I haven’t seen the press conference, so this might have been covered, but. . .
As I understand it, melanoma, while commonly called a type of ‘skin cancer’ is really a cancer arising in the pigmentation cells, not the connective skin tissue itself, like basal cell or squamous cell. His original surgery was for a liver biopsy, and his press conference indicated that there are spots on his brain, too.
Not questioning the metastatic nature of cancer spread. I got that. But since it was diagnosed as melanoma, are there other places other than the skin where pigmentation cells exist? Or had they already identified a primary site on his skin somewhere?
So I had a Stage IA melanoma removed from my left leg. While this is basically one of the “best” invasive cancers (Stage IA means it has invaded skin tissue, albeit not deeply, Stage 0 or melanoma in situ exists on top of the skin but hasn’t invaded the epidermis) in terms of long term survivability rates it still lead me to do a lot of research and ask a lot of questions of my doctors, because hey, it’s cancer–I felt I needed to know.
As I would read about specific cases of melanoma that had spread, I had the same question. “How can they diagnose melanoma when they can’t find a primary on the skin?” And “how do they know someone didn’t have a melanoma on their skin and independently developed say, lung, liver, brain, or lymphoma unrelated to the melanoma?” In my case I have reasonable belief that my melanoma developed ten years prior to its removal, as that is when a mole grew in size, darkened, and then sat like that for ten years. I was one of the lucky ones–my melanoma was apparently not growing, and I’ve heard case stories of people who had a melanoma that sat there for 40+ years without spreading any further. I’ve also read case stories of people who see a weird skin growth and who are in the ground four months later.
The answer as I understand it, is when melanoma metastasizes it first goes to the near lymph nodes, and then on the lymphatic superhighway can spread to far organs. The way they can know that it is a case of metastatic melanoma and not simply independent cancers, is that the melanocytes that normally only exist on the outer layer of the skin and give skin its pigmentation, are actually found in those cancers in the lymph nodes and removed organs. So that would be how, if Carter’s cancer is metastatic melanoma, they’d know that, the tumors they’ve found in his brain or liver would have melanocytes in them. That’s my layman’s understanding based on my understanding of what my personal doctor sand the Internet told me, so I may be getting it wrong.
FWIW I’ve also read that is why there is some hope that melanoma may be the first metastatic cancer that can be truly “cured.” Its behavior in that it spreads “identifiable cells” throughout the body, that are distinct from the cells of surrounding tissue, gives researchers hope that they can engineer drugs that teach the immune system to target these cells specifically and destroy them. With most other cancers the cancerous growths are extremely hard to “mark” as different from healthy tissue.
One pigmented area is the iris. And indeed it is possible, according to my doctor, for the eye to be the primary site of melanomia. Rare but it happens. My son’s sister-in-law died of melanomia a couple days after her 32nd birthday. They examined her closely but were never able to find a primary site. Another surprise, again according to my doctor, is that it can start in places that the sun don’t shine, even though tanning may be the real cause. I don’t understand this; maybe some doctor can explain it. It’s as though tanning releases some toxin that can cause melanomia somewhere else.
It’s my understanding that exposure to UV weakens the skin’s resistance, thus allowing the cancer to develop. It’s perfectly possible for a melanoma to develop in skin that has never been exposed to UV.
All of these conditions are seen on a Bell curve of the population. There are 5 to 10% who will get “it” whatever they do, and 5 to 10% who will never get “it”. The rest can improve or weaken their chances by being careful.
(Stage IV melanoma patient here; in-transit, lymph node, and lung mets, but clean brain MRI so far)
When cancer metastasizes, it retains its original form wherever it goes. It’s not unknown for the primary site to resolve and never be located, while the melanoma has spread to other organs without their own melanocytes.
Metastasis to the brain has a poor outlook even by melanoma standards. Carter is probably getting stereotactic radiosurgery, possibly followed by immune therapy (I am in a study receiving a combination of such drugs). Chemo is not very effective against melanoma.
I was startled by Obama and Clinton at least initially yammering away about a “fast and full” or “speedy” recovery. A ninety-year-old sincere Christian with that diagnosis who has led a very productive and admired life deserves better-thought-out comment.
A page explaining some of the basics of Carter’s diagnosis:
Yes, eyes can be a source: the retina (more commonly but more precisely the chorioid/posterior uvea); the iris; the ciliary body; and rarely the outside covering of the eye surface, the conjunctiva (which is what my mother, dead from very late appearing, like 15 years later later, brain mets, several years back now, had).
Skin and the nervous system share the same embryologic origin: ectoderm. (The retina is actually an outgrowth of the brain btw, the conjunctiva from the skin.) So the unanswered and possibly unanswerable question is regarding melanomas that are first identified in the brain: are they primary to the brain (and melanocytes are found in the leptomeninges, substantia nigra and locus coerulus) or are they metastatic to the brain with a disappearing primary source, one thatthe body successfully fought off on its own but not before it had seeded elsewhere? My experience is that most oncologists favor the disappearing primary hypothesis over the brain melanocyte/melanocyte precursor hypothesis in those circumstances but from a practical POV it does not matter much: if you have melanoma in the brain the odds are not so good you will do well.
Best wishes for a very prolonged period of quiescence FeAudrey. Yeah, even smart people can say stupid things when they mean well.
Carter himself said his doctors told him that 2% of melanomas are found elsewhere than the skin.
News reports also said that the 5-year prognosis showed a 15-20% chance of survival and that Carter’s age wouldn’t make a difference. I don’t know what that means for him individually, but this is still not an automatic quick death sentence.
I don’t disagree with the quoted 10 to 15 percent chance of (5-year) survival for metastatic melanoma. CITE.
That said, of all metastatic locations, brain and liver are pretty much the worst in terms of long-term prognosis. And, FWIW, the cite above points out that older people with the disease tend to fare less well than younger victims.
His age makes a difference in one sense: that 5-year prognosis means that if he didn’t die of something else first there is an 80 to 85% chance that he will die from the melanoma within 5 years. Of course the life expectancy of a man who has reached 90 is 94 anyway, so he might very well die of something else (the “dies of old age” thing) before the melanoma kills him.
But that 5-year prognosis is misleading. More than half of those with melanoma brain mets are dead before 8 months is up, and those are better than numbers had historically been, based on improved local control interventions.
Apparently pleural mets are the worst.
The odds are significantly against him living another year … but no it is not automatic. I wish him comfort and dignity to the end of his time and if his faith helps him achieve that more power to him and his beliefs.
Melanomas can develop in numerous organs of the body, including liver as a primary site (this is very rare). There are melanocytes present in various mucosal surfaces of the body which can be the source of melanomas.
“Primary mucosal melanomas arise from melanocytes located in mucosal membranes lining respiratory, gastrointestinal and urogenital tract. Although a majority of mucosal melanomas originate from the mucosa of the nasal cavity and accessory sinuses, oral cavity, anorectum, vulva and vagina, they can arise in almost any part of mucosal membranes. Most of mucosal melanomas occur in occult sites, which together with the lack of early and specific signs contribute to late diagnosis, and poor prognosis.”
It is entirely possible that Carter never had a melanoma of the skin but that the primary source was elsewhere in the body and not detectable by usual tests.
I had my second treatment this week – no major side effects so far, and the doctor thinks that the involved lymph nodes in my left axilla are softening and diminishing a bit.
Friends have been praising me for doing as much as I can as long as I can, and there is Jimmy Carter, older and sicker than I am, moaning about not being able to go to Nepal to build houses for poor people! :o
Possible, yes. But in a light-skinned guy who worked as a farmer in the US south, the likelihood of it being a primary cutaneous melanoma is probably even greater than the “98 percent” chance that Carter himself mentioned.
Small quibble here: While there are bonafide melanocytes in the leptomeninges (especially around the brainstem) to my knowledge they are not in the SN or LC. The cells there are pigmented and thus resemble melanocyres, but the pigment in those cells is not melanin, but neuromelanin, which is related to other things those cells make (dopamine in the SN and norepinephrine in the LC).
I grant that they are differentiated into a neuronal line rather than into skin pigment melanocytes.
Melanocytes are not only of ectodermal origin, they are, along with neurons and not other skin cells, specificallyof dorsal neural crest cell origin that then migrate to skin locations.
Interesting experiment: transplanting skin melanocytes into striatum of hemi-parkinsonian model rats or mice lesioned with 6-hydroxydopamine significantly improved the Parkinson-like behaviors. (The line of research is to see if one can autograft skin origin melanocytes as a Parkinson’s treatment.) It seems that putting melanocytes into the signaling environment of neuromelanin producing neurons (accepting that calling them melanocytes may be a step too far) can get them to subserve some of those functions lost in these Parkinson models.
This is also interesting: a zebrafish model showing some shared pathways specifically between dopa pathways and skin melanocyte function.
Minimally these pigmented neurons in the SN and LC share much more than a mere superficial commonality with differentiated skin melanocytes.
Sorry for the digression. I’d love for Mr. Carter to die knowing he outlived Guinea worms on this planet!