Abhishek Mahajan (narrator / author)

Finally, the seed must survive, adapting its local environment to suit its needs.

There is evidence that endometriosis lesions can secrete immunomodulatory factors that help them evade immune clearance, release angiogenesis factors that promote blood supply to them, and tamp down its responsiveness to progesterone levels as to prevent natural hormonal suppression of growth.

How does it do all of these?

Simple.

The acquisition of somatic mutations and epigenetic changes that reprogram the lesion's cellular behavior.

Which explains why people have observed so many genetic anomalies in endometriosis lesions, and also why simple retrograde menstruation isn't alone enough to cause endometriosis.

And yet, we still haven't explained everything about the origins of endometriosis.

What causes circulating latent stem cells to transform into endometrial-like cells?

Why does spontaneous regression of endometriosis sometimes occur?

Why do some endometriosis lesions remain stable for years?

Why don't all genetically or hormonally predisposed people develop it?

All unclear.

Still much work left to do to account for all of these.

And, you know, upon reading about the above pathogenesis of endometriosis, one may immediately remark on how similar it feels to another condition.

Subheading.

It is nearly equivalent to cancer.

Spontaneous start and stop.

That sounds an awful lot like cancer, doesn't it?

And not just the typical, innocuous gynecological disease that one may initially assume endometriosis is.

If you aren't yet convinced, let's return back to the seed metaphor we were using in the last section.