The Cause of Lipomatosis

Talk about anything and everything related to lipomas and related healthcare issues here.

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Re: The Cause of Lipomatosis

Post by caribou » Tue Feb 28, 2012 6:53 pm

Of course if there was a way to get rid of lipomas easily and non-invasively, I wouldn't care that much if it was caused by a genetic defect or something else.

It is interesting that a HMGIC mutation in hyaline cartilage (synovial joints) does not cause neoplasia.
It doesn't necessarily mean anything in terms of lipomatosis though. I doubt the mutation was inherited, or was it stated that these persons had the mutation in other tissues as well? It seems more likely to have been either spontaneous (as mutations do happen all the time, in individual cells), or maybe due to mechanical stress caused by more friction as the cartilage in the joint had degraded. Or somehow related to the arthritis anyway, who knows. Those who have inherited the mutation and have it in all their cells, don't still get lipomas in all their fat cells, but only haphazardly when something goes awry and the genes that have translocated in the wrong parts of the chromosome stop working as they should.

I have to look into this ozone therapy when I have the time, but I have to say the logic behind it seems very faint and it sounds like just the kind of thing that is meant to scam people with false hope. :/ I don't deem all alternative medicine bogus, I do think there are some viewpoints and therapies that modern medicine has dismissed and or not understood yet, but even if you should an open mind, if something doesn't make sense or seem logical at all then I would be very critical about it.
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Re: The Cause of Lipomatosis

Post by matt » Tue Feb 28, 2012 7:42 pm

The ozone therapy scam would have then found it's way all the way to the pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10741810 :shock:

PS. Do you happen to have access to pubmed? I have the original publication of this study but it's very poor quality because it's scanned...
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Re: The Cause of Lipomatosis

Post by caribou » Tue Feb 28, 2012 9:39 pm

I'm not very experienced in finding medical articles yet. In my understanding, Pubmed does not have full-text articles, because it's only a search site. My university library doesn't have access to that journal (The International Journal of Artificial Organs), so I'm afraid I can't get the full article. It's a shame though, I really would have wanted to read it.

Since you have a copy, does it explain in what mechanism the oxidation of blood (or adding oxygen and ozone to blood) works and how it could alleviate the symptoms of several diseases, as the researches seem to claim? (They had a few more articles on Pubmed about blood oxidation by the same authors). Maybe there is something behind it, it's hard to say. According to their other abstracts, the ozone in the blood reacts with biomolecules creating reactive oxygens, mainly hydrogen peroxide. Hydrogen peroxide is quite harmful (or toxic, even), but it's used in peroxisomes to deal with toxins. I don't know how increasing the levels of it would affect health (it could be very detrimental at worst, I would imagine), maybe in small amounts it could work as hormesis. It's rather interesting if it could somehow make lipomas disappear, I don't understand how.

Edit. Here's the other abstract so you know what I'm referring to:
Some biochemical effects determined on human blood after addition of a gas mixture composed of oxygen (approximately 96%) and ozone (approximately 4%) have been evaluated. Ozone was used in a mild concentration ranging between 0.21 and 1.68 mM. Within few minutes after rapid mixing of the equal gas-liquid volumes, the ozone was consumed because by instantaneously reacting with biomolecules, generating reactive oxygen species (particularly hydrogen peroxide) having very short lifetime and lipid oxidation products. The following results are oxygen-ozone dose dependent: (1) The pO(2) values have risen from about 40 up to 400 mmHg. (2) By testing the highest ozone concentration, the total antioxidant capacity of blood decreased within 1 min from 1.35 to 0.91 mM but regained its normal values within 20 min owing to the rapid reduction of oxidized antioxidants operated by erythrocytes. (3) Similarly, intraerythrocytic reduced glutathione after ozonation decreased from the initial value of 5.71 to 4.56 micromol/g Hb. (4) Both hemolysis and methemoglobin showed a negligible increase.
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Re: The Cause of Lipomatosis

Post by sjohn » Tue Feb 28, 2012 11:24 pm

Dr Bocci is in the same Department as Dr Di Paolo. In this update they mention that most of the biological mechanisms of action of ozone have been clarified. So, all you need is access, basically.
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Re: The Cause of Lipomatosis

Post by caribou » Wed Feb 29, 2012 9:34 am

Thanks for that, sjohn. Unfortunately I don't have access to the journal "Blood Purification" either, and I'm not willing to pay 33$ for the article. :/

I've been thinking that perhaps ozone treatment might only be effective for Madelung's disease, which isn't truly in the same category as FML. Since madelung's is not of genetic origin and is probably caused by environmental factors, it could respond well to environmental stimuli and lifestyle changes and treatments such as this. But I still don't understand in which mechanism it could treat FML. Does anyone know if the guy whose two lipomas disappeared had FML or Madelung's? I assume no one here knows, but I'm afraid he might have had the latter, if Madelung's is what they decided to test with ozone therapy later on.
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Re: The Cause of Lipomatosis

Post by sjohn » Wed Feb 29, 2012 9:43 am

Dr Herbst just recently published a study in which she compares these three fat disorders (MSL, DD, FML) using a certain biomarker. I didn't really had the time to break it down, perhaps maybe you can do it and tell us what u think! Cheers!
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Re: The Cause of Lipomatosis

Post by matt » Wed Feb 29, 2012 10:14 am

Hi,

I'm not so sure that FML is always inherited but even if it is what makes it so different from Madelung's or even Dercum's? I know the medical world loves to categorize and do diagnoses but it is sometimes extemely difficult to separate these conditions from each other. Misdiagnoses have been known to happen.

The only supporting thing for the inheritance in the FML is currently the prevalence in the family. Still this study found no genetic indications of inheritance. Their genetic encoding had no mutations and still they shared lipomatosis. The researchers claim it's the first such analysis ever made. :?

They don't even know whether Madelung's disease is inherited or not. So we can't say for sure Madelung's has no genetic origin.

The same applies to Dercums Disease.

Dr. Karen Herbst is probably the most educated doctor there is when it comes to the rare adipose disorders and she says nothing about genetics in her study. The study is all about differences in the desaturation index.

Do you know if there are other studies which would indicate differently?
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Re: The Cause of Lipomatosis

Post by caribou » Wed Feb 29, 2012 11:13 am

Karen Herbst didn't mention the genetic backround of FML because she wasn't researching the cause of FML in the study, but rather the activity of a certain enzyme involved in lipid metabolism and how it might function differently in rare adipose disorders. I think her main concern was the enzyme's activity in Adiposis Delarosa. This is what Karen Herbst states on her website about FML, as I'm sure you know:
It is most likely an autosomal dominant disorder(4) and is seen in men and women(5). The genetic defect is thought to be secondary to a translocation involving high-mobility-group protein isoform I-C (HMGIC)on chromosome 12 and the lipoma preferred partner gene (LLP) on chromosome 3(6, 7), however, chromosomal abnormalities are not seen in all families(8), and the lipomas evaluated for translocation were a small number of a much larger group of mesenchymal tumors(9).
And this is all the medical community knows about FML (as far as I know). We don't know why there were families where chromosomal defects weren't observed. However, at least in my family, it does seem to be an autosomal dominant disorder based on how it's inherited (doesn't skip generations). I'd like to find out about other people's experiences in case FML doesn't always follow the pattern of an autosomal dominant disease (which was part of the reason why I started this survey). If that were the case, maybe there were more to it than just genes.

Still it seems like the most probable theory is that FML is usually caused by a specific mutation, particularly in the chromosome region 12q13-14 where HMGA2 gene is located. But we do need more research to know for sure.

I'm not too familiar with Madelung's or Dercum's, although when I looked them up on Wikipedia, Madelung's seemed to be a syndrome caused by alcoholism in some people genetically susceptible to it. I hadn't checked what Dr. Herbst had on her website until now:
Individuals with MSL have increased fat, usually in a symmetrical distribution either on the neck, upper back (buffalo hump) or interscapular region, on the upper arms or chest, in the mediastinum or thighs, sparing the distal limbs(10). The fat in MSL is thin and watery when removed by needle biopsy unless the individual has undergone numerous liposuction or excision surgeries. When transporting fat in media, the fat will stick to the top of a polystyrene container distinguishing this fat from AD or FML. Because the appearance and location of the lipomatosis can vary, MSL has been divided into three types:(6, 11): TypeI or diffuse lipomatosis of the neck (‘horsecollar lipomata’); Type II or multiple symmetric lipomata of the shoulder girdle, the upper arms, the thorax, the thighs and sometimes the abdomen giving the patients the so called ‘pseudoathletic’ appearance; and Type III or a rare type with preponderance of the lipomatosis in the thigh girth (‘gynecoid type’). Women tend to have Type II and III(10).

Associated disorders include liver disease, hyperlipidemia including elevated high density lipoprotein (HDL) levels (in patients with a history of alcohol use), hypertriglyceridemia, hypothyroidism, diabetes mellitus, and neurological changes(12). MSL is an inherited disorder associated with mitochondrial mutations in a few familial cases,(13, 14) however, Klopstock et al.(15) found mitochondrial mutations in only 2 of 12 patients studied. In addition, Chalk et al. found no mitochondrial pathology or mutations in four siblings with MSL with a pattern favoring autosomal recessive (16).
Basically it could be genetic (through an autosomal recessive pattern, possibly), or it could not be. It's hard to say when so little research has been done. Similarly it's hard to say much about FML, even though it seems to me to be an autosomal dominant disorder. These things do matter when assessing the potential of treatments such as ozone therapy to treat FML. I would be inclined to think that ozone therapy doesn't help with FML, unless it would be tested on people with FML with positive results. Obviously it would be ideal if this could be done, it might shed some light on the nature of FML whatever the result of the test.
The only supporting thing for the inheritance in the FML is currently the prevalence in the family.
But this is a very important point, and it does strongly imply an autosomal dominant inheritance pattern, n'est-ce pas?
Last edited by caribou on Wed Feb 29, 2012 11:28 am, edited 2 times in total.
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Re: The Cause of Lipomatosis

Post by caribou » Wed Feb 29, 2012 11:24 am

Dr Herbst just recently published a study in which she compares these three fat disorders (MSL, DD, FML) using a certain biomarker. I didn't really had the time to break it down, perhaps maybe you can do it and tell us what u think! Cheers!
I'll try to have a better look at it at some point when I have time, although I'm not an expert in reading or understanding medical studies, by no means. Based on a cursory glance, it seemed like Dr. Herbst was assessing if the enzyme stearoyl-CoA desaturase (an enzyme in the synthesis of unsaturated fatty acids) was acting in some way abnormally in Dercum's disease or in other adipose disorders. It seemed to be abnormal in DD possibly leading somehow to accelerated fat accumulation and she was hypothesizing that it could be caused by factors such as inflammation or problems in the lymphatic system. It doesn't seem like this enzyme is very relevant in FML.
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Re: The Cause of Lipomatosis

Post by matt » Sun May 27, 2012 6:11 am

But this is a very important point, and it does strongly imply an autosomal dominant inheritance pattern, n'est-ce pas?
I'm sorry, but you if anyone should not make assumptions which are not based on a scientific fact. Especially when we have a study which indicates contradictory.

I think we are mixing together here the mutation and heredity. Mutation can occur without the inheritance. How and why lipomatosis is sometimes shared within family members we do not actually know yet, although it would make sense it's because of the heredity. Still, we have not enough proof for it.

So it's anyone's guess at the moment.

I do agree the mutation causes the tumor. But what causes the mutation is still somewhat unclear to me? It's possible the mutation is inherited but it's definitely not 100 % sure yet. This is what I want to emphasize.
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Re: The Cause of Lipomatosis

Post by Sparky » Fri Jun 08, 2012 11:01 am

This post and the other similar http://www.lipomaboard.com/general-f2/genetics-t81.html post have been a very interesting read.

I'm not a medical person, nor do I possess a sizable brain, so I'd like to make some conclusions as to what has been discussed here and to affirm my understanding:

- In preposition terms (genetic origin?), can we conclude then that mutated / translocated chromosmal defects, and specifically in chromosome 12q as the dominant and underlying 'enabler' as to why I have lipoma (ie. if I have the translocation, I am at risk of developing lipoma). Can I extend this assumption by saying I 'have' lipoma therfore I must have this translocation?
- (stick my neck out a bit with this one) - typical 12q translocation with q13/q14 results in common subcutaneous lipoma, translocation elsewhere rusults in other lipoma types.
- Is it possible for an autosomal dominant inheritance pattern to remain dominant for a couple of generations providing an illusion of non-FML / genetic mutation inheritance? For me, I believe the reason why I have lipoma is due to chromosonal inheritance (males in the chain mainly, but my daughter also has her first one). I'd like to learn about any evidence of 12q mutation not related to FML.

Overindingly then it appears chromosomal mutation is at the centre of the preposition to lipoma. Most studdies I have read confirm this position, although there have been cases that no defect has been found that challenge this position (doh).

As to the 'why dont all 12q defect cells / people develop lipoma' - well, this is the great mystery..... what is the trigger? your guess is as good as mine.

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Re: The Cause of Lipomatosis

Post by Guest » Sat Jun 09, 2012 8:35 pm

1. Sparky: Do you have many small bumps just underneath your skin? They feel rubbery and you can move them around somewhat with your fingers? If you have common FML then there is a very high probability that you have a 12q translocation mutation. There are many other disorders loosely called "lipoma" that having nothing to do with a 12q mutation.

2. "Translocations elsewhere" can result in disorders unrelated to any type of lipoma.

3. I am not 100 % clear on what you are asking. If you have common FML, then the mutation probably did not start with you, but was instead inherited by you.

4. No, the studies finding no 12q mutation are a different type of "lipoma". As just one of many examples, someone who gets their arm banged in an auto accident can eventually get a "lipoma" in that spot. But that person has no 12Q translocation. The existence of disorders called "lipoma" that are not associated with a 12q translocation mutation does not disprove that common FML is due to a 12q translocation mutation.

5. Valid question and no one knows the complete answer. But there are some hints....which are difficult to describe in a couple sentences. The mutation makes the cell susceptible to tumor formation, but more than just the mutation needs to happen in order for a tumor to form. Protein signaling that controls cell division is a very complex process with a lot of variables.
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Re: The Cause of Lipomatosis

Post by Sparky » Sun Jun 10, 2012 11:02 am

Thanks for your reply Guest.

1. Preposition/genetic origin. Yes, I have the symptoms you describe. I have had two rounds of removal (8 or so), doctors simply confirmed lipoma and benign, I am very sure I have FML.
There are many other disorders loosely called "lipoma" that having nothing to do with a 12q mutation.
Yes, I know this, but in a true lipoma case (mine, yours and others here), can I say with some certainty that we have all had a preposition to acquire lipoma because we have the 12q mutation (either through inheritance or some chromosomal damage/change). Put another way, in a preposition sense (not trigger) can a lipoma develop without a 12q mutation?

2. Sorry, I wasn’t clear with my question. Specifically looking at 12q. If translocation occurrs with q13/q14 then it seems a result is the common conventional lipoma (Q2.p1) but if 12q translocates elsewhere does this result and explain the different, less prevalent lipoma types? I was trying to understand simply if a distinction could be made in this way.

3.
If you have common FML, then the mutation probably did not start with you, but was instead inherited by you.
Yes, I get this bit. But if we accept that 12q is an autosomal dominant inheritance pattern, and it can remain so for a couple of generations, then I was questioning how a person without current family members with lipoma would know FML or just had numerous lipoma? I'm somewhat relating this question to my first with regards to chromosome mutation, and would like to about any tests/cases/evidence of 12q mutation which NOT related to FML.

4.
studies finding no 12q mutation are a different type of "lipoma"
Yes, thanks. "pathogenetic link between soft tissue trauma and the formation of posttraumatic lipomas is still controversially discussed" (pub med id - PMID: 17975353).

So, it seems that there are cases (often post traumatic) where lipoma 'like' lesions have been discovered, but as they are not truly lipoma, then I'm back to 12q mutation as being the only pre-position underpinning why we get lipoma.

5.
Protein signalling that controls cell division is a very complex process with a lot of variables
Unless it is possible to re-correct my translocation somehow, I'm resigned to the "susceptibility" of lipoma generation for the remainder of my life. However, I believe that by understanding the potential trigger/s is the key to unlocking a successful treatment.

I'm desperate to understand the pathology/bio makeup of lipoma over the surrounding adipose tissue/fat. Furstratingly, I am finding VERY limited information. There MUST be a difference and thus clues as to why. I am currently looking at fat metabolization and its connection with lower HSL (hormone sensitive lipase) in lipoma - not sure if this has been discussed here yet?

Many, thanks again for your input guest (got a name?) Come on folks, let your fingers loose and help me/others understand these important points.

Sparky.
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Re: The Cause of Lipomatosis

Post by Guest » Sun Jun 10, 2012 12:50 pm

Hi.

1. Some lipomas have been associated with other locations such as 6p and 13q. But by some accounts these 6p lipomas have a slightly different appearance and can be more infiltrating. So we should say that you very likely have a 12q translocation rather than us being 100 % certain. (If you are that curious, you could simply walk into a local genetics lab and have them test you. I have already posted extensively about these labs on this board.)

2. Some of the tumors caused by translocations other than t(3;12)(q27-28;q14-15) do look just like standard FML tumors. So there are exceptions. But the vast majority of common FML tumors are t(3;12)(q27-28;q14-15).

3. The diagnosis of FML can be made based on the symptoms, independent of family members symptoms. The expression of the mutation can vary between individuals.

4. I would modify your statement slightly, to recognize my point in # 1 above.

5. There is tons of information on the pathology. Common FML is not related to fat metabolism. Metabolic processes are completely different from cell division control. So you could learn everything about fat metabolism and it will not help you understand common lipomatosis.

Regarding the "trigger"--one thing we do know that it is not external environmental factors. Unfortunately, it is "endogenous", meaning it is part of your make up. These cellular signaling process are very complex with a lot of interactions and dependencies, not all of which are understood. And since it is endogenous, even if the medical community understood it better, it would still be very difficult to cure.

Apparently your doctor doesn't explain this to you. I have learned from other posts on this board that people have very bad experiences communicating with their doctors on this stuff. Some posters even claimed that their doctors don't seem to be informed, but some of that might be just communication issues.
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Re: The Cause of Lipomatosis

Post by Sparky » Sun Jun 10, 2012 7:54 pm

Once again, many thanks for sharing these points with me guest.

1. Ok, we've evolved this question now somewhat. Can I now say with confidence, that from what we know, a person with FML or common conventional lipoma (most here I suspect) 'must' have a chromosomal translocation mutation, and that in 'most' cases this is attributed to q12 (q13-q15) as we have discussed?

2. Understood, as I suspected thanks.

3. If you accept my conclusion #1 then surely the vast majority of people presenting lipoma will have had their chromosomal mutation passed down to them? What I am proposing therefore is that in these cases there is no difference between FML and common conventional lipoma.

4. Understood, thanks.

5. This question has evolved somewhat, but let's keep the momentum going though....
There is tons of information on the pathology. Common FML is not related to fat metabolism
General pathology concluding "mature adipose tissue" isnt far from what I can find. What I'm looking for is case specific lipoma pathology, compartive if you like, in questioning how do lipomas differ to that surrounding adipose? What is the encapsulation, what role does it play in the decisions of the lipoma life and the ability/possibility for the body to gain access to the stored adipose. Ulitimately, I guess I'm looking for pointers of how to enable/trick the body in gaining access to the stored adipose. The following is some example comparitive information I seek.

1. Lipoprotein lipase activity and hormone-sensitive lipase activity were investigated in subcutaneous lipomas removed from two patients and compared with the enzyme activities in subcutaneous adipose tissue from two normal subjects. 2. Confirmation was obtained of the presence of lipoprotein lipase activity in lipomas with an activity fifteen to forty-five times that in the two control samples. 3. Hormone-sensitive lipase activity was demonstrated in lipomas under basal conditions of assay as well as in the presence of adrenaline plus theophylline. However, compared with the non-lipomatous fat samples, these activities were lower, as was the magnitude of the lipolytic response to adrenaline plus theophylline. 4. The significance of these measurements of enzyme activity and their role in the pathogenesis of lipomas are briefly discussed.

As for doctors.... it's been many years for me, but yes, very limited information flow. By 'endogeous', can I take it that that relates to the preposition point I keep harping on about and by having a chromosome mutation? just trying to piece things together.

Sparky.
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Re: The Cause of Lipomatosis

Post by Guest » Tue Jun 12, 2012 12:24 am

Sparky:

Hi.


1. Yes, you now state it correctly.

3. Yes, most people with common lipmatosis have had the translocation passed down to them. That isn't just your theory, it is a proven fact.

5. A tumor is not "stored adipose tissue" that the body can somehow "gain access to". As to the encapsulation--it is fibrous connective tissue. At the cellular level, there isn't much difference between healthy fat and the fat in a common FML tumor (other than of course the uncontrolled growth.) The article that you quote doesn't seem like a common FML tumor to me. It sounds more like some lipodystrophy syndrome such as MSL. Remember, the term "lipoma" gets used for many very different disorders. If you could confirm that the authors are are referring to an FML tumor, then I would be extremely interested in reading the whole study--but I think that is extremely unlikely.

Regarding "endogenous"--no this doesn't refer to just the translocation mutation. It is any factor within the body. This is difficult to explain, so here is an analogy: imagine a goalie has bad peripheral vision in his right eye. Most games it is no problem. But one day he gets paired up with a bad full-back on his right side. Still usually not a problem. But on this day the opposing team's wing luckily gets way outside the right fullback and gets a clear shot from the far right. The goalie has a slow reaction due to his bad peripheral vision and the opposing team scores a goal. For the rest of the season, the goalie's bad peripheral vision does not cause any problem, because these particular combination of circumstances did not recur.

The point is that the translocation creates the tumor susceptibility, but it is the interaction of the translocation with other factors that is needed to cause the tumor. And these factors are within the body's invisible cellular processes, not an external influence such as drinking too much coffee. That is why there is not much you can do in this regard.

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Re: The Cause of Lipomatosis

Post by matt » Tue Jun 12, 2012 10:41 am

Hi guys, nice conversation going on here, please keep it up!

Unfortunally there are again too strong statements from Guest (Tom apparently?) so let me correct some of them:
  • It is thought that FML is inherited, this is certainly not a proven fact. Infact the only study about the inheritance in FML proved the other way around.
  • We do not know whether FML is endogenous, this is only speculation. Infact there are many examples pointing that some external factors might have something to do with the onset of the lipomatosis.
  • To say that common FML is not related to fat metabolism is pure insanity. Of course it is because it's fat we're dealing here with!
  • "The diagnosis of FML can be made based on the symptoms". Sad but true. Anyone with a medical doctor's degree can do the diagnosis based purely on his/her experience and knowlidge. No tests needed.
  • "Yes, most people with common lipmatosis have had the translocation passed down to them. That isn't just your theory, it is a proven fact." No, this is only a proven fact in Guest's head.
It's true that in most tumors there are mutations but even in one single lipoma there can be none, one or multiple mutations depending on the spot where the sample was taken.

Warts are a type of tumors caused by a human papillomavirus. Warts are often transmitted inside the family via contact. They are not inherited genetically. One can have one or sometimes multiple warts around the body. Often common warts appear in the extremities.

There are a variety of papillomaviruses which can cause a variety of symptoms and conditions for which the common superficial warts are just one example. Common warts are considered as benign but some human papillomavirus lesions may undergo malignant transformation.

Abnormal chromosomal structures are often found in conditions concerning the human papillomavirus.

Have you ever considered why microbes can sometimes create these tumors? Are they to protect themselves from the immune system or perhaps the body protects itself from the microbes?
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Re: The Cause of Lipomatosis

Post by Sparky » Tue Jun 12, 2012 12:24 pm

Firstly, Tom, thanks very much for your replies once again.

The details I attached are the abstract from a document on pubmed. It's not a free document, so I dont have access to the full text.. perhaps you do? (PMID: 1261213)

I understand your comments regards lipoma tumour and access to the energy stored. As you say though, there is very little difference in the fat cell make up of a lipoma over the surrounding adipose. It is for exactly this reason that this poses a tantalising thought for me as to the possibility of creating a treatment by creating a situation whereby the body does see the lipoma fat as a store to draw from.

Matt, I dont think Tom was saying FML is inherited per se. What he and I have discussed is that it is in regards to inherited chromosomal mutation and preposition / susceptibility that we associate linkage (may or may not develop) FML and common conventional lipoma.

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Re: The Cause of Lipomatosis

Post by matt » Tue Jun 12, 2012 12:40 pm

Sparky,

I understand you but please note that this linkage or the mutation have not been scientifically proven except that FML tends to appear inside the family.

That is why I gave you the example about the warts. We need more precise information in the chromosomal level before we can draw any definitive conclusions, right?
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Re: The Cause of Lipomatosis

Post by Sparky » Tue Jun 12, 2012 2:48 pm

Matt, you said in your last post....
I do agree the mutation causes the tumor. But what causes the mutation is still somewhat unclear to me?
But it appears that the mutation provides only the preposition for the tumor, not the cause though? (I think that's what you meant?)

Ok, so let's look at the mutation part. If we agree that the mutation is fundamental (allbeit apparently not exclusively) in this discussion, then the next question is how do we get the mutation? Well, the two ways we have discussed is either through inheritance or some other development through external / localised ingress or event, right?

Understanding that then, I have inherited the mutation, every one of my cells has it, I have only 50 or so lipoma (remember mutation just provides the preposition, another trigger or event must occurr also), so not too bad given the cell numbers. But aparently it's also possible for someone to develop the mutation and also have lipoma, must be very unlucky dont you think?

So then, looking at these two paths for the mutation, which do you consider the more probable? Can you see why there is strong bias to FML?

Sparky.
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