Abhishek Mahajan (narrator / author)

For a seed to survive, it must manipulate its immediate environment, happening upon somatic mutations that allow it to do so.

Very cancer-wise sounding.

And, curiously enough, many of the mutations that cells found in endometrial lesions are identical to those found in cancerous tumours.

A cell paper from 2018, which compared somatic mutations between normal endometrial tissue and endometriosis tissue had this to say.

While we were preparing to submit this manuscript, Anglesio et al.

reported that 21% of the lesions in patients with deep infiltrating endometriosis harbored somatic mutations in ARID1A, PIK3CA, KRAS, and PPP2R1A.

our results corroborated their findings in a larger cohort of subjects with a more common type of endometriosis.

End quote.

For context, all of the named genes are recognized as known oncologic mutations.

Of course, clonality should be considered when assessing results like this, as in, what fraction of the assessed cell population had the mutation?

If it's a low proportion, it is background noise.

If it's high, it may be what is keeping the cell population afloat.

And indeed, endometrial tissue, on average, had much higher fractions of KIS and PIK3CA mutations than normal endometrial tissue.

We could push this even further and ask the question, does a higher mutational burden of these genes cause endometriosis to be even more aggressive, just like how it does for cancer aggressiveness?

One paper studied this, though only through the lens of KIS, and the answer was pretty clear.

Yes.

Quote

KIS mutation presence was higher in subjects with deep infiltrating endometriosis or endometrioma lesions only, 57.9%.

11 19ths and subjects with mixed subtypes, 60.6%.

40 66ths compared with those with superficial endometriosis only, 35.1%.