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This is a problem taken from "Concepts of Genetics", Klug et al, 10e. I'm given the following table about the mutations in the BRCA1 gene: $$\begin{array}{c|c|c|c|c} \text{Kindred}&\text{Codon}&\text{Nucleotide}&\text{Coding}&\text{Frequency in}\\ &&\text{change}&\text{effect}&\text{control chromosomes}\\ \hline 1&24&-11\text{ bp}&\text{Frameshift or splice}&0/180\\ 2&1313&\text{C}\to\text{T}&\text{gln}\to\text{stop}&0/170\\ 3&1756&\text{Extra C}&\text{Frameshift}&0/162\\ 4&1775&\text{T}\to\text{G}&\text{met}\to\text{arg}&0/120\\ 5&\text{N/A}&?&\text{Loss of transcript}&\text{N/A}\end{array}$$ Footnote: "*N/A indicates not applicable, as the regulatory gene is inferred, and the position has not been identified."

Using this information, how can I decide whether the gene is a tumor suppressor or an oncogene?

I already know that BRCA1 is a tumor suppressor, so put another way, how can I arrive at this conclusion given the data above?

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I assume these are all carcinogenic mutations. Because some them are clearly recessive loss-of-function mutations (like loss of transcript), you can conclude that the function of the gene consists of "holding back cancer". When these mutations occur, they can generally be complemented by a healthy allele on the sister chromosome.

Oncogenes on the other hand, require gain-of-function mutations, like translocation to a more active promotor or dominant negative mutations (like a loss-of-function mutation in a protein which forms multimers, which get "polluted" by the mutant and thus can not be complemented by the other allele). In most cases this "increases" their stimulation of cell division and thus cancerous growth.

Loss of transcript of an oncogene would not cause cancer.

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