You might be interested in this paper: https://www.frontiersin.org/articles/10.3389/fgene.2011.00100/full

Outlines in vivo studies in mice showing how Ras zygosity effects tumour identity differently based on the type of mutation they've got. While Ras knockouts seem to make fetuses unviable, Ras Gain-of-function seems to still permit viability, but also confers shorter lifespans because of tumours.

A lot of Ras mutations are acquired from what i know, with different mutations being linked more to certain organs because of the nature of carcinogens that organ is exposed to. So I don't know if it's super worth looking deeper into heredity of this sort of thing, even if its very cool.

Certain cancers (I believe Ras-linked cancers?) Potentially experience this actually.

I think it was an in vitro study where overactive Ras was studied in homozygous WT, heterozygous, and homozygous mutant, while growth of cell populations was observed. They actually found that heterozygous conditions exhibited more severe progression of the disease.

It's thought that certain cancerous signals operate within a sweet spot, where their results are not so severe that feedback mechanisms halt them, but are severe enough to cause a diseased phenotype.

I'll take another look at my notes and double check the details of this because it was really a quite fascinating example of this exact phenomenon you're asking about.

If you're interested as to why - Ras at normal levels induces normal proliferation. Certain mutations to Ras are able to push this into excessive proliferation. However beyond this, even more proliferative signaling through Ras induces senescence instead and causes cells to age and effectively die. Hence there is a 'sweet spot' possible where some mutant Ras is present but the signaling is not so excessive that cancer cells die.

EDIT: After going to my notes to check it was in fact mutation of Ras which alters it's nucleotide binding such that it is constitutively active.

If you want to read more about it, the paper describes it as the 'sweet spot' model here: https://www.nature.com/articles/s41568-018-0076-6

It seems there is some nuance to do with the signaling power of given mutations which might contribute to oncogenesis as well, so perhaps not a perfect model of heterozygosity being more pathogenic than homozygosity, however the concept is still somewhat there I think.

Do you think we should be doing more to address the inaccessibility of information contained within reports of scientific research. I study within the area and am constantly frustrated by the lack of clarity within figures and written sections where it seems easily possible to make yourself more clear at the expense of sounding marginally less academic and abbreviated.