BASAL CELL CARCINOMA

Basal cell carcinoma (BCC) is type of skin cancer that found the most in human. There are about one million American diagnosed and an estimated 20,000 people who die from skin cancer or basal cell carcinoma worldwide each year.

Basal cell carcinoma mostly appears on the face, ears shoulder and neck where the skin is easily exposed to sunlight or dust, X –ray treatment, low vitamins intake and some chemical may cause serious BCC. However, it can also appear on other parts of body such as the abdomen, leg, and scalp exposed to sun’s ultraviolet rays. Early diagnostic and treatment will help to reduce damage the skin and cause an ulcer known as a rodent ulcer. In some cases, contact with arsenic, exposure to radiation, open sores, lesions that do not heal, inflammatory skin conditions, and complications of burn scars, infection, vaccination, or even tattoos are contributing factors

Basal Cell Carcinoma Causes

-          There is some people develops basal cell carcinomas by exposed to fiberglass dust and dry cleaning. Also, prior non-diagnostic X-ray treatment for skin conditions increased risk of both cancers.

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-          Several studies have shown an association between cumulative ultraviolet exposure and risk of basal cell carcinoma, although the magnitude of risk conferred has been small.

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-          There is also other non-ultraviolet environmental exposures that have been associated with increased risk of basal cell carcinoma include ionizing radiation, high dietary energy (especially fat), low intake of vitamins, and various chemicals and dust. Exposure to arsenic predisposes to multiple basal cell carcinomas.

-          Lately UK has also been reported that 2% of such tumors could be associated with exposure to radon.

-          Some research found squamous cell carcinomas in people exposed to insecticides, herbicides, fungicides and seed treatments as well petroleum products, grease, and several other exposures.

Basal Cell Carcinoma Prevention

-          If you would like to get tan, do so slowly, starting at 15 minutes a day, max. Work up to greater exposure, but only if there is no damage, not even slight damage, to your skin. Basal cell carcinoma tends to be more virulent among people who get most of the tanning from tanning beds.

-          The most important nutrients for preventing basal cell carcinoma are antioxidants supplement and vegetable. The main principal is using n-acetyl cysteine (NAC), selenium, and vitamins C and E. NAC works synergistically with vitamins C and E to protect the “watchdog” gene p53 that keeps skin cells with damaged DNA from continuing to grow and multiply. Selenium and vitamin E help the skin make the “super-antioxidant” glutathione, and another antioxidant, alpha-lipoic acid, will help keep glutathione from being broken down in the liver. Alpha-lipoic acid is especially important for people who work or exercise outdoors.

-          What else can you do to relieve and prevent basal carcinoma? Number one, wear sunscreen or sun block lotion. The recommendation used to be to use at least SPF-15 on sun-exposed skin in the summer. Now more doctors tell their patients to use a stronger (higher number) sun screen any time of year.

Basal Cell Carcinoma Treatment

Treatment of BCC is depending on the size, depth, and location of the basal cell cancer. Here are treatments options that available include:

MOHS surgery

Radiation therapy

Cryosurgery (freezing cancer cells)

Topical chemotherapy

Photodynamic therapy.

Treating Basal cell with MOHS is by far the best way to prevent the Basal cell cancer from coming back (about a one percent chance of returning) while other types of basal cell treatment are less effective (about a ten percent return rate). MOHS is a surgical procedure that involves removing tumor tissue layer by layer. Each of the layers of removed tissue is then scanned for cancer cells under a microscope

SKIN DISEASES: VITILIGO

What is vitiligo, and what causes it?

Vitiligo (pronounced vit-ill-EYE-go) is a pigmentation disorder in which melanocytes (the cells that make pigment) in the skin are destroyed. As a result, white patches appear on the skin in different parts of the body. Similar patches also appear on both the mucous membranes (tissues that line the inside of the mouth and nose) and the retina (inner layer of the eyeball). The hair that grows on areas affected by vitiligo sometimes turns white.

The cause of vitiligo is not known, but doctors and researchers have several different theories. There is strong evidence that people with vitiligo inherit a group of three genes that make them susceptible to depigmentation. The most widely accepted view is that the depigmentation occurs because vitiligo is an autoimmune disease -- a disease in which a person's immune system reacts against the body's own organs or tissues. People's bodies produce proteins called cytokines that, in vitiligo, alter their pigment-producing cells and cause these cells to die. Another theory is that melanocytes destroy themselves. Finally, some people have reported that a single event such as sunburn or emotional distress triggered vitiligo; however, these events have not been scientifically proven as causes of vitiligo.

Who is affected by vitiligo?

About 0.5 to 1 percent of the world's population, or as many as 65 million people, have vitiligo. In the United States, 1 to 2 million people have the disorder. Half the people who have vitiligo develop it before age 20; most develop it before their 40th birthday. The disorder affects both sexes and all races equally; however, it is more noticeable in people with dark skin.

Vitiligo seems to be somewhat more common in people with certain autoimmune diseases, including hyperthyroidism (an overactive thyroid gland), adrenocortical insufficiency (the adrenal gland does not produce enough of the hormone called corticosteroid), alopecia areata (patches of baldness), and pernicious anemia (a low level of red blood cells caused by the failure of the body to absorb vitamin B₁₂). Scientists do not know the reason for the association between vitiligo and these autoimmune diseases. However, most people with vitiligo have no other autoimmune disease.

Vitiligo may also be hereditary; that is, it can run in families. Children whose parents have the disorder are more likely to develop vitiligo. In fact, 30 percent of people with vitiligo have a family member with the disease. However, only 5 to 7 percent of children will get vitiligo even if a parent has it, and most people with vitiligo do not have a family history of the disorder.

This year the San Raffaele Scientific Institute in Milano will host the First World Vitiligo Congress, between 23 - 24 September. This conference will focus on vitiligo cure research.

Anti-Vitiligo has originated in the subcontinent and its success in the brown races has been tested over centuries. Its recent availability across the globe has made it possible to evaluate its healing potential in other races as well, and the data has shown that success of anti-vitiligo is not specific to any race.
Anti-Vitiligo has been found to improve all variants of the vitiligo disorder including generalized vitiligo1 (universal vitiligo, acrofacial vitiligo and vitiligo vulgaris) and localized vitiligo1 (segmental vitiligo and focal vitiligo)


Vitiligo is a disorder characterized by patchy loss of skin pigmentation due to immune attacks on melanocytes, which can be caused by defects in many genes. Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo. The immune system genes are associated with other autoimmune disorders.
In one case, the gene TYR, which makes the melanocyte more susceptible to the immune system in vitiligo, also makes the melanocyte more susceptible to the immune system in the skin cancer malignant melanoma. So people with vitiligo caused by the TYR gene are less likely to have malignant melanoma.
A genomewide association study found 10 independent susceptibility loci for generalized vitiligo, responsible for 7.4% of the genetic risk. Some patients had vitiligo alone; others had generalized vitiligo with other autoimmune diseases. Most loci were associated with both forms. (The exception was PTPN22, which was only associated with generalized vitiligo.) In the MHC region, which controls the immune system, major association signals were identified in the class I gene region (between HLA-A and HLA-HGC9) and class II gene region (between HLA-DRB1 and HLA-DQA1). Outside the MHC region, association signals were identified near RERE, PTPN22, LPP, IL2RA, GZMB, UBASH3A and C1QTNF6 genes, which are associated with other autoimmune diseases. TYR encodes tyrosinase, which is not a component of the immune system, but is an enzyme of the melanocyte that catalyzes melanin biosynthesis, and a major autoantigen in generalized vitiligo. The major alleles of TYR are associated with vitiligo, and the minor alleles are associated with malignant melanoma. Vitiligo-associated 402R tyrosinase may be more efficiently presented to the immune system. Melanoma-associated 402Q may fail to be identified by the immune system.
The transcriptional profile of melanocytes from vitiligo patients have been studied. Oligonucleotide microarrays containing approximately 16,000 unique genes were used to analyse mRNA expression in melanocytes from vitiligo patients and age-matched healthy controls. In total, 859 genes were identified as differentially expressed.
Vitiligo is sometime associated with autoimmune and inflammatory diseases,commonly thyroid overexpression and underexpression. A study comparing 656 people with and without vitiligo in 114 families found several mutations (single-nucleotide polymorphisms) in the NALP1 gene.The NALP1 gene, which is on chromosome 17 located at 17p13, is on a cascade that regulates inflammation and cell death, including myeloid and lymphoid cells, which are white cells that are part of the immune response. NALP1 is expressed at high levels in T cells and Langerhan cells, white blood cells that are involved in skin autoimmunity.
Among the inflammatory products of NALP1 are caspase 1 and caspase 5, which activate the inflammatory cytokine interleukin-1β. Interleukin-1β is expressed at high levels in patients with vitiligo. There are compounds which inhibit caspase and interleukin-1β, and so might be useful drugs for vitiligo and associated autoimmune diseases. In one of the mutations, the amino acid leucine in the NALP1 protein was replaced by histidine (Leu155->His). The original protein and sequence is highly conserved in evolution, and found in humans, chimpanzee, rhesus monkey, and bush baby, which means that it is an important protein and an alteration is likely to be harmful. Addison's disease (typically an autoimmune destruction of the adrenal glands) may cause vitiligo.