I would like to outline some of the recent research
into the causes of lipomatosis. The revolution in genetic research
has enabled big advances in the understanding of tumors over the last
few years. Although this work has NOT identified any easy cures or
treatments, it at least points us in the right direction. Below is
my overview. I'll use the term generic term "lipoma" but my
perspective is FML. I am not sure to what extent this applies to
other lipoma types such as Dercum's.
THE CAUSE OF LIPOMATOSIS
WHAT IS LIPOMA: Every cell contains very complex biochemical
controls that tell it when it should divide and when it should not
divide. The "blueprint" for this mechanism is encoded in each cell's
DNA, which dictates which proteins are produced and when. When this
cell-division control mechanism does not function properly, cells
continue to divide uncontrollably. This is the definition of a
tumor. If the tumor is of the type in which the damaged DNA is able
to spread throughout the body (e.g.—"metastasize") then this tumor is
classified as a "cancer". Tumors that do not spread to other,
healthy tissues are called "benign tumors". Lipoma is a benign
WHAT CAUSES TUMORS: There are many ways in which the cell's growth-
control machinery can become damaged in a way that causes tumors.
For example, some tumors are caused when a virus alters the DNA.
Some environmental factors can also damage healthy DNA. However, in
the case of most lipomatosis, the cause is a translocation mutation.
Translocation mutations are not caused by environmental factors and
they don't happen after someone is born.
HOW A TRANSLOCATION MUTATION OCCURS: Each cell except for sperm and
egg has 46 chromosomes. Sperm and egg each have 23 chromosomes, so
that a combination of a sperm and an egg results in the correct
number of 46. In order for the body to create an egg or sperm it
must break a 46-chromosome cell down into two 23-chromosome cells.
This requires a physical ripping apart of the chromosome pairs.
Sometimes this process goes awry and chromosomes break. The egg or
sperm with a broken chromosome is unable to conceive. Sometimes a
part of the chromosome breaks off but then reattaches itself just as
good as new. But there is a third possibility, and herein lies our
Sometimes two chromosomes break at the same time. Then, instead of
the broken off pieces reattaching themselves to the chromosome from
which they came, they switch spots. This creates two "repaired"
chromosomes, but a piece of them has been switched. This is called
a "balanced reciprocal translocation". Breakages in chromosomes
occur most frequently at the normal weak points in the physical
chromosome structure. One of these weak points is on chromosome 12,
near the halfway point of the large or "q" half. Guess which gene
happens to reside at that weak point? A key gene that codes some of
the signaling proteins that play a key role in regulating cell
Unlike many mutations, the egg or sperm with a translocation mutation
is viable for conception. So the baby is born. The mutation does
not prevent birth because the genes that have been "translocated" to
an incorrect chromosome can, for the most part, still perform their
function. These genes are not missing (as in a "deletion mutation"),
they are just located on the wrong chromosome.
If someone with this mutation has a cytogenetic analysis run on
themselves, the lab can easily see that some of the genetic material
that should be on chromosome 12 is located on a different chromosome
(usually 13). Some researchers have published the relationship
between different specific mutations and the specific associated
types of lipomas. Also, fusion of that common break point on 12
with some genes will cause disorders more serious then lipoma. For
example, if a specific portion of 15 is the translocation
counterpart, then the person will suffer not from lipoma but from
WHEN DID THE MUTATION OCCUR: This mutation during the formation of
sperm or egg may not have occurred in the immediate parents of the
lipoma patient. It may have occurred a thousand years ago, in one of
their ancestors. Since it is a "dominant" trait, pairing with it a
non-mutant gene from an unaffected mate does not prevent the
formation of the tumors.
CLINICAL MANIFESTATION: A person can live for years without
suffering from any adverse effect from this mutation. Imagine a
quarterback that is great at running-plays and short passes, but bad
at long passes. He looks fine until his team gets behind and they
really need to throw long bombs. Then the quarterback starts to
throw interceptions and can't do his job. Another analogy: the
quarterback works great with his favorite receiver John, but always
misses when he tries to throw to the other receiver Joe. This is
isn't Joe's fault--John and Joe are equally good receivers. The
quarterback looked great when John was in the game, but as soon as
the coach put Joe in the game, the quarterback couldn't do his job.
In reality, the quarterback brought his weakness into the game from
the start, but it only became apparent later, due to interactive
factors (when he had to start throwing to Joe).
At some point, in some cells, the translocated genes can no longer do
their job while being located on the wrong chromosome. The "on-off
switch" in the cell division machinery in this cell gets stuck on
the "on" setting. The cells continue to divide. All the daughter
cells of this cell also continue to divide. This creates a mass of
tissue, in which all cells are continuing to divide when they
shouldn't be dividing. This is a lipoma tumor.
IMPLICATION FOR TREATMENTS: So what do we know about how to fix
this? Well, unfortunately that gene that got shifted to the new
location does not act alone in controlling fat cell division. It's
just one player on a big team. And we don't even know the plays or
who the other players are. We don't know exactly how this gene
interacts with others to encode proteins that regulate cell growth.
So we don't know that the quarterback is able to throw to John but
not to Joe. We don't even know that John or Joe (other genes in the
DNA code) are in this game. So all we can say is: this quarterback
has a problem in which sometimes he can be successful and other times
Hopefully, this background can help you better understand some
aspects of lipomatosis. For example, some people ask: "If my lipoma
is due to a mutation that I was born with, then why didn't I start
getting any tumors until I was 20--—the same year in which I started
to drink a lot of coffee?" Hopefully the explanation above might
help people understand that a mutation can exist for years without
manifesting any problem. Yes, you may have started to see lipomas at
the same time as you started to drink coffee. You also hear a
rooster crow before you see the sun rise, but you recognize that this
doesn't prove that the rooster is causing the sun to rise.
Another implication is that some of the justifications for some of
the homeopathic treatments are obviously invalid. For example, one
treatment is supposed to eliminate lipomas by "cleansing the body of
toxins". Anyone who understands the real cause of lipomatosis would
recognize that the problem is not due to "toxins" that can
be "cleansed". This "toxic cleansing treatment" is a scam that preys
on uninformed patients.
Let me offer one last example of how understanding these mechanisms
can help a lipomatosis patient. Some uninformed patients fear that
their lipoma might somehow "turn to cancer". Well….most lipomas are
12q13-15 reciprocating with 13q12-14. (Other lipomas involve 6p and
13q.) In most lipomsarcoma the 12q rearranges and fuses with the
16p. So if a person was born with a 12 to 13 mutation, why should he
fear that he would somehow contract a disease that results from a 12
to 16 mutation? Do you see how powerful it is to understand the real
cause of lipomatosis?
HOW THIS EXPLAINS CLINICAL VARIATION: My siblings have five lipomas
each, while I have had 130 appear. I mentioned in my previous post #
1542 that longitudinal studies have found no observable cause for
this variation in expression of the mutation. Coffee drinkers with
the mutation don't get more lipomas than non-coffee drinkers with the
mutation. These studies have ruled out all measurable environmental
factors, yet there are clearly different disease severities among
people with the same mutation. The reason is that, while my siblings
and I both have the same quarterback with the same problem (the
translocation mutation), my playbook is written to use Joe more than
my sibling's playbooks. So our shared inherent flaw in the
quarterback shows up more with me than my siblings. The hidden
factor that no one participating in a longitudinal study will ever
write in their diary is the interaction of the translocated genes
with other normal genes.
This also helps explain why the efforts of the misinformed people
posting to Dave's board are futile. People keep asking questions
such as: "Do all of us lift weights? Is that the cause of the
lipomas?" They are looking at visible factors (that would have shown
up in longitudinal studies decades ago) and are unaware of endogenous
invisible interactions between DNA segments.
TRANSMISSION OF THE MUTATION: Your 46 chromosomes are structured as
23 pairs of two. Let's say that your translocation is between
chromosomes 12 and 13. On these two chromosome pairs, you have one
unmutated chromosome and one mutated chromosome. So you have an
unmutated 12, a mutated 12, an unmutated 13 and a mutated 13. The
key gene that is supposed to be located on chromosome 12 is located
on chromosome 13 in your mutated 13, but on your unmutated 12 it
correctly resides on your 12.
Now it's your turn to produce egg or sperm. You will donate one
chromosome from each pair. There is an equal chance of it being your
good chromosome as your mutated chromosome. Any given egg or sperm
has an equal chance of getting any of the following combinations:
1. Good 12 and good 13—your child has no lipomas at all.
2. Mutated 12 and mutated 13--you successfully conceive but your
child has lipomatosis. The gene is supposed to be on chromosome 12
is on chromosome 13.
3. Mutated 12 and good 13—this is an "unbalanced translocation" It
doesn't work because now the combination is missing the gene that is
supposed to be on chromosome 12. This egg will either not conceive
or you (or your wife) will have a miscarriage before you are even
aware that you became pregnant.
4. Good 12 and mutated 13: Same. Unbalanced and not viable. You
have the key gene twice, once on the good 12 and once from the
IMPACT OF THIS TRANSMISSION MECHANISM: Your successful conceptions
will have a 50-50 chance of getting the mutation. I have one
brother who has no lipomas. He got the good chromosomes from both
pairs. He is not a "carrier". There is no such thing as a "carrier
for dominant traits. The mutation is completely gone from this
brother's line. Another implication is that someone with lipomatosis
may take longer to conceive.
Hopefully, this note will answer a variety of questions that lipoma
patients might have. Sorry for the length, but I thought that one
long post might cover a lot of questions that people have.
http://health.groups.yahoo.com/group/Li ... ssage/1571
There's more but you have to be registered (fee) to read full articles, but it may be possible to get free tem pass.Eur J Hum Genet. 2001 Sep;9(9):690-4.
Multiple lipomas linked to an RB1 gene mutation in a large pedigree with low penetrance retinoblastoma.
Genuardi M, Klutz M, Devriendt K, Caruso D, Stirpe M, Lohmann DR.
SourceMedical Genetics, A. Gemelli School of Medicine, Catholic University, Rome, Italy.
Hereditary predisposition to lipomas is observed in familial multiple lipomatosis (OMIM 151900) and benign cervical lipomatosis (OMIM 151800) and can also be associated with mutations in the MEN1 and PTEN genes (OMIM 131100 and 153480, respectively). In addition, a recent report indicates that a few patients with hereditary retinoblastoma also have lipomas. Here we report on an extended family segregating a splice site mutation in the RB1 gene. Almost all adult carriers of this mutation had multiple lipomas while penetrance for retinoblastoma was incomplete. In an unrelated pedigree, which was reported previously, the identical mutation was only associated with low-penetrance retinoblastoma but not lipomas. Our data indicate that lipoma predisposition in hereditary retinoblastoma is not associated with specific RB1 gene mutations but is influenced by modifying factors linked to this gene.
Cancer Genet. 2011 Jan;204(1):53-6.
Translocation (Y;12) in lipoma.
Liang CW, Mariño-Enríquez A, Johannessen C, Hornick JL, Dal Cin P.
SourceCathay General Hospital, Taipei, Taiwan.
Lipomas are the most common benign mesenchymal neoplasm in adults, and have been extensively characterized at the cytogenetic level. Chromosomal aberrations have been observed in the majority of lipomas, two-thirds of which involve chromosomal region 12q14.3. To date, structural rearrangements have been reported affecting every chromosome except chromosome Y. Here we report a case of a lipoma that shows a novel apparently balanced translocation involving chromosomes Y and 12. Fluorescence in situ hybridization using a break-apart HMGA2 in-house probe set detected a single signal on the normal chromosome 12 but not on either the derivative chromosome Y or 12, indicating a cryptic loss of 12q14.3, where HMGA2 is mapped. Immunohistochemical studies, however, revealed overexpression of HMGA2 with nuclear expression in the majority of tumor cells, whereas MDM2 and CDK4 were negative. The overexpression of HMGA2 may be caused by a cryptic chromosomal aberration affecting either the cytogenetically unaltered HMGA2 allele or HMGA2 regulators elsewhere. The current case broadens our knowledge about the translocation partners of HMGA2 in lipomas and highlights the biological complexity in regulating HMGA2 expression.
Copyright © 2011 Elsevier Inc. All rights reserved.
PMID:21356192[PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, SubstancesPublication TypesCase ReportsMeSH TermsAllelesChromosome BandingChromosomes, Human, Pair 12/genetics*Chromosomes, Human, Y*CytogeneticsHMGA2 Protein/geneticsHumansImmunohistochemistry/methodsIn Situ Hybridization, FluorescenceKaryotypingLipoma/genetics*MaleMiddle AgedTranslocation, Genetic*SubstancesHMGA2 Protein
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Int J Cancer. 2007 Jul 15;121(2):308-15.
Gains and complex rearrangements of the 12q13-15 chromosomal region in ordinary lipomas: the "missing link" between lipomas and liposarcomas?
Italiano A, Cardot N, Dupré F, Monticelli I, Keslair F, Piche M, Mainguené C, Coindre JM, Pedeutour F.
SourceFaculty of Medicine, Laboratory of Solid Tumors Genetics, Nice University Hospital and CNRS UMR 6543, Nice, France.
Well-differentiated liposarcomas (WDLPS) classically contain high-level amplification of 12q14-15 sequences, including the MDM2 and CDK4 genes, while lipomas are characterized by simple structural chromosome aberrations often involving HMGA2 at 12q15. Previous studies have shown that low-level gain of the 12q14-15 region, such as trisomy 12 and 12q15-24 duplication, might be sufficient for the development of minimal atypia and formation of WDLPS. Moreover, because some features, such as overexpression of HMGA2, are shared by both lipomas and WDLPS, it has been hypothesized that lipomas and WDLPS may form a genetic and morphological continuum. We report here the results of molecular cytogenetic analysis of 8 lipomas that had unusual chromosomal features resulting in gains of 12q14-15. While 3 cases had simple numerical rearrangements (trisomy 12) or structural rearrangements (unbalanced translocations with 12q gains), 5 cases were particularly intriguing because of peculiar features such as giant chromosomes, supernumerary chromosomes or neocentromeres that usually are the hallmark of WDLPS. Gain of 12q14-15 sequences including extra copies of MDM2 and CDK4 were detected by fluorescence in situ hybridization analysis in all analyzed cases but no expression of MDM2 and CDK4 was observed suggesting that these genomic imbalances had no functional consequence. We observed rearrangements of HMGA2 in 5 out 8 cases. Altogether, our results indicate that moderate gains of 12q are not always associated with a malignant phenotype, and that some intermediary forms exist between classical lipomas and classical WDLPS. Some of these intermediary forms may correspond to a genomic premalignant condition while some may have no malignant potential.
(c) 2007 Wiley-Liss, Inc.
PMID:17372913[PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, SubstancesPublication TypesCase ReportsResearch Support, Non-U.S. Gov'tMeSH TermsAgedAged, 80 and overChromosome Aberrations*Chromosome BandingChromosome DeletionChromosomes, Human, Pair 12/genetics*Cyclin-Dependent Kinase 4/geneticsFemaleHMGA2 Protein/geneticsHumansIn Situ Hybridization, FluorescenceKaryotypingLipoma/genetics*Lipoma/pathology*Liposarcoma/geneticsLiposarcoma/pathologyMaleMiddle AgedProto-Oncogene Proteins c-mdm2/geneticsTranslocation, GeneticTrisomySubstancesHMGA2 ProteinCDK4 protein, humanCyclin-Dependent Kinase 4MDM2 protein, humanProto-Oncogene Proteins c-mdm2
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" The combined data indicate that the pathogenetically significant event is fusion, truncation or transcriptional activation of HMGA2, but it can not be excluded that EBF, which has been implicated in adipogenesis, contributes to the tumor development."
Cytogenet Genome Res. 2006;112(1-2):60-6.
Truncation and fusion of HMGA2 in lipomas with rearrangements of 5q32-->q33 and 12q14-->q15.
Nilsson M, Mertens F, Höglund M, Mandahl N, Panagopoulos I.
SourceDepartment of Clinical Genetics, University Hospital, Lund, Sweden.
Chromosome segment 12q13-->q15 recombines with many different chromosome bands in lipomas and at least ten recurrent translocations have been identified. The HMGA2 gene is often rearranged, but little is known about the molecular consequences at other breakpoints. Fusion genes between HMGA2 (12q14-->q15) and LPP (3q27-->q28), LHFP (13q12) and CMKOR1 (2q37) have been reported. In the present study, eight lipomas with rearrangements involving chromosome bands 12q14-->q15 and 5q32-->q33 were analyzed. In chromosome 5, five of the cases had a breakpoint in the 5' part of EBF in 5q33, while three cases had breakpoints located about 200 kb 3' of EBF. In chromosome 12, the breakpoints clustered to the region of HMGA2. Four cases had breaks within the gene and four had breaks 5' to HMGA2 where the gene BC058822 is located. Two versions of an HMGA2/EBF fusion transcript were detected in one case; one transcript was in frame and the other out of frame. Identical EBF/BC058822 fusion transcripts, seen in two cases, one of which also had the HMGA2/EBF transcript, were out of frame and resulted in truncation of EBF. Since EBF and HMGA2 have different orientations, the findings must be explained by complex aberrations including multiple breaks. The combined data indicate that the pathogenetically significant event is fusion, truncation or transcriptional activation of HMGA2, but it can not be excluded that EBF, which has been implicated in adipogenesis, contributes to the tumor development.
Copyright 2006 S. Karger AG, Basel.
PMID:16276091[PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, SubstancesPublication TypesResearch Support, Non-U.S. Gov'tMeSH TermsAdultAgedBase SequenceChromosome MappingChromosomes, Human, Pair 12*Chromosomes, Human, Pair 5*DNA PrimersFemaleGene FusionGene RearrangementGenetic MarkersHMGA2 Protein/genetics*HumansKaryotypingLipoma/genetics*MaleMiddle AgedReverse Transcriptase Polymerase Chain ReactionSequence DeletionTranscription, GeneticTranscriptional ActivationSubstancesDNA PrimersGenetic MarkersHMGA2 Protein
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More reason to have these looked at by doctor!
It appears that the research done regarding cancerous Lipomsarcomas may lead to help for those of us suffering with "harmless" (sure) Lipomas:
Pathol Res Pract. 2001;197(8):563-8.
Distinction between lipoma and liposarcoma by MDM2 alterations: a case report of simultaneously occurring tumors and review of the literature.
Boltze C, Schneider-Stock R, Jäger V, Roessner A.
SourceDepartment of Pathology, Otto-von-Guericke-University, Magdeburg, Germany. firstname.lastname@example.org
We investigated a lipoma and a well-differentiated/dedifferentiated liposarcoma (WD/DDL), occurring simultaneously in one patient for the possible role of p53 and mdm2 in the molecular oncogenesis of liposarcoma and tumor progression. The hypothesis tested was if there is a continuum in the development from lipoma to liposarcoma. Lipoma was characterized by a lack of p53 mutation, p53 LOH and p53 protein expression, as well as by mdm2 amplification and mdm2 protein expression. p53 mutation and p53 LOH were found neither in the well-differentiated nor in the dedifferentiated parts of the liposarcoma. In contrast, mdm2 amplification and an increase in mdm2 protein expression were found to be associated with malignancy and dedifferentiation, whereas p53 protein expression was only slightly increased. These findings indicate that mdm2 constitutes one of the most common targets for molecular aberration in WD/DDL. We suggest that mdm2 is a marker distinguishing between ordinary lipoma and well-differentiated liposarcoma, and that the genesis of these tumors is different.
PMID:11518050[PubMed - indexed for MEDLINE]
- Lipoma Guru
- Posts: 1172
- Joined: Tue Mar 29, 2011 8:01 am
- Number of lipomas: 61-100
- Location: Finland
First of all, thank you Laura and other for sharing this. I read these kinds of posts in the old lipomaforum years ago (Dave's forum, like the writer mentions). At the time it made me kind of depressed since it tend to say there's nothing I can do about it. I felt I was like a miserable passenger in an airline jet. The post is suggesting that it's all because of our genes and because of the translocation which may have happend thousands of years ago. It sounds a lot like we should just accept it and live with it, doesn't it?
The post is at first glance very expert like. Something like what a person who is well informed in the medical field would write. Perhaps the writer was medically educated. Medically educated may sometimes hold limitations in their perspectives since they are influenced by the big Pharma. I am not a medically educated person but I have opinions. These opinions may be wrong but let me share some of them.
The whole separation between tumors which metastasize and which are benign is in my opinion somewhat wrong. Some researchers like Dr. Simoncini have suggested that basically all tumors are alike but their ability to metastasize depends on the location they are formed at. And I'm not completely sure about the fact that lipomas do not metastasize. In my opinion a benign tumor is the kind of which the body has some sort of control. The whole cancer field is still under a great debate although we've known the disease forever.
This has got to raise some questions to anyone who follows the field at all. Every now and then a promising new treatment is published but then it silently fades away and everybody forgets it. I tend to think that unfortunally the reason is money. You may think that I persue some conspiracy and maybe I do. At least some huge pharmaceutical company's shareholders would lose a lot of money in the long run if cancer was completely curable. Now they can come up with a new cancer drug every year or so and sell that. Every new drug is supposed to be better than the old.
It's very common to blame our genes in almost every disease, especially if the cause of the disease is not well understood.
The writer tells us
How does the writer know this? Because the writer has seen it with own eyes? Or because the writer is told so? Mitochondrial translocations are thought to born this way but not all translocations. This is of course how translocation usually happens. But... even a physical stress to some kidney cells can mutate the DNA http://pubs.rsc.org/en/Content/ArticleL ... C0IB00018C Mitochondrial translocation happens sometimes by viral or cellular oncogenes: http://www.febsletters.org/article/S001 ... 0/abstract So it is also known that viruses are capable to induce translocations or even mix their own DNA or RNA. So I'm quite puzzled with the quote.Translocation mutations are not caused by environmental factors and they don't happen after someone is born.
The rest of the post is based on this fact. Yes, the writer throughs in some impressive chromosome talk which might be true, except the part that translocation mutations don't happen after a person has born. The whole microbiology is something that only a handful of people are familiar with and understand. Or think they understand. The field is under a constant change because of new discoveries. I am really not sure about the above quote. Actually I'm highly against it.
It has also been discovered that this translocation is not always found in lipoma cells, actually in just around 70%. At least not there where it is in majority of cases. They don't even know why the rest 20-30% have lipomas, even if genecatically tested. So yes, the writer explains a nice story what happens AFTER THE TRANSLOCATION and simply manifests that translocations are something that don't happen after conceival. I don't believe it.
Why don't I believe so? Well, I don't understand why a patient would get rid of lipomas with EBOO ozone treatment if it's all in his genes? Does the ozone somehow re-mutate the translocated chromosome? Or does it perhaps eliminate the REASON for the translocation? And why do so many long term alcoholics and HIV patients develop lipomas (more than would be statiscally coherent) http://onlinelibrary.wiley.com/doi/10.1 ... .20406/pdf and http://aidsmap.com/Pubic-lipomas-a-new- ... e/1427281/ and why does a drug for AIDS induce lipomas: http://www.aidsmap.com/Rosiglitazone-ca ... e/1418747/
As a matter of fact it has been suggested that it might actually be the anti-HIV drugs that cause the mitochondrial damage (DNA damage): http://www.thebody.com/content/art2145.html
Yet, Mitochondria, does also have their own distinct DNA. Their DNA when attacked by ROS is highly vulnerable to mutation, and such mutation can cause at least 40 types of diseases affecting:
1. The brain
2. Nerve cells
The source continues:
Deficiency in consumption of Vitamin B6, B12, C, D, Folic Acid and niacin can also lead to mitochondrial damage.
I am not to say that genes don't play any role but I'm pretty sure they are not the only reason. And I might aswell be totally on off-track. Just wondering.
I would also like to know if the detected translocations in the lipoma cells are visible in a non-lipoma cell. I'm sorry but the quarterback John was just Gibberish to me so I didn't quite get how lipomatosis can start later on in life...
Well thanks a lot Genius! Ofc people with FML would have genetic differences from everybody else. After all it is a Familial condition as it's name suggests. And yes, now we know which genes are responsible. But is that all?
The article fails to answer questions like:
What regulates lipoma growth?
Why are some lipomas bigger than others?
What regulates lipoma shape?
Why are some lipomas a lot softer than others?
What regulates lipoma size?
What regulates the severeness of the condition? (some people have a lot more than others)
What regulates lipoma location (why are they created on the trunk and not on our feet)
(i could ask a hundred more questions)
And in the end what in the hell those mutations really mean? How do they express themselves in biochemical terms inside the body? Why do they get worse with age?
The article is basically some generalities concerning FML that are very nicely written. But sadly nothing more.
Read this today on a surgeons website.
This was also on the surgeons website.http://www.lipex.lv/en/beauty-services/ ... ts-etc.htm.
Not sure what "relapses never occur" means.Charlupa wrote:Treatment of chondromas, lipomas and fibromas is a surgical excision. After their removal relapses never occur.
This was also on the surgeons website.http://www.lipex.lv/en/beauty-services/ ... ts-etc.htm.
I had several lipomas removed from my arms, and new ones came back, some in exact location, others right next to it.
I can track this because I still have faint surgery scars, with lipomas under them or near them.
The physician's website also said something I've never heard of:
"6.Lipoma (fatty tumor, lipoma) is a benign tumor. Lipomas are the result of blockage of the discharge outlet of the sebaceous gland channel. It is painless and can intensively grow but it does not present any danger. Lipomas, which are in subcutaneous fat, regenerate in liposarcomas extremely seldom."
- Lipoma Guru
- Posts: 1172
- Joined: Tue Mar 29, 2011 8:01 am
- Number of lipomas: 61-100
- Location: Finland
And relapses do happen to the very exact location from where the lipoma was surgically removed. This can happen because not all lipoma cells were removed or there were smaller lipomas under the old lipoma. And I have also my own hypothesis that some lipomas are capable of generating somekind of "satellite fat cells" although lipomas shouldn't metastasize.
In January 2006 I wrote a post that detailed my scare with the many cases of the Lipoma disorder I had found in Veterans medical records. I posted my scary experience below this post so please read before you go on.
I must say that it's been almost 4 years later and I've found some interesting evidence that should be looked at more carefully.
On one occasions I did find a case that ruled in favor of a veteran being service connected for multiple lipomas. I also found another who was exposed to agent orange in 1996 and was denied. Not sure if that person appealed. However, I did come across this "ANNUAL REPORT TO CONGRESS" in 2002. It lists the multiple symptoms of Gulf War Veterans and included are "lipomas".
I recently went to the Veterans hospital to have 5 very large lipomas out of my 45 removed. And of course every time I explain where I believe they come from they smirk! Every nurse, every xxxxxxx doctor, every student. The funny thing is they've never spent a day in the dirt fighting for this country and it's offensive.
This condition is actually called: Dercums Disease a.k.a. Adiposis dolorosa
A service connected disorder that has been granted compensation in the past.
Thanks for hearing me out!
"Among the 19 skin conditions, only
“miscellaneous benign conditions” were
significantly more prevalent in disabled Gulf
War veterans than in healthy Gulf War veterans
(12.6% vs. 4.1%). There were no differences in
the rates of this group of benign conditions in
disabled Gulf War veterans, compared to
disabled Bosnia and era veterans (12.6% vs.
10.5%). This diverse group of benign skin
conditions included congenital nevi, urticaria,
lipoma, dermatofibroma, and vitiligo."
2002 Report see link --->
http://www.research.va.gov/resources/pu ... rRpt02.pdf
2001 Post (below)
I thought someone might benefit from my story. I’m not sure where to begin, but I do feel that sharing this information with others is important.
It wasn’t long ago that I worked in the laboratory at the V.A. hospital. The hospital will remain nameless; however, I have an extensive science background in the cellular biological sciences. I was asked to review lab data directly for the directing Physician. In particular this information came to me when medical students who were taking notes on the floor had to have their work reviewed prior to being entered into the medical charts.
The VA is always backlogged as you all know so processing this stuff became mundane. I noticed after about the 50th doc, that almost every veteran had the same symptom and condition. I was worried but didn’t tell anyone what I thought I’d found, nor spoke to anyone but family until now. I thought nothing of it but coincidence. The next day I processed about forty five more docs and by the end of week found one hundred and ninety one cases of this problem. This is when I began to worry. But who and what would I do about it. Go tell all VETS in the hospital? No way!!!
Even though I’m aware of how to read medical docs, I truly wouldn’t have found this disorder, but was lucky enough to inquire about the sudden emergence of this problem during my last hospital visit a week earlier. The first Physician couldn’t even tell me what it was. The second knew but referred me back to my nurse who said they were lipomas. It’s a small to large fat sac that will suddenly appear out of nowhere on the trunk, forearms, thighs, ribs, legs and back.
I was told by the primary care nurse who visits many patients, that this was nothing to worry about. I beg to differ; after seeing the medical notations myself I do believe this is related to either the Persian Gulf War or to vaccinations given to soldiers. According to clear medical documentation I’ve read in JAMA lipomas are a primary in older patients over the age of 65 with a history alcohol use, and or parents with severe alcohol use. In some cases this may be hereditary, but they are rarely and I mean rarely found in anyone under the age of 65. A genetic predisposition to such ailment is rare and for me to find this many documented cased at a V.A. hospital in patients less than 65 yrs. old remains a mystery.
I bring this small issue to the table first, because there are so many other manifested side effects in V.A. patients. Side effects that are a constant in all V.A. medical records, I believe this and other small health things we take for granted or maybe ignore sometimes have been a common problem across state lines.
What’s bothers me about this is that it wouldn’t surprise me if the V.A. is banking on the fact that we never figure out that there are commonalities in abundance within medical records. I hope this helps. I had approximately 3 lipomas in 1996 and then a gradual increase with a period of spurious growth in 2000 to 35. I’ve had one removed because it became so large; another biopsied (neg for cancer) because they weren’t sure why so many showed up and rapidly.
I’m way under the age of 65 and way too young to see anything like this ruin my life. I hadn’t thought there was anything to this whole thing until I found my 36th fully invading my testicle sac. The V.A. said it would go away, I have no children – so I’ve been praying and hope this sh%t goes away.
I think it is broken. Can you check and repost?
Very interesting post.
I wonder if it would be possible to get a congressman or senator who is military friendly to investigate or call for investigaton?
I agree that probably the VA hopes no one will add 2 + 2.
However, I've had liopmas since I was 20, as had my brother. My other sisters do not have them.
We are in age ranked:
Sister 63 - no lipomas. Blond with green eyes. Fair skin and freckles.
Brother 60 - lipomas, brown hair, gray eyes. Average skin color, some freckles.
Sister 55 - no lipomas, brown hair and brown eyes. Average skin color, no freckls.
Myself 52 (femail) lipomas, brown hair, brown eyes. Average skin color, some freckles.
Neither of my parents had lipomas. My mother was from a british country. My father born in US, served in WWII.
My mother was adopted and I don't know much about her parents.
Im not sure how to make it so you can just click on the link. I have copied and pasted the link in the search bar and it worked. If it is still not working you can try to google- lipomas caused by agent orange. Like many of my ideas, it maybe useless but it does explain why doctors keep using the same robotic reply that lipomas are painless and require no treatment. Yea sure, if a doctor has a child born with a lipoma on his face, im guessing the doctor might start doing a little actual research ( like all of us have) I hope the link works as there are some interesting comments from vets and their wives.I have always wondered if vaccines might be a cause. Sure they are usually harmless but lets say they might effect 1 out of every 100 people. Is that enough to stop. Maybe someone is covering their butt and keeping their mouth shut. Or maybe its just genes. The more I type the less I know lol. Take Care!
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