Hello tat268,
Several studies have shown that insulin and an insulin-like factor may
stimulate melanoma cell growth. Bear in mind that most of these
studies are on cells in a petri dish, and not in the human body. Many
factors come into play apart from melanoma cells and insulin, such as
enzymes and hormones, and the interactions are not yet fully
understood. Insulin is not listed as a cause of melanoma in current
medical literature.
What Causes Melanoma?
?Ultraviolet radiation is considered the main cause of melanoma. Many
test have been done and some scientist think melanoma is sometimes
genetically linked. A recent study reported that about 10% of people
with melanoma had a defective gene called the p16 melanoma
susceptibility gene. In its normal state the gene acts as a tumor
suppressor; when defective it fails to stop the cells from multiplying
and becoming cancerous (5). Other tests have shown that the risk of
melanoma is also greater if one or more of a person's close relatives
have been diagnosed with melanoma?
http://www.unc.edu/~meghankj/causes.html
?One of the biggest risk factors for melanoma is chronic exposure to
ultraviolet rays, primarily through tanning under the sun or in a
tanning bed. Although sunscreens with an SPF (sun protection factor)
of 15 or greater are effective for protecting exposed skin from
damaging UV rays, many people mistakenly believe they can slather on
the sunscreen and then lie lizard-like on the sand, patio, or poolside
to get a gradual gentle tan. "There is no safe way to tan. How many
times do we have to say this? It increases melanoma risk absolutely,"
Naylor says.?
http://content.health.msn.com/content/article/82/97076.htm
?Ultraviolet (UV) radiation can damage DNA. Most melanomas have
abnormalities in their chromosomes, which is where DNA is found. This
damage makes the DNA less able to control how and when cells grow and
divide. In some situations, this results in the beginning of a cancer.
Most UV radiation comes from sunlight, but some may come from
artificial sources such as tanning booths. Some of this exposure may
have occurred within the few years before the beginning of the cancer.
However, much of it may be due to exposures that happened many years
earlier. Children and young adults often receive a lot of intense UV
sun exposure that may not result in an actual cancer for many years or
even decades.
Scientists continue to study connections between DNA and melanoma.
They have found the DNA of certain genes is often damaged in melanoma
cells. These DNA changes are not inherited. Instead they may be the
result of damage caused by sunlight. But there is evidence that some
people can repair their damaged DNA better than others and are less
likely to develop melanoma. In the future, better understanding of the
way these DNA changes lead to melanoma might be used in gene therapy
to overcome or repair that damage.?
http://www.cancer.org/docroot/CRI/content/CRI_2_4_2X_Do_we_know_what_causes_melanoma_50.asp?sitearea=
Here is what I found connecting insulin and melanoma:
?A number of studies have shown that insulin and insulin growth factor
stimulate melanoma cell growth, both in vivo and in vitro. However,
Kahn et al found that insulin can alternatively inhibit or stimulate
the proliferation of melanoma cells, depending on their genotype?
http://arpa.allenpress.com/arpaonline/?request=get-document&doi=10.1043%2F0003-9985(2001)125%3C1295:MM%3E2.0.CO%3B2
This study shows that Insulin-like growth factor may stimulate melanoma.
?Insulin-like growth factor-I (IGF-I) stimulates melanoma cells to
grow, survive, and
migrate.?
http://www.wistar.upenn.edu/herlyn/sup_pdfs/Satya_IL-8,_Cell_Growth_Diff.pd.pdf
?A better understanding of melanoma biology was made possible in
recent years by the development of tissue culture techniques and the
establishment of cell lines from normal epidermal melanocytes and
melanomas at different stages of progression . It has been
demonstrated that normal melanocytes require at least four mitogens to
grow in culture media: insulin or insulin-like growth factor,
fibroblast growth factor-alpha, melanocyte-stimulating hormone, and
phorbol esters. In contrast, cell lines derived from intermediate
stages of melanoma show successive loss of growth factor requirements,
and metastatic melanomas proliferate in the absence of any exogenous
proteins or phorbol esters. These findings support the hypothesis that
tumor cells produce autocrine growth factors and develop growth
autonomy?
http://www.cancernetwork.com/textbook/morev32.htm
?Melanocytes can form abnormal moles, also called atypical moles or
dysplastic nevi. These moles are not malignant themselves, but their
presence is a warning of an inherited tendency to develop melanoma.
Some people have only 1 or 2 atypical moles; some people may have more
than 100. The tendency to develop atypical moles can run in families
(inherited predisposition).?
http://content.health.msn.com/hw/cancer/hw206559.asp
You may also be referring to Acanthosis Nigricans, which while can
turn malignant (cancerous), it usually is not. Acanthosis Nigricans
has been confused with melanoma, but it is a hyperpigmentation
disorder.
The American Osteopathic College of Dermatology says ?Acanthosis
nigricans is a disorder that may begin at any age. It causes velvety,
light-brown-to-black, markings usually on the neck, under the arms or
in the groin. Acanthosis nigricans is most often associated with being
overweight.
Eating too much of the wrong foods, especially starches and sugars,
raises insulin levels. Most patients with acanthosis nigricans have a
high insulin level, higher than those of the same weight who don't
have acanthosis nigricans. Elevated levels of insulin in most cases
probably cause acanthosis nigricans. This happens when there is
insulin "spillover" into the skin. This activates insulin receptors in
the skin and forces it to grow abnormally. Reducing the circulating
insulin by a special diet can lead to a rapid improvement of the skin
problem.?
http://www.aocd.org/skin/dermatologic_diseases/acanthosis_nigrica.html
?While acanthosis nigricans may signal an underlying malignancy (e.g.,
gastrointestinal tumor), it more often is associated with insulin
resistance (type 2 diabetes, polycystic ovary syndrome) or obesity.?
Acanthosis Nigricans is caused by a stimulation of malanocytes and
other early skin cell proliferations, and some believe the stimulating
factor is insulin, or an insulin-like growth factor. In the malignant
form, stimulating factors may be a tumor produced substance, in
reaction to the tumor, and/or medications.
http://www.aafp.org/afp/20031115/1963.html
http://www.emedicine.com/derm/topic1.htm
According to this LookSmart article from American Family Physician,
Nov 15, 2003 by Daniel L. Stulberg, Nicole Clark, Daniel Tovey
?Acanthosis nigricans, usually related to insulin resistance or
obesity, ranges in appearance from a thickened, velvety brown
streaking to a leathery, verrucous, papillomatous lesion (Table 2).
The condition commonly occurs on the neck or in skin folds (e.g., in
the axilla, under the breast, at the belt line, in the groin), but it
may develop in other parts of the body. Patients with this condition
may complain that they have a "dirty area" that cannot be cleansed?
?It is important for physicians to recognize acanthosis nigricans,
because the condition can be associated with insulin resistance (as
occurs in type 2 diabetes and polycystic ovary syndrome), obesity and,
occasionally, malignancy. Type 2 diabetes is increasing in incidence
in the United States, especially among black and hispanic children; 60
to 92 percent of these children have acanthosis nigricans. According
to one study that compared 50 children with type 2 diabetes and 50
children with type 1 diabetes, acanthosis nigricans was present in 86
percent of the children with type 2 diabetes but in none of the
children with type 1 diabetes.
If a patient rapidly develops acanthosis nigricans, especially on the
palms or soles, occult malignancy is a possibility. A thorough
physical examination, a review of systems, a complete blood count,
fecal occult blood testing, and chest radiography should be considered
if the patient does not fit the typical clinical pattern of insulin
resistance. Adenocarcinomas are the most common malignancies found in
patients with acanthosis nigricans; the tumors are most often present
in the stomach (60 percent), followed by the colon, ovary, pancreas,
rectum, and uterus.?
http://articles.findarticles.com/p/articles/mi_m3225/is_10_68/ai_110488909
Photos of Acanthosis nigricans
http://www.atlas-dermato.org/images2/acanthosis29.jpg
http://tray.dermatology.uiowa.edu/Images/Clin/AcanNigr01.jpg
Additional Information:
A previously asked question regarding melanoma:
http://answers.google.com/answers/threadview?id=333242
As an interesting aside, insulin is being used to treat cancers in
this alternative medicine clinic! ? During IPT, a small dose of
insulin is given to the patient that induces a state of low blood
sugar (hypoglycemia). When the patient begins to have feelings of
lightheadedness and weakness, low dose chemotherapy is given
intravenously. The insulin fools the cells into thinking they are
going to be fed food, when in reality they are going to be destroyed
by chemotherapy. The doses of chemotherapy used during IPT are usually
one tenth to one fourth of the traditional doses given by oncologists,
therefore the side effects are minimal.?
http://www.caringmedical.com/symptoms/condition_detail.asp?condition_id=648
Tropical fish are helping scientists learn about melanoma.
http://www.cancerwise.org/May_2002/display.cfm?id=FB4FBA60-0465-406F-B13877C447FCEA26&method=displayFull&color=green
If you are concerned about moles you may have, print out this useful
chart, mark your moles and take it with you to your doctor.
http://www.mdanderson.org/pdf/skinchart.pdf
Hope this helps you out! If any part of my answer is unclear, please
request an Answer Clarification, before rating. This will allow me to
assist you further, if possible.
Sincerely,
crabcakes
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