function mutation (for example, a receptor or pathway becomes constitutively active), then you would only need one mutation in one allele - so I guess you could call this a dominant mutation. If the mutation results in loss-of-function (for example, a tumour suppressor gene such as p53), then you will still have the other normal allele producing normal p53, therefore you would need two mutations in both alleles to cause cancer (potentially). I don’t know if familial cancers are usually caused by dominant mutations - you could either inherit a single dominant mutation (a gain-of-function mutation) or a recessive mutation (loss-of-function mutation). In either case you are at increased risk of cancer. An example might be families which have a mutation in the BRCA1/2 genes. BRCA1 encodes a tumour suppressor protein and therefore you would need to have a mutation in both alleles in order to have non-functional BRCA1. Under normal circumstances, you would need to have mutations in both alleles, however, if you have already inherited one of those mutations from birth, it only takes one mutation in the other allele to completely knock out functional BRCA1 - predisposing to cancer.

An example of autosomal dominant cancer is familial adenomatous polyposis - in this condition, all individuals develop many polyps which may become cancerous by their forties.
As for penetrance - you’re right, even if you inherit a dominant mutation, you may not develop the condition since often, expression of genes is dependent on other genes.

Epistasis is about how different genetic loci interact. Penetrance relates to how strongly the phenotype reflects the genotype.

The concept of epistasis arose from classical genetic interactions and not from a molecular biology perspective. I don't often hear about epistasis being discussed in the context of cancer research. Probably because epistasis is often discussed in a developmental biology context. I always found the pathways incredibly complex e.g. in C. elegans development.

Cancer is actually far more interesting in my view. You are absolutely correct in saying that the transcriptome (genes that are expressed) massively affects the development of cancer. For example, say we have gene X: its transcript mRNA X could vary widely in different individuals. Factors which could affect expression include: levels of vitamin D, factors that affect the epigenome (e.g. diet or stress), factors affecting post-transcriptional regulation (splicing, polyadenylation 5'-capping), levels of inflammation, the redox status of the cell via sirtuins, Fe levels in the blood if it has an IRE upstream of the gene (and so gender, because female versus male Fe metabolism differs) etc... there are so many things that could affect it. Similarly, very few cancers are from only a single gene. Two that I can think of are the sarcoma (src gene) and retinoblastoma (pRb). Usually familial cancers simply increase the frequency at which the cancer develops (familial clustering) and lowers the age of onset. Indicating that there is at least a "second-hit" required. From what I have read, typically the cell needs ~20 hits in significant genes to develop into a cancer. By significant genes we can think of those that are seen as involved in the "hallmarks of cancer" as this provides a framework for understanding what is happening.