The second form of FAP, known as attenuated familial adenomatous polyposis has the APC gene functional but slightly impaired.

Individuals at risk (due to family links or genetic testing) are usually offered routine monitoring of the intestinal tract every 1–3 years for life, from puberty for FAP and early adulthood for attenuated forms.

International polyposis registries exist that track known cases of FAP or APC gene defects, for research and clinical purposes.

Mutation of APC also occurs commonly in incident cases of colorectal carcinoma, emphasizing its importance in this form of cancer.

[citation needed] Depending on the nature of the defect in the APC gene, and whether it is the full or attenuated form, familial polyposis may manifest as polyps in colon or in the duodenal tract, or in any combination of these.

[1] The genetic determinant in familial polyposis may also predispose carriers to other malignancies, e.g., of the duodenum and stomach (particularly ampullary adenocarcinoma).

(APC regulates β-catenin, a protein that plays a crucial role in cell communication, signalling, growth, and controlled destruction, but which left uncontrolled also gives rise to numerous cancers[1]).

[citation needed] Although the polyps are inherently benign, the first step of the two-hit hypothesis has already taken place: the inherited APC mutation.

[citation needed] The normal function of the APC gene product is still being investigated; it is present in both the cell nucleus and the membrane.

Mutation of APC also occurs commonly in incident cases of colorectal carcinoma, emphasizing its importance in this form of cancer.

MYH glycosylase fixes these mistakes by base excision repair, such that mutations do not accumulate in the DNA and lead to tumor formation.

When MYH glycosylase does not function correctly, DNA errors may accrue to initiate tumorigenesis with a clinical presentation similar to that in patients with APC mutations.

Making the diagnosis of FAP before the development of colon cancer is important not just for the individual, but also for the sake of other family members who may be affected.

[citation needed] NCBI states that when an individual is identified as having FAP, or the mutations resulting in FAP: "It is appropriate to evaluate the parents of an affected individual (a) with molecular genetic testing of APC if the disease-causing mutation is known in the proband [person first identified with the condition] or (b) for clinical manifestations of APC-associated polyposis conditions".

Most individuals with the APC mutation will develop colon cancer by the age of 40, although the less-common attenuated version typically manifests later in life (40–70).

Treatment for the two milder forms of FAP may be substantially different from the more usual variant, as the number of polyps is far fewer, allowing more options.

The drug eflornithine, an inhibitor of ornithine decarboxylase typically used to treat trypanosomiasis, is being investigated as a potential preventive medication in combination with the NSAID celecoxib for treatment of FAP.

[9][10][11] Prior to reaching the advanced stages of colorectal cancer, the polyps are confined to the inner wall and thickness of the intestinal tract and do not metastasize or 'spread'.

The purpose of these registries is to increase knowledge about the transmissibility of FAP, but also to document, track, and notify family members of affected individuals.

One study has shown that the use of a registry to notify family members (call-ups) significantly reduced mortality when compared with probands.