The answer is that the distribution of cells bearing the mutation(s) is spatially restricted, local to the organ that hosts the tumor. For example, a squamous cell carcinoma results from mutations in dermal skin cells, causing cancerous growth. The mutated cells are limited to the tumor itself. Hence, removal of the tumor will remove all of the mutated cells. Some cancers can become malignant and will spread to other organs. The mutated cells are defined by the original parent tumor and the sites of metastasis where those cells have migrated, elsewhere in the body.

Some cancers come back because whatever treatment - surgery, chemo, immunotherapy - has failed to eradicate all of the cells bearing the cancer-causing mutations.

I think of myself as an expert on the biological basis of homosexuality, and concur with the statement above. I published several papers on the topic, including the 1999 Williams Nature paper that I cited below, before my professional interests turned exclusively to neurobiology.

As I noted below, the fraternal birth order effect is the most well-established finding we currently have on the cause of male homosexuality, and it is amenable to an epigenetic intepretation. For example, circumstantial evidence suggests that increasing parity immunizes or innoculates mothers against HY antigens, which *could* underlie the development of male homosexuality. Such a mechanism would probably involve immune cells and cytokines from the mother passing through the placenta and influencing epigenetic marks on the developing fetus' genome. That, in turn, could influence brain and bodily development.

EDIT: Note that the fraternal birth order finding implies that something occurs in utero to affect the psychosexual development of the male fetus in a way that heightens the likelihood that the boy will be gay. We do not know what that something is.

It is considered well-established in this field that prenatal androgen levels sexually differentiate the brain and the body in a male-like direction. Abundant evidence supports this general idea. And since sexual attraction is a sexually dimorphic trait (most men are attracted to women and only women, and vice versa), its reasonable to suppose that something about prenatal androgen could be involved in male homosexuality.

The strongest data we have on the cause of male homosexuality is the fraternal birth order effect, which says that the likelihood of being gay increases with each additional older brother. This phenomenon can be interpreted as a genetic effect if the hypothetical gene(s) predispose women to greater fertility - more likely to have more children. That predisposition to have more children, coupled to a predisposition to launch an immune response to cellular 'male-ness' could explain the fraternal birth order effect.

This finding was supported by a 2000 paper by Williams et al, which found that finger length ratio in gay men, a physical characteristic set before birth, is related to their fraternal birth order.

There are extracellular adhesion molecules, expressed specifically at synapses, that promote and stabilize synapses. Some examples include ephrins, neuroligins, and neural cell adhesion molecules. Also, perineuronal nets also seem to promote synapse stability.