The Skin Cancer Blog

Skin Cancer Treatment Tips

Mon, 23 Aug 2010 06:40:00 +0000

Skin cancer is the most common form of human cancer. It is evaluated that over 1 million new cases occur annually. Skin cancer is the most common form of cancer in the United States. Skin cancer generally develops in the epidermis (the outermost layer of skin), so a tumor is usually clearly visible. The two most common types are basal cell cancer and squamous cell cancer. It accounts for more than 75 percent of all skin cancers. Squamous cell carcinomas arise from the upper levels of the epidermis, usually on places that have been exposed to the sun. Squamous cell carcinoma also can spread internally. They account for about 20 percent of skin cancers in the United States.Melanoma is generally the most serious form of skin cancer because it tends to spread (metastasize) throughout the body quickly.

They usually form on the head, face, neck, hands and arms. Skin cancer is most closely associated with chronic inflammation of the skin. Sunburn or excessive sun damage, especially early in life. UVA & UVB have both been involved in causing DNA damage resulting in cancer. Chronic non-healing wounds, especially burns.

Treatment for skin cancer and the precancerous skin lesions known as actinic keratoses varies, depending on the size, type, depth and location of the lesions. The best ways to lower the risk of non-melanoma skin cancer are to avoid intense sunlight for long periods of time and to practice sun safety. For low-risk disease, radiation therapy and cryotherapy (freezing the cancer off) can provide adequate control of the disease; both, however, have lower overall cure rates than surgery.

Interferon and interleukin-2 are under study to treat melanoma and nonmelanoma skin cancers. Wear sunglasses with 99% to 100% UV absorption to provide optimal protection for the eyes and the surrounding skin. Wearing protective clothing (long sleeves and hats) when outdoors. Photodynamic therapy destroys skin cancer cells with a combination of laser light and drugs that makes cancer cells sensitive to light. Avoid other sources of UV light. Tanning beds and sun lamps are dangerous because they can damage your skin. Avoid the sun between 10 a.m. and 4 p.m. Radiation may destroy basal and squamous cell carcinomas if surgery isn’t an option. Reapply sun block every 2 hours and after swimming. In chemotherapy, drugs are used to kill cancer cells.

Skin Cancer Treatment and Prevention Tips

1. Radiation may destroy basal and squamous cell carcinomas.

2. Reducing exposure to ultraviolet (UV) radiation, especially in early years.

3. Avoiding sun exposure during the day (usually from 10 AM to 3 PM).

4. Wearing protective clothing (long sleeves and hats) when outdoors.

5. Using a broad-spectrum sunscreen that blocks both UVA and UVB radiation.

6. Wear sunglasses with 99% to 100% UV absorption to provide optimal protection for the eyes.

Juliet Cohen writes articles for women health blog and skin treatment. She also writes articles for hair styles.
Article Sourceskin cancer

Cell Nucleus

Sun, 22 Aug 2010 09:28:29 +0000

History

Oldest known depiction of cells and their nuclei by Antonie van Leeuwenhoek, 1719.

Drawing of a Chironomus salivary gland cell published by Walther Flemming in 1882. The nucleus contains Polytene chromosomes.

The nucleus was the first organelle to be discovered. The probably oldest preserved drawing dates back to the early microscopist Antonie van Leeuwenhoek (1632 1723). He observed a “Lumen”, the nucleus, in the red blood cells of salmon. Unlike mammalian red blood cells, those of other vertebrates still possess nuclei. The nucleus was also described by Franz Bauer in 1804 and in more detail in 1831 by Scottish botanist Robert Brown in a talk at the Linnean Society of London. Brown was studying orchids microscopically when he observed an opaque area, which he called the areola or nucleus, in the cells of the flower’s outer layer. He did not suggest a potential function. In 1838 Matthias Schleiden proposed that the nucleus plays a role in generating cells, thus he introduced the name “Cytoblast” (cell builder). He believed that he had observed new cells assembling around “cytoblasts”. Franz Meyen was a strong opponent of this view having already described cells multiplying by division and believing that many cells would have no nuclei. The idea that cells can be generated de novo, by the “cytoblast” or otherwise, contradicted work by Robert Remak (1852) and Rudolf Virchow (1855) who decisively propagated the new paradigm that cells are generated solely by cells (“Omnis cellula e cellula”). The function of the nucleus remained unclear.

Between 1876 and 1878 Oscar Hertwig published several studies on the fertilization of sea urchin eggs, showing that the nucleus of the sperm enters the oocyte and fuses with its nucleus. This was the first time it was suggested that an individual develops from a (single) nucleated cell. This was in contradiction to Ernst Haeckel’s theory that the complete phylogeny of a species would be repeated during embryonic development, including generation of the first nucleated cell from a “Monerula”, a structureless mass of primordial mucus (“Urschleim”). Therefore, the necessity of the sperm nucleus for fertilization was discussed for quite some time. However, Hertwig confirmed his observation in other animal groups, e.g. amphibians and molluscs. Eduard Strasburger produced the same results for plants (1884). This paved the way to assign the nucleus an important role in heredity. In 1873 August Weismann postulated the equivalence of the maternal and paternal germ cells for heredity. The function of the nucleus as carrier of genetic information became clear only later, after mitosis was discovered and the Mendelian rules were rediscovered at the beginning of the 20th century; the chromosome theory of heredity was developed. :)

Structures

The nucleus is the largest cellular organelle in animals. In mammalian cells, the average diameter of the nucleus is approximately 6 micrometers (m), which occupies about 10% of the total cell volume. The viscous liquid within it is called nucleoplasm, and is similar in composition to the cytosol found outside the nucleus. It appears as a dense, roughly spherical organelle.

Nuclear envelope and pores

Main articles: Nuclear envelope and Nuclear pores

The eukaryotic cell nucleus. Visible in this diagram are the ribosome-studded double membranes of the nuclear envelope, the DNA (complexed as chromatin), and the nucleolus. Within the cell nucleus is a viscous liquid called nucleoplasm, similar to the cytoplasm found outside the nucleus.

A cross section of a nuclear pore on the surface of the nuclear envelope (1). Other diagram labels show (2) the outer ring, (3) spokes, (4) basket, and (5) filaments.

The nuclear envelope otherwise known as nuclear membrane consists of two cellular membranes, an inner and an outer membrane, arranged parallel to one another and separated by 10 to 50 nanometers (nm). The nuclear envelope completely encloses the nucleus and separates the cell’s genetic material from the surrounding cytoplasm, serving as a barrier to prevent macromolecules from diffusing freely between the nucleoplasm and the cytoplasm. The outer nuclear membrane is continuous with the membrane of the rough endoplasmic reticulum (RER), and is similarly studded with ribosomes. The space between the membranes is called the perinuclear space and is continuous with the RER lumen.

Nuclear pores, which provide aqueous channels through the envelope, are composed of multiple proteins, collectively referred to as nucleoporins. The pores are about 125 million daltons in molecular weight and consist of around 50 (in yeast) to 100 proteins (in vertebrates). The pores are 100 nm in total diameter; however, the gap through which molecules freely diffuse is only about 9 nm wide, due to the presence of regulatory systems within the center of the pore. This size allows the free passage of small water-soluble molecules while preventing larger molecules, such as nucleic acids and larger proteins, from inappropriately entering or exiting the nucleus. These large molecules must be actively transported into the nucleus instead. The nucleus of a typical mammalian cell will have about 3000 to 4000 pores throughout its envelope, each of which contains a donut-shaped, eightfold-symmetric ring-shaped structure at a position where the inner and outer membranes fuse. Attached to the ring is a structure called the nuclear basket that extends into the nucleoplasm, and a series of filamentous extensions that reach into the cytoplasm. Both structures serve to mediate binding to nuclear transport proteins.

Most proteins, ribosomal subunits, and some RNAs are transported through the pore complexes in a process mediated by a family of transport factors known as karyopherins. Those karyopherins that mediate movement into the nucleus are also called importins, while those that mediate movement out of the nucleus are called exportins. Most karyopherins interact directly with their cargo, although some use adaptor proteins. Steroid hormones such as cortisol and aldosterone, as well as other small lipid-soluble molecules involved in intercellular signaling can diffuse through the cell membrane and into the cytoplasm, where they bind nuclear receptor proteins that are trafficked into the nucleus. There they serve as transcription factors when bound to their ligand; in the absence of ligand many such receptors function as histone deacetylases that repress gene expression.

Nuclear lamina

Main article: Nuclear lamina

In animal cells, two networks of intermediate filaments provide the nucleus with mechanical support: the nuclear lamina forms an organized meshwork on the internal face of the envelope, while less organized support is provided on the cytosolic face of the envelope. Both systems provide structural support for the nuclear envelope and anchoring sites for chromosomes and nuclear pores.

The nuclear lamina is mostly composed of lamin proteins. Like all proteins, lamins are synthesized in the cytoplasm and later transported into the nucleus interior, where they are assembled before being incorporated into the existing network of nuclear lamina. Lamins are also found inside the nucleoplasm where they form another regular structure, known as the nucleoplasmic veil, that is visible using fluorescence microscopy. The actual function of the veil is not clear, although it is excluded from the nucleolus and is present during interphase. The lamin structures that make up the veil bind chromatin and disrupting their structure inhibits transcription of protein-coding genes.

Like the components of other intermediate filaments, the lamin monomer contains an alpha-helical domain used by two monomers to coil around each other, forming a dimer structure called a coiled coil. Two of these dimer structures then join side by side, in an antiparallel arrangement, to form a tetramer called a protofilament. Eight of these protofilaments form a lateral arrangement that is twisted to form a ropelike filament. These filaments can be assembled or disassembled in a dynamic manner, meaning that changes in the length of the filament depend on the competing rates of filament addition and removal.

Mutations in lamin genes leading to defects in filament assembly are known as laminopathies. The most notable laminopathy is the family of diseases known as progeria, which causes the appearance of premature aging in its sufferers. The exact mechanism by which the associated biochemical changes give rise to the aged phenotype is not well understood.

Chromosomes

Main article: Chromosome

A mouse fibroblast nucleus in which DNA is stained blue. The distinct chromosome territories of chromosome 2 (red) and chromosome 9 (green) are visible stained with fluorescent in situ hybridization.

The cell nucleus contains the majority of the cell’s genetic material, in the form of multiple linear DNA molecules organized into structures called chromosomes. During most of the cell cycle these are organized in a DNA-protein complex known as chromatin, and during cell division the chromatin can be seen to form the well defined chromosomes familiar from a karyotype. A small fraction of the cell’s genes are located instead in the mitochondria.

There are two types of chromatin. Euchromatin is the less compact DNA form, and contains genes that are frequently expressed by the cell. The other type, heterochromatin, is the more compact form, and contains DNA that are infrequently transcribed. This structure is further categorized into facultative heterochromatin, consisting of genes that are organized as heterochromatin only in certain cell types or at certain stages of development, and constitutive heterochromatin that consists of chromosome structural components such as telomeres and centromeres. During interphase the chromatin organizes itself into discrete individual patches, called chromosome territories. Active genes, which are generally found in the euchromatic region of the chromosome, tend to be located towards the chromosome’s territory boundary.

Antibodies to certain types of chromatin organization, particularly nucleosomes, have been associated with a number of autoimmune diseases, such as systemic lupus erythematosus. These are known as anti-nuclear antibodies (ANA) and have also been observed in concert with multiple sclerosis as part of general immune system dysfunction. As in the case of progeria, the role played by the antibodies in inducing the symptoms of autoimmune diseases is not obvious.

Nucleolus

Main article: Nucleolus

An electron micrograph of a cell nucleus, showing the darkly stained nucleolus.

The nucleolus is a discrete densely stained structure found in the nucleus. It is not surrounded by a membrane, and is sometimes called a suborganelle. It forms around tandem repeats of rDNA, DNA coding for ribosomal RNA (rRNA). These regions are called nucleolar organizer regions (NOR). The main roles of the nucleolus are to synthesize rRNA and assemble ribosomes. The structural cohesion of the nucleolus depends on its activity, as ribosomal assembly in the nucleolus results in the transient association of nucleolar components, facilitating further ribosomal assembly, and hence further association. This model is supported by observations that inactivation of rDNA results in intermingling of nucleolar structures.

The first step in ribosomal assembly is transcription of the rDNA, by a protein called RNA polymerase I, forming a large pre-rRNA precursor. This is cleaved into the subunits 5.8S, 18S, and 28S rRNA. The transcription, post-transcriptional processing, and assembly of rRNA occurs in the nucleolus, aided by small nucleolar RNA (snoRNA) molecules, some of which are derived from spliced introns from messenger RNAs encoding genes related to ribosomal function. The assembled ribosomal subunits are the largest structures passed through the nuclear pores.

When observed under the electron microscope, the nucleolus can be seen to consist of three distinguishable regions: the innermost fibrillar centers (FCs), surrounded by the dense fibrillar component (DFC), which in turn is bordered by the granular component (GC). Transcription of the rDNA occurs either in the FC or at the FC-DFC boundary, and therefore when rDNA transcription in the cell is increased more FCs are detected. Most of the cleavage and modification of rRNAs occurs in the DFC, while the latter steps involving protein assembly onto the ribosomal subunits occurs in the GC.

Other subnuclear bodies

Subnuclear structure sizes

Structure name

Structure diameter

Cajal bodies

0.22.0 m

PIKA

5 m

PML bodies

0.21.0 m

Paraspeckles

0.21.0 m

Speckles

2025 nm

Besides the nucleolus, the nucleus contains a number of other non-membrane delineated bodies. These include Cajal bodies, Gemini of coiled bodies, polymorphic interphase karyosomal association (PIKA), promyelocytic leukaemia (PML) bodies, paraspeckles and splicing speckles. Although little is known about a number of these domains, they are significant in that they show that the nucleoplasm is not uniform mixture, but rather contains organized functional subdomains.

Other subnuclear structures appear as part of abnormal disease processes. For example, the presence of small intranuclear rods have been reported in some cases of nemaline myopathy. This condition typically results from mutations in actin, and the rods themselves consist of mutant actin as well as other cytoskeletal proteins.

Cajal bodies and gems

A nucleus typically contains between 1 and 10 compact structures called Cajal bodies or coiled bodies (CB), whose diameter measures between 0.2 m and 2.0 m depending on the cell type and species. When seen under an electron microscope, they resemble balls of tangled thread and are dense foci of distribution for the protein coilin. CBs are involved in a number of different roles relating to RNA processing, specifically small nucleolar RNA (snoRNA) and small nuclear RNA (snRNA) maturation, and histone mRNA modification.

Similar to Cajal bodies are Gemini of coiled bodies, or gems, whose name is derived from the Gemini constellation in reference to their close “twin” relationship with CBs. Gems are similar in size and shape to CBs, and in fact are virtually indistinguishable under the microscope. Unlike CBs, gems do not contain small nuclear ribonucleoproteins (snRNPs), but do contain a protein called survivor of motor neurons (SMN) whose function relates to snRNP biogenesis. Gems are believed to assist CBs in snRNP biogenesis, though it has also been suggested from microscopy evidence that CBs and gems are different manifestations of the same structure.

PIKA and PTF domains

PIKA domains, or polymorphic interphase karyosomal associations, were first described in microscopy studies in 1991. Their function was and remains unclear, though they were not thought to be associated with active DNA replication, transcription, or RNA processing. They have been found to often associate with discrete domains defined by dense localization of the transcription factor PTF, which promotes transcription of snRNA.

PML bodies

Promyelocytic leukaemia bodies (PML bodies) are spherical bodies found scattered throughout the nucleoplasm, measuring around 0.21.0 m. They are known by a number of other names, including nuclear domain 10 (ND10), Kremer bodies, and PML oncogenic domains. They are often seen in the nucleus in association with Cajal bodies and cleavage bodies. It has been suggested that they play a role in regulating transcription.

Paraspeckles

Main article: Paraspeckle

Discovered by Fox et al. in 2002, paraspeckles are irregularly shaped compartments in the nucleus’ interchromatin space. First documented in HeLa cells, where there are generally 1030 per nucleus, paraspeckles are now known to also exist in all human primary cells, transformed cell lines and tissue sections. Their name is derived from their distribution in the nucleus; the “para” is short for parallel and the “speckles” refers to the splicing speckles to which they are always in close proximity.

Paraspeckles are dynamic structures that are altered in response to changes in cellular metabolic activity. They are transcription dependent and in the absence of RNA Pol II transcription, the paraspeckle disappears and all of its associated protein components (PSP1, p54nrb, PSP2, CFI(m)68 and PSF) form a crescent shaped perinucleolar cap in the nucleolus. This phenomenon is demonstrated during the cell cycle. In the cell cycle, paraspeckles are present during interphase and during all of mitosis except for telophase. During telophase, when the two daughter nuclei are formed, there is no RNA Pol II transcription so the protein components instead form a perinucleolar cap.

Splicing speckles

Sometimes referred to as interchromatin granule clusters or as splicing-factor compartments, speckles are rich in splicing snRNPs and other splicing proteins necessary for pre-mRNA processing. Because of a cell’s changing requirements, the composition and location of these bodies changes according to mRNA transcription and regulation via phosphorylation of specific proteins.

Function

The main function of the cell nucleus is to control gene expression and mediate the replication of DNA during the cell cycle. The nucleus provides a site for genetic transcription that is segregated from the location of translation in the cytoplasm, allowing levels of gene regulation that are not available to prokaryotes.

Cell compartmentalization

The nuclear envelope allows the nucleus to control its contents, and separate them from the rest of the cytoplasm where necessary. This is important for controlling processes on either side of the nuclear membrane. In some cases where a cytoplasmic process needs to be restricted, a key participant is removed to the nucleus, where it interacts with transcription factors to downregulate the production of certain enzymes in the pathway. This regulatory mechanism occurs in the case of glycolysis, a cellular pathway for breaking down glucose to produce energy. Hexokinase is an enzyme responsible for the first the step of glycolysis, forming glucose-6-phosphate from glucose. At high concentrations of fructose-6-phosphate, a molecule made later from glucose-6-phosphate, a regulator protein removes hexokinase to the nucleus, where it forms a transcriptional repressor complex with nuclear proteins to reduce the expression of genes involved in glycolysis.

In order to control which genes are being transcribed, the cell separates some transcription factor proteins responsible for regulating gene expression from physical access to the DNA until they are activated by other signaling pathways. This prevents even low levels of inappropriate gene expression. For example in the case of NF-B-controlled genes, which are involved in most inflammatory responses, transcription is induced in response to a signal pathway such as that initiated by the signaling molecule TNF-, binds to a cell membrane receptor, resulting in the recruitment of signalling proteins, and eventually activating the transcription factor NF-B. A nuclear localisation signal on the NF-B protein allows it to be transported through the nuclear pore and into the nucleus, where it stimulates the transcription of the target genes.

The compartmentalization allows the cell to prevent translation of unspliced mRNA. Eukaryotic mRNA contains introns that must be removed before being translated to produce functional proteins. The splicing is done inside the nucleus before the mRNA can be accessed by ribosomes for translation. Without the nucleus ribosomes would translate newly transcribed (unprocessed) mRNA resulting in misformed and nonfunctional proteins.

Gene expression

Main article: Gene expression

A micrograph of ongoing gene transcription of ribosomal RNA illustrating the growing primary transcripts. “Begin” indicates the 3′ end of the DNA, where new RNA synthesis begins; “end” indicates the 5′ end, where the primary transcripts are almost complete.

Gene expression first involves transcription, in which DNA is used as a template to produce RNA. In the case of genes encoding proteins, that RNA produced from this process is messenger RNA (mRNA), which then needs to be translated by ribosomes to form a protein. As ribosomes are located outside the nucleus, mRNA produced needs to be exported.

Since the nucleus is the site of transcription, it also contains a variety of proteins which either directly mediate transcription or are involved in regulating the process. These proteins include helicases that unwind the double-stranded DNA molecule to facilitate access to it, RNA polymerases that synthesize the growing RNA molecule, topoisomerases that change the amount of supercoiling in DNA, helping it wind and unwind, as well as a large variety of transcription factors that regulate expression.

Processing of pre-mRNA

Main article: Post-transcriptional modification

Newly synthesized mRNA molecules are known as primary transcripts or pre-mRNA. They must undergo post-transcriptional modification in the nucleus before being exported to the cytoplasm; mRNA that appears in the nucleus without these modifications is degraded rather than used for protein translation. The three main modifications are 5′ capping, 3′ polyadenylation, and RNA splicing. While in the nucleus, pre-mRNA is associated with a variety of proteins in complexes known as heterogeneous ribonucleoprotein particles (hnRNPs). Addition of the 5′ cap occurs co-transcriptionally and is the first step in post-transcriptional modification. The 3′ poly-adenine tail is only added after transcription is complete.

RNA splicing, carried out by a complex called the spliceosome, is the process by which introns, or regions of DNA that do not code for protein, are removed from the pre-mRNA and the remaining exons connected to re-form a single continuous molecule. This process normally occurs after 5′ capping and 3′ polyadenylation but can begin before synthesis is complete in transcripts with many exons. Many pre-mRNAs, including those encoding antibodies, can be spliced in multiple ways to produce different mature mRNAs that encode different protein sequences. This process is known as alternative splicing, and allows production of a large variety of proteins from a limited amount of DNA.

Dynamics and regulation

Nuclear transport

Main article: Nuclear transport

Macromolecules, such as RNA and proteins, are actively transported across the nuclear membrane in a process called the Ran-GTP nuclear transport cycle.

The entry and exit of large molecules from the nucleus is tightly controlled by the nuclear pore complexes. Although small molecules can enter the nucleus without regulation, macromolecules such as RNA and proteins require association karyopherins called importins to enter the nucleus and exportins to exit. “Cargo” proteins that must be translocated from the cytoplasm to the nucleus contain short amino acid sequences known as nuclear localization signals which are bound by importins, while those transported from the nucleus to the cytoplasm carry nuclear export signals bound by exportins. The ability of importins and exportins to transport their cargo is regulated by GTPases, enzymes that hydrolyze the molecule guanosine triphosphate to release energy. The key GTPase in nuclear transport is Ran, which can bind either GTP or GDP (guanosine diphosphate) depending on whether it is located in the nucleus or the cytoplasm. Whereas importins depend on RanGTP to dissociate from their cargo, exportins require RanGTP in order to bind to their cargo.

Nuclear import depends on the importin binding its cargo in the cytoplasm and carrying it through the nuclear pore into the nucleus. Inside the nucleus, RanGTP acts to separate the cargo from the importin, allowing the importin to exit the nucleus and be reused. Nuclear export is similar, as the exportin binds the cargo inside the nucleus in a process facilitated by RanGTP, exits through the nuclear pore, and separates from its cargo in the cytoplasm.

Specialized export proteins exist for translocation of mature mRNA and tRNA to the cytoplasm after post-transcriptional modification is complete. This quality-control mechanism is important due to the these molecules’ central role in protein translation; mis-expression of a protein due to incomplete excision of exons or mis-incorporation of amino acids could have negative consequences for the cell; thus incompletely modified RNA that reaches the cytoplasm is degraded rather than used in translation.

Assembly and disassembly

An image of a newt lung cell stained with fluorescent dyes during metaphase. The mitotic spindle can be seen, stained green, attached to the two sets of chromosomes, stained light blue. All chromosomes but one are already at the metaphase plate.

During its lifetime a nucleus may be broken down, either in the process of cell division or as a consequence of apoptosis, a regulated form of cell death. During these events, the structural components of the nucleushe envelope and laminare systematically degraded.

During the cell cycle the cell divides to form two cells. In order for this process to be possible, each of the new daughter cells must have a full set of genes, a process requiring replication of the chromosomes as well as segregation of the separate sets. This occurs by the replicated chromosomes, the sister chromatids, attaching to microtubules, which in turn are attached to different centrosomes. The sister chromatids can then be pulled to separate locations in the cell. In many cells the centrosome is located in the cytoplasm, outside the nucleus, the microtubules would be unable to attach to the chromatids in the presence of the nuclear envelope. Therefore the early stages in the cell cycle, beginning in prophase and until around prometaphase, the nuclear membrane is dismantled. Likewise, during the same period, the nuclear lamina is also disassembled, a process regulated by phosphorylation of the lamins. Towards the end of the cell cycle, the nuclear membrane is reformed, and around the same time, the nuclear lamina are reassembled by dephosphorylating the lamins.

However, in dinoflagellates the nuclear envelope remains intact, the centrosomes are located in the cytoplasm, and the microtubules come in contact with chromosomes, whose centromeric regions are incorporated into the nuclear envelope (the so-called closed mitosis with extranuclear spindle). In many other protists (e.g. ciliates, sporozoans) and fungi the centrosomes are intranuclear, and their nuclear envelope also does not disassemle during cell division.

Apoptosis is a controlled process in which the cell’s structural components are destroyed, resulting in death of the cell. Changes associated with apoptosis directly affect the nucleus and its contents, for example in the condensation of chromatin and the disintegration of the nuclear envelope and lamina. The destruction of the lamin networks is controlled by specialized apoptotic proteases called caspases, which cleave the lamin proteins and thus degrade the nucleus’ structural integrity. Lamin cleavage is sometimes used as a laboratory indicator of caspase activity in assays for early apoptotic activity. Cells that express mutant caspase-resistant lamins are deficient in nuclear changes related to apoptosis, suggesting that lamins play a role in initiating the events that lead to apoptotic degradation of the nucleus. Inhibition of lamin assembly itself is an inducer of apoptosis.

The nuclear envelope acts as a barrier that prevents both DNA and RNA viruses from entering the nucleus. Some viruses require access to proteins inside the nucleus in order to replicate and/or assemble. DNA viruses, such as herpesvirus replicate and assemble in the cell nucleus, and exit by budding through the inner nuclear membrane. This process is accompanied by disassembly of the lamina on the nuclear face of the inner membrane.

Anucleated and polynucleated cells

Human red blood cells, like those of other mammals, lack nuclei. This occurs as a normal part of the cells’ development.

Although most cells have a single nucleus, some eukaryotic cell types have no nucleus, and others have many nuclei. This can be a normal process, as in the maturation of mammalian red blood cells, or a result of faulty cell division.

Anucleated cells contain no nucleus and are therefore incapable of dividing to produce daughter cells. The best-known anucleated cell is the mammalian red blood cell, or erythrocyte, which also lacks other organelles such as mitochondria and serves primarily as a transport vessel to ferry oxygen from the lungs to the body’s tissues. Erythrocytes mature through erythropoiesis in the bone marrow, where they lose their nuclei, organelles, and ribosomes. The nucleus is expelled during the process of differentiation from an erythroblast to a reticulocyte, which is the immediate precursor of the mature erythrocyte. The presence of mutagens may induce the release of some immature “micronucleated” erythrocytes into the bloodstream. Anucleated cells can also arise from flawed cell division in which one daughter lacks a nucleus and the other has two nuclei.

Polynucleated cells contain multiple nuclei. Most Acantharean species of protozoa and some fungi in mycorrhizae have naturally polynucleated cells. Other examples include the intestinal parasites in the genus Giardia, which have two nuclei per cell. In humans, skeletal muscle cells, called myocytes, become polynucleated during development; the resulting arrangement of nuclei near the periphery of the cells allows maximal intracellular space for myofibrils. Multinucleated cells can also be abnormal in humans; for example, cells arising from the fusion of monocytes and macrophages, known as giant multinucleated cells, sometimes accompany inflammation and are also implicated in tumor formation.

Evolution

As the major defining characteristic of the eukaryotic cell, the nucleus’ evolutionary origin has been the subject of much speculation. Four major theories have been proposed to explain the existence of the nucleus, although none have yet earned widespread support.

The theory known as the “syntrophic model” proposes that a symbiotic relationship between the archaea and bacteria created the nucleus-containing eukaryotic cell. It is hypothesized that the symbiosis originated when ancient archaea, similar to modern methanogenic archaea, invaded and lived within bacteria similar to modern myxobacteria, eventually forming the early nucleus. This theory is analogous to the accepted theory for the origin of eukaryotic mitochondria and chloroplasts, which are thought to have developed from a similar endosymbiotic relationship between proto-eukaryotes and aerobic bacteria. The archaeal origin of the nucleus is supported by observations that archaea and eukarya have similar genes for certain proteins, including histones. Observations that myxobacteria are motile, can form multicellular complexes, and possess kinases and G proteins similar to eukarya, support a bacterial origin for the eukaryotic cell.

A second model proposes that proto-eukaryotic cells evolved from bacteria without an endosymbiotic stage. This model is based on the existence of modern planctomycetes bacteria that possess a nuclear structure with primitive pores and other compartmentalized membrane structures. A similar proposal states that a eukaryote-like cell, the chronocyte, evolved first and phagocytosed archaea and bacteria to generate the nucleus and the eukaryotic cell.

The most controversial model, known as viral eukaryogenesis, posits that the membrane-bound nucleus, along with other eukaryotic features, originated from the infection of a prokaryote by a virus. The suggestion is based on similarities between eukaryotes and viruses such as linear DNA strands, mRNA capping, and tight binding to proteins (analogizing histones to viral envelopes). One version of the proposal suggests that the nucleus evolved in concert with phagocytosis to form an early cellular “predator”. Another variant proposes that eukaryotes originated from early archaea infected by poxviruses, on the basis of observed similarity between the DNA polymerases in modern poxviruses and eukaryotes. It has been suggested that the unresolved question of the evolution of sex could be related to the viral eukaryogenesis hypothesis.

Finally, a very recent proposal suggests that traditional variants of the endosymbiont theory are insufficiently powerful to explain the origin of the eukaryotic nucleus. This model, termed the exomembrane hypothesis, suggests that the nucleus instead originated from a single ancestral cell that evolved a second exterior cell membrane; the interior membrane enclosing the original cell then became the nuclear membrane and evolved increasingly elaborate pore structures for passage of internally synthesized cellular components such as ribosomal subunits.

References

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^ Spann TP, Goldman AE, Wang C, Huang S, Goldman RD. (2002). “Alteration of nuclear lamin organization inhibits RNA polymerase IIependent transcription”. Journal of Cell Biology 156 (4): 603608. doi:10.1083/jcb.200112047. PMID 11854306.

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^ NF Rothfield, BD Stollar (1967). “The Relation of Immunoglobulin Class, Pattern of Antinuclear Antibody, and Complement-Fixing Antibodies to DNA in Sera from Patients with Systemic Lupus Erythematosus”. J Clin Invest 46 (11): 17851794. doi:10.1172/JCI105669 (inactive 2009-11-14). PMID 4168731.

^ S Barned, AD Goodman, DH Mattson (1995). “Frequency of anti-nuclear antibodies in multiple sclerosis”. Neurology 45 (2): 384385. PMID 7854544.

^ Hernandez-Verdun, Daniele (2006). “Nucleolus: from structure to dynamics”. Histochem. Cell. Biol 125 (125): 127137. doi:10.1007/s00418-005-0046-4.

^ a b Lamond, Angus I.; Judith E. Sleeman. “Nuclear substructure and dynamics”. Current Biology 13 (21): R825828. doi:10.1016/j.cub.2003.10.012. PMID 14588256.

^ a b c Cioce M, Lamond A. “Cajal bodies: a long history of discovery”. Annu Rev Cell Dev Biol 21: 105131. doi:10.1146/annurev.cellbio.20.010403.103738. PMID 16212489.

^ a b c Pollard, Thomas D.; William C. Earnshaw (2004). Cell Biology. Philadelphia: Saunders. ISBN 0-7216-3360-9.

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^ Fox, Archa. Interview with R. Sundby. Paraspeckle Size. E-mail Correspondence. 2007-03-07.

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^ Pombo A, Cuello P, Schul W, Yoon J, Roeder R, Cook P, Murphy S (1998). “Regional and temporal specialization in the nucleus: a transcriptionally active nuclear domain rich in PTF, Oct1 and PIKA antigens associates with specific chromosomes early in the cell cycle”. EMBO J 17 (6): 17681778. doi:10.1093/emboj/17.6.1768. PMID 9501098.

^ a b Fox, Archa; Lam, YW; Leung, AK; Lyon, CE; Andersen, J; Mann, M; Lamond, AI (2002). “Paraspeckles:A Novel Nuclear Domain”. Current Biology 12 (1): 1325. doi:10.1016/S0960-9822(01)00632-7. PMID 11790299. http://www.current-biology.com/content/article/abstract?uid=PIIS0960982201006327.

^ a b Fox, Archa; Wendy Bickmore (2004). “Nuclear Compartments: Paraspeckles”. Nuclear Protein Database. http://npd.hgu.mrc.ac.uk/compartments/paraspeckles.html. Retrieved 2007-03-06.

^ a b Fox, A. et al. (2005). “P54nrb Forms a Heterodimer with PSP1 That Localizes to Paraspeckles in an RNA-dependent Manner”. Molecular Biology of the Cell 16: 53045315. doi:10.1091/mbc.E05-06-0587. PMID 16148043. http://www.molbiolcell.org/cgi/reprint/16/11/5304. PMID 16148043

^ Lamond AI, Spector DL (August 2003). “Nuclear speckles: a model for nuclear organelles”. Nat. Rev. Mol. Cell Biol. 4 (8): 60512. doi:10.1038/nrm1172. PMID 12923522.

^ Handwerger, Korie E.; Joseph G. Gall (January 2006). “Subnuclear organelles: new insights into form and function”. TRENDS in Cell Biology 16 (1): 1926. doi:10.1016/j.tcb.2005.11.005. PMID 16325406.

^ Lehninger, Albert L.; David L. Nelson, Michael M. Cox. (2000). Lehninger principles of biochemistry (3rd ed.). New York: Worth Publishers. ISBN 1-57259-931-6.

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^ Grlich, Dirk; Ulrike Kutay (1999). “Transport between the cell nucleus and the cytoplasm”. Ann. Rev. Cell Dev. Biol. (15): 607660. doi:10.1042/BST0330265. PMID 10611974.

^ Nierhaus, Knud H.; Daniel N. Wilson (2004). Protein Synthesis and Ribosome Structure: Translating the Genome. Wiley-VCH. ISBN 3527306382.

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^ Torous, DK; Dertinger SD, Hall NE, Tometsko CR. (2000). “Enumeration of micronucleated reticulocytes in rat peripheral blood: a flow cytometric study”. Mutat Res (465(12)): 9199. doi:10.1083/jcb.153.3.621. PMID 10708974.

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^ Pennisi E. (2004). “Evolutionary biology. The birth of the nucleus”. Science 305 (5685): 766768. doi:10.1126/science.305.5685.766. PMID 15297641.

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Further reading

Goldman, Robert D.; Gruenbaum, Y; Moir, RD; Shumaker, DK; Spann, TP (2002). “Nuclear lamins: building blocks of nuclear architecture”. Genes & Dev. 16 (16): 533547. doi:10.1101/gad.960502. PMID 11877373.

A review article about nuclear lamins, explaining their structure and various roles

Grlich, Dirk; Kutay, U (1999). “Transport between the cell nucleus and the cytoplasm”. Ann. Rev. Cell Dev. Biol. 15 (15): 607660. doi:10.1146/annurev.cellbio.15.1.607. PMID 10611974.

A review article about nuclear transport, explains the principles of the mechanism, and the various transport pathways

Lamond, Angus I.; Earnshaw, WC (1998-04-24). “Structure and Function in the Nucleus”. Science 280 (5363): 547553. doi:10.1126/science.280.5363.547. PMID 9554838.

A review article about the nucleus, explaining the structure of chromosomes within the organelle, and describing the nucleolus and other subnuclear bodies

Pennisi E. (2004). “Evolutionary biology. The birth of the nucleus”. Science 305 (5685): 766768. doi:10.1126/science.305.5685.766. PMID 15297641.

A review article about the evolution of the nucleus, explaining a number of different theories

Pollard, Thomas D.; William C. Earnshaw (2004). Cell Biology. Philadelphia: Saunders. ISBN 0-7216-3360-9.

A university level textbook focusing on cell biology. Contains information on nucleus structure and function, including nuclear transport, and subnuclear domains

External links

cellnucleus.com Website covering structure and function of the nucleus from the Department of Oncology at the University of Alberta.

The Nuclear Protein Database Information on nuclear components.

The Nucleus Collection in the Image & Video Library of The American Society for Cell Biology contains peer-reviewed still images and video clips that illustrate the nucleus.

Nuclear Envelope and Nuclear Import Section from Landmark Papers in Cell Biology, Joseph G. Gall, J. Richard McIntosh, eds., contains digitized commentaries and links to seminal research papers on the nucleus. Published online in the Image & Video Library of The American Society for Cell Biology

Cytoplasmic patterns generated by human antibodies

Gallery of nucleus images

Comparison of human and chimpanzee chromosomes.

Mouse chromosome territories in different cell types.

24 chromosome territories in human cells.

v d e

Structures of the cell

Endomembrane system

Cell membrane – Nucleus (and Nucleolus) – Endoplasmic reticulum – Golgi apparatus – Peroxisome – Parenthesome

Vesicles (Exosome – Lysosome – Endosome – Phagosome – Vacuole)

Cytoplasmic granules (Melanosome – Microbody – Glyoxysome – Weibel-Palade body)

Endosymbionts

Mitochondrion – Plastids (Chloroplast – Chromoplast – Leucoplast)

Cytoskeleton

Microfilaments – Intermediate filaments – Microtubules – Prokaryotic cytoskeleton

External

Cell wall – Cilium/Flagellum – Acrosome

Other

Cytoplasm – Ribosome – MTOCs (Centrosome/Centriole – Basal body – Spindle pole body) – Vault – Proteasome

Categories: OrganellesHidden categories: Pages with DOIs broken since 2009 | Wikipedia indefinitely move-protected pages | Articles containing Latin language text | Featured articles I am an expert from Cheap On Sales, usually analyzes all kind of industries situation, such as plastic organizer box , air tight food storage.
Article Sourceskin cancer

Facts and Treatment of Skin Cancer

Sat, 21 Aug 2010 20:21:35 +0000

Skin cancer — the abnormal growth of skin cells — most often develops on skin exposed to the sun. But this common form of cancer can also occur on areas of the skin not ordinarily exposed to sunlight. Skin cancer is a disease in which cancer (malignant) cells are found in the outer layers of your skin. Your skin protects your body against heat, light, infection, and injury. It also stores water, fat, and vitamin D.

Melanoma is a form of skin cancer that occurs in the melanocytes, which are cells in the outer layer of the skin (the epidermis). Melanoma is the most serious form of skin cancer. Melanoma may be cured if caught and treated early, but if left untreated the majority of melanomas eventually spread to other parts of the body. Early detection and surgery to remove the melanoma are successful in curing most cases of melanoma; however it is rarely curable in its later stages.

Facts

There are three types of skin cancer: the two most common are Basal Cell and Squamous Cell Carcinomas. They are easily treated and rarely fatal. The third and most dangerous is the malignant melanoma.

Skin cancer is the second most common cancer in the United Kingdom, with about 40,500 new cases each year, of which 6,000 are malignant melanomas. About 1,500 people die from melanomas in Britain every year.

Melanomas can spread two ways: horizontally, which gives rise to the superficial spreading melanoma, or they can grow downwards and the cells will invade the lymph glands, which is much more dangerous.

Over the past 60 years, damage to the planet’s ozone layer has increased the amount of harmful radiation that reaches your skin.

Causes

Skin cancer begins in your skin’s top layer — the epidermis. The epidermis is as thin as a pencil line, and it provides a protective layer of skin cells that your body continually sheds. The epidermis contains three types of cells:

Sunburn and Ultra Violet light exposure causes maximum damage resulting in DNA damage to the skin. The body can usually repair this damage before gene mutations occur. But when a person’s body cannot repair the damaged DNA, then it results in skin cancer.

Squamous cells lie just below the outer surface.

Basal cells, which produce new skin cells, sit beneath the squamous cells.

Melanocytes, which produce melanin — the pigment that gives skin its normal color, are located in the lower part of your epidermis. Melanocytes produce more melanin when you’re in the sun to help protect the deeper layers of your skin. Extra melanin produces the darker color of tanned skin.

Treatment

Freezing. Your doctor may destroy actinic keratoses and some small, early skin cancers by freezing them with liquid nitrogen (cryosurgery). The dead tissue sloughs off when it thaws. The treatment may leave a small, white scar. You may need a repeat treatment to remove the growth completely.

Excision: Small cancers can be removed by excising them out. It will be done under local anaesthetic.

Laser therapy. A precise, intense beam of light vaporizes growths, generally with little damage to surrounding tissue and with minimal bleeding, swelling and scarring. A doctor may use this therapy to treat superficial skin cancers or precancerous growths on lips.

Radiation therapy. Radiation may destroy basal and squamous cell carcinomas if surgery isn’t an option.

Mohs surgery. This procedure is for larger, recurring or difficult-to-treat skin cancers, which may include both basal and squamous cell carcinomas. Your doctor removes the skin growth layer by layer, examining each layer under the microscope, until no abnormal cells remain.

Read about Acne Cure and Treatments and Breast Enlargement Enhancement. Also read about Beauty and Makeup Tips
Article Sourceskin cancer

Removing Skin Moles – Do You Feel Embarrassed Going Out in Public All of the Time?

Sat, 21 Aug 2010 00:11:42 +0000

Do you suffer with skin moles and because you do they are getting you down emotionally. There is nothing worse than other people looking at you and your moles. Do you wish you had a magic skin mole removal at your fingertips so that you would not have to feel so bad about yourself? Do you always want to feel embarrassed about your moles but feel powerless because you can’t seem to find a cure for your problem?

The last thing that you probably want to do is to go and see your doctor as they will only probe around looking for something to say that you want to hear RIGHT! But all that you really want is a cure for your mole problem. I bet that you have tried many over the counter products that promise you a cure for removing skin moles, but none of them seem to have worked
Properly.

When you first saw your skin moles especially if they were visible to everyone I an sure that you must of feeling. Like being swallowed up by a large hole to hide the embarrassment. Did you feel any of the following?

- “My life is ruined now!”
- “How can I be seen in public looking like this?”
- “The first thing that people are going to notice is this horrible mole, wart or skin tag!”
- “I bet everyone will think I have some kind of disease
- “How can I get rid of this thing tonight?!”
- “What boy is going to want to go out with me now?”
- “I am never coming out of my bedroom until this mole goes away!”

Would you like all those feeling to go away and to start to live your life again?

Are you looking for a solution to your mole,wart or skin tag problem, then here is my No 1 recommended solution to Removing Skin Moles.
If you would like more information on Removing Skin Moles then Click Here.
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Herbal Skin Mole Eradication Solutions – How Effective Are They?

Fri, 20 Aug 2010 09:04:24 +0000

Today, you can find 100s of different products for mole treatment, however, which one to select? Which product will probably be the best for you. In this short article I will show you what is the most beneficial mole remover as well as what to expect from such solutions.

In reality, most herbal products that are proven to be very good skin mole removers have one typical element. it is tea tree essential oil. This oil has been employed for 1000’s of years. It could recover your skin from burns and traumas. This oil has many unique features which make it an excellent option for skin mole elimination. It is pretty easy to make use of it. The only thing what you should do is to apply 1 drop of the oil on mole several times daily and soon enough you will see good changes.

There is one important fact regarding the oil. It was implemented by ancient Greeks and Egyptians. These people used it as a home remedy not just for skin injury but also as a beauty product.

It is just one of the most beneficial solutions you can think about. Yet, if you are searching for a tested mole remover, there is a product named Heal Moles. It’s made by a very reputable firm which has been out there for 10 years. The product is really a blend of essential oils created from various plants. That’s why it doesn’t have any negative effects and you will not see any scars or skin damage.

Right now, you know about a pair of possible choices which may help you to remove skin mole once and for all. So what are you waiting for? It’s time to start removing those unsightly spots on your skin. I hope you found this posting useful and it will help you. Best of luck.

Find out extra information about Heal Moles mole remover at the website.
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Natural Way to Get Rid of Skin Moles

Thu, 19 Aug 2010 12:23:17 +0000

Do you want to find effective ways to remove your skin moles? Do not want to spend much money on mole removal procedures? If so, natural mole removal is what you need to clean your skin. This remedies cannot rid your from moles overnight however if you continue to use them for a few weeks, you will see positive results. There are so many folks across the globe who managed to rid themselves from skin moles using 100 percent natural techniques.

In most cases, you will need to apply a special mix on your moles a few times per day. Your mole will become drier and than it will finally fall off. As you know natural herbs do not contain any acids and that is why you will not harm your precious skin. As a result, you will not see scars on your skin.

Most of the ingredients used in mole removal with home remedies may be easily available in your local grocery stores. These ingredients are also very cheap and everybody can affort them. The fact that herbal remedies do not have side effects make them extremely popular.

One of the simple home remedies is potato peel. Just cut potatoe and rub one piece into your mole. Just repeat this actions a couple times per day and you will soon notice positive changes. Experts claim that you can even use radish or pineapples instead, however potatoe is more effective.

Garlic can also remove your moles. Just take a few garlic pods and squeeze them, you will get a little bit juice. Apply the squeezed garlic with the juice to the moles.

The truth is, there are many other ingredients that can help you with your problem. I hope you will find these two remedies effective. it is time to get rid of your ugly moles. I wish you all the best.

mole removal

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Solar Keratosis can be Cured Naturally

Wed, 18 Aug 2010 17:56:37 +0000

A solar keratosis is a small, rough, bump which develops on the skin. It is caused by continuous exposure to sun. Treatment is usually advised as there is a small risk that it may eventually turn into skin cancer.
Freezing a solar keratosis with liquid nitrogen is the common treatment. Cutting out or scrapping off the solar keratosis are other options. Although not all solar keratosis progress into a melanoma, if you have SK then your risk of developing a melanoma at some other part of your skin is increased.

People with fair skin who do not tan easily are most commonly affected. Because their skin has less protective pigment, they are the most susceptible to sunburn and other forms of sun damage. The more serious type of skin cancer, melanoma, most commonly occurs in people who have had a lot of sun exposure.

So, tell a doctor soon if you notice any changes in any part of your skin such as new moles, small dark patches developing, etc. There are other spots, called seborrheic keratoses, that are not caused by sun exposure and have no relationship to skin cancers. Because their growth is often hard to predict,many skin specialists think it is safest to consider them as a form of squamous cell skin cancer.

Treatment is usually advised if you have more than one solar keratosis. Doctors can usually diagnose an actinic keratosis just by examining it. For instance, for every 100 cases of solar keratosis, 50 per cent will get better in a few years, and 50 per cent will stay the same or get worse. SK is caused by continuous exposure to sun and changes the size, shape, structure and organisation of our skin cells.

Cancers that develop from melanocytes, the pigment-making cells of the skin, are called melanomas. This is not the most serious form of skin cancer. If you spend much time in the sun you have an increased risk of developing solar keratoses, certain types of skin cancer and various other skin problems.

The vast majority of these cancers develop in areas of severe sun damage, particularly within or contiguous to areas of solar keratoses, but it has not been possible thus far to predict who will develop these potentially dangerous skin cancers.

So, although solar keratosis does not always progress into a melanoma, if you have SK then your risk of developing a melanoma at some other part of your skin is increased. The natural cure for SK is crocodile oil, this has been used for centuries for many skin problems. Many sufferers hav testified that they no longer have to have their SK burnt off as their skin has healed naturally with this balm.

For more information on crocodile oil, visit http://www.crocodileoil.com
Article Sourceskin cancer

Skin Cancer Signs To Watch Out For

Tue, 17 Aug 2010 23:36:29 +0000

Cancer of the skin is common for people who have spent lots of time under the sun, without protection from the rays. It affects people of all skin tones. Skin cancer signs primarily develops on parts of the body that are most exposed to the sun, such as the hands, legs, neck, face, lips, and ears. There are also various stages of skin cancer, and each with their own symptoms.

Signs of skin cancer may be tricky to diagnose, but once you think you have the following then you should see a doctor at the soonest possible time:

1. Basal cell carcinoma is the most common of skin cancer signs. However, it is also the most easily treated, and signs of skin cancer tend to appear as a bump on your face or neck with a shiny exterior, or a flat lesion on the chest or back that may be flesh or brown in color.

2. Squamous cell carcinoma has a higher tendency to spread compared to basal cell carcinoma, and can only be treated if detected early. Skin cancer signs include a firm, red roundish lump on the hands, arms, face, neck or ears. It may also exhibit itself as a flat lesion with a more scaly and crusty surface on these same locations in the body.

3. Melanoma is the most severe and serious form of skin cancer. It is fatal and has led to many deaths, which is why early detection is extremely important in survival. Skin cancer signs of melanoma exhibit itself differently for men and women. Men should watch out for signs of melanoma on their head, neck, or trunk, while for women, it commonly affects the arms or legs. Signs of skin cancer to watch out for:

a. Small lesions with irregular borders with white, blue, or red spots.
b. A mole anywhere in the body that changes shape frequently and has irregular borders. It may also change color and size and may bleed.
c. Dark-colored lesions located in the fingertips, toes, palms, hands, or on mucous membranes such as the anus, lips, or vagina.
d. Firm bumpy moles that have a waxy or pearly exterior that may appear anywhere on the body.

4. Kaposi sarcoma is a form of skin cancer that is not common, but it is as severe as melanoma. Because it forms in the skin’s blood vessels, signs of skin cancer include the appearance of purple and red colored patches in the skin and mucous membranes.

5. Sebaceous gland carcinoma is characterized by painless nodules and often diagnosed as benign cancer. These can appear anywhere, although common affected sites are the eyelids. It is not a popular case but still, it is considered very dangerous.

If you are unsure about skin cancer signs, you may want to get the opinion of a doctor or dermatologist as waiting until the signs are more aggressive is a bad idea. Catching skin cancer early on is the best bet for survival.

Neelima Reddy is an author and publisher of many health related websites. For more information on skin cancer basics, prevention methods and treatment options, visit his website at: Skin Cancer Information
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Tanning Skin Cancer – Symptoms And Treatment

Tue, 17 Aug 2010 08:58:37 +0000

Although most women love to be under the sun and work on that golden tan, they often don’t realize that in the long term this is the biggest contributing factor to skin cancer. Even if you use tanning beds for an artificial tan, the ultraviolet radiation produced by these lamps also contributes to tanning skin cancer. The immediate effects of tanning skin cancer may not be felt or seen early on, but in your later years this will show through wrinkles, fine lines, and may also lead to cancer.

To prevent tanning skin cancer, one must always take precaution to protect their skin by avoiding the harsh rays of the sun, usually from 10am to 3pm. Furthermore, it is recommended to always use sun block even on cloudy days, and protect parts of your body that are also exposed to the sun such as your lips, head, neck, and forearms.

Precaution against tanning skin cancer, even if you do not always spend time under the sun, entails regular observance of symptoms in your body. These are symptoms of tanning skin cancer that you should watch out for:

A red spot or mole that is firm to the touch;
A mole that changes color or shape;
A mole that has irregular borders and changes size over time;
Red or brown flat, scaly patches on your skin;
A spot anywhere on your skin that may bleed or become crusty, and does not go away with medication.

If you see any of these symptoms anywhere in your body and are suspicious, you should go see a doctor right away. Early detection of tanning skin cancer increases your chances for being cured and surviving.

Today, there are many options for treatment of tanning skin cancer available depending how early on the cancer is. Oftentimes, the abnormal cells can be removed with the use of topical medications, or just through the use of a local anesthetic in an outpatient procedure.

However, other cases of tanning skin cancer treatment options include:

Early skin cancers can be treated through freezing or cryosurgery, wherein the dead abnormal tissue can be sloughed off after the freezing.
Excision of the cancerous tissue through surgery can also be done in some cases. However, to avoid scarring, it’s best to consult a doctor who is experienced in skin reconstruction as the cutting of the skin usually leaves significant traces. You may ask for a cosmetic surgery done to get rid of the ugly signs.
Laser therapy is effective in vaporizing growths caused by tanning skin cancer. This is usually used to treat precancerous growths and superficial cancers.
Severe cases require more extreme forms of treatment, such as radiation therapy. Radiation is used as an option to surgery, to remove basal and squamous cell forms of cancers.
Tanning skin cancer discovered in its much later phases often has to be treated through the use of chemotherapy. In chemotherapy, drugs are used on a regular basis to kill the cancer cells.
Nishanth Reddy is an author and publisher of many health related websites. For more information on skin cancer basics, prevention methods and treatment options, visit his website at: Skin Cancer Information
Article Sourceskin cancer

Using Skin Cancer Images as a Baseline for Skin Examination

Mon, 16 Aug 2010 09:45:08 +0000

If you know what early warning signs to look for, skin cancer can be detected at an early stage and cured without the use of aggressive treatments which cause severe side effects. Unlike other cancers, skin cancer’s earliest warning signs are openly visible on the skin. The advantage of early detection is lost if you don’t know what to look for and if you fail to do regular skin examinations or consult a doctor if you find any irregularities. Skin cancer images can be used as a guide when doing a skin self-examination, showing you what kind of irregularities require medical attention.

Early detection of skin cancer is extremely important. When detected early, skin cancer can usually be removed through a simple outpatient surgery; this can even be true for the most serious form of skin cancer, melanoma. If the disease is allowed to advance and the tumor is allowed to grow to the point that it may begin to metastasize, local lymph nodes may need to be removed and tested for cancerous cells. If cancerous cells have spread to nearby lymph nodes, radiation or chemotherapy may be necessary to destroy any remaining cancer cells throughout the body.

If skin cancer has further progressed before treatment, other tumors may begin to grow in other parts of the body. These tumors, though they may be in other organs or systems, are made up of the same cancerous skin cells. If one or more tumors appear in other parts of the body, further surgeries and more aggressive treatments may be necessary, and the point may be reached where curing the cancer is impossible and only the symptoms are treated.

Early detection being so important and skin cancer being such a common disease, people need to learn not just prevention methods but also methods of early detection. Just as women need to do regular breast self-examinations, everyone needs to do periodic skin self-examinations, checking thoroughly all parts of their skin for any irregularities that may be a sign of skin cancer. Exemplary images of skin cancer symptoms can help people recognize skin irregularities which require medical examination to find out whether they are cancerous.

Warning signs for melanoma include any changes in moles or nevi, especially dysplastic nevi, or moles which are irregularly shaped or colored. Nonmelanoma skin cancer can be more difficult to detect for people who don’t know what to look for, as it can present itself as small, relatively harmless-looking lumps, or as sores or rashes that don’t seem to heal properly. If a person sees an image of this type of skin cancer, they will know to see a doctor rather than waiting it out and seeing if it heals on its own.

As long as they are accompanied by some background information, skin cancer images can be an important tool for people who wish to detect skin cancer in its early stages.

To learn much more about how you can benefit from skin cancer images, visit http://www.SkinCancer-101.com where you’ll find this and much more, including how detecting skin cancer signs can save.
Article Sourceskin cancer