An autosomal recessive trait with impaired cell-mediated immunity. About 15 human papillomaviruses are implicated in associated infection, four of which lead to skin neoplasms. The disease begins in childhood with red papules and later spreads over the body as gray or yellow scales.
Benign epidermal proliferations or tumors; some are viral in origin.
A genus of DNA viruses in the family PAPILLOMAVIRIDAE, causing cutaneous lesions in humans. Infections exist in latent form in the general population and are activated under conditions of IMMUNOSUPPRESSION.
A family of small, non-enveloped DNA viruses infecting birds and most mammals, especially humans. They are grouped into multiple genera, but the viruses are highly host-species specific and tissue-restricted. They are commonly divided into hundreds of papillomavirus "types", each with specific gene function and gene control regions, despite sequence homology. Human papillomaviruses are found in the genera ALPHAPAPILLOMAVIRUS; BETAPAPILLOMAVIRUS; GAMMAPAPILLOMAVIRUS; and MUPAPILLOMAVIRUS.
Skin diseases caused by bacteria, fungi, parasites, or viruses.
A persistent progressive non-elevated red scaly or crusted plaque which is due to an intradermal carcinoma and is potentially malignant. Atypical squamous cells proliferate through the whole thickness of the epidermis. The lesions may occur anywhere on the skin surface or on mucosal surfaces. The cause most frequently found is trivalent arsenic compounds. Freezing, cauterization or diathermy coagulation is often effective. (From Rook et al., Textbook of Dermatology, 4th ed, pp2428-9)
Tumors or cancer of the SKIN.
Neoplasms of the skin and mucous membranes caused by papillomaviruses. They are usually benign but some have a high risk for malignant progression.
Deoxyribonucleic acid that makes up the genetic material of viruses.
Infections produced by oncogenic viruses. The infections caused by DNA viruses are less numerous but more diverse than those caused by the RNA oncogenic viruses.
Products of viral oncogenes, most commonly retroviral oncogenes. They usually have transforming and often protein kinase activities.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
An autosomal dominantly inherited skin disorder characterized by warty malodorous papules that coalesce into plaques. It is caused by mutations in the ATP2A2 gene encoding SERCA2 protein, one of the SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. The condition is similar, clinically and histologically, to BENIGN FAMILIAL PEMPHIGUS, another autosomal dominant skin disorder. Both diseases have defective calcium pumps (CALCIUM-TRANSPORTING ATPASES) and unstable desmosomal adhesion junctions (DESMOSOMES) between KERATINOCYTES.
Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)
Skin diseases caused by viruses.

A susceptibility locus for epidermodysplasia verruciformis, an abnormal predisposition to infection with the oncogenic human papillomavirus type 5, maps to chromosome 17qter in a region containing a psoriasis locus. (1/60)

Epidermodysplasia verruciformis (EV) is a rare genodermatosis characterized by an abnormal susceptibility to infection with a specific group of related human papillomavirus (HPV) genotypes, including the oncogenic HPV5 associated with the skin carcinomas developing in about half of EV patients. EV is usually considered as an autosomal recessive condition. Taking EV as a model to identify a locus underlying the susceptibility to HPV infections, we performed a genome-wide search for linkage with 255 microsatellite genetic markers in three consanguineous EV families comprising six patients, using the homozygosity mapping approach. Homozygosity restricted to affected individuals was observed for a marker of chromosome 17q (D17S784) in two families and a marker about 17 centiMorgan (cM) distal (D17S1807) in the third family. Ten additional microsatellite markers spanning 29 cM in this region were analyzed. Two-point lod score values greater than 3 were obtained for four markers and multipoint linkage analysis yielded a maximum lod score of 10.17 between markers D17S939 and D17S802. Recombination events observed in two families allowed a candidate region for the EV susceptibility locus to be mapped to the 1 cM region defined by these two markers. The EV locus (named EV1) is included in the 17qter region recently found to contain a dominant locus for the susceptibility to familial psoriasis. It has been shown that patients suffering from psoriasis are likely to constitute the reservoir of HPV5. It is thus tempting to speculate that distinct defects affecting the same gene may be involved in the two skin conditions.  (+info)

High prevalence of a variety of epidermodysplasia verruciformis-associated human papillomaviruses in psoriatic skin of patients treated or not treated with PUVA. (2/60)

Epidermodysplasia verruciformis-associated human papillomaviruses and in particular human papillomavirus type 5 were recently shown to be highly prevalent in psoriatic skin. We have analyzed lesional skin from 54 psoriasis patients for infections with genital-specific and epidermodysplasia verruciformis-specific human papillomaviruses to define the spectrum of involved human papillomavirus types and to test if it is influenced by psoralen ultraviolet A therapy. Using polymerase chain reaction analysis we could detect human papillomavirus sequences in skin lesions of 83% of the tested patients. In contrast, human papillomavirus-DNA was only demonstrated in 19% of skin samples from 42 dermatologically healthy, immunocompetent individuals. Sequence analysis of the polymerase chain reaction amplimers revealed 14 human papillomavirus types, all belonging to the epidermodysplasia verruciformis or epidermodysplasia verruciformis-related papillomaviruses. Only in one case we identified sequences related to those of genital viruses, which, however, represented a putatively new human papillomavirus type. The most prevalent human papillomavirus type in our patient series was human papillomavirus type 36, found in 62% of the patients positive for human papillomavirus-DNA, followed by human papillomavirus type 5 (38%) and human papillomavirus type 38 (24%). Multiple infections with two to five different human papillomavirus types could be detected in skin samples of 63% of the analyzed patients. The overall human papillomavirus detection rate did not differ significantly between patients which have been subjected to psoralen ultraviolet A photochemotherapy or solely treated with topical preparations (77 vs 89%). Human papillomavirus type 5, however, could be detected significantly more frequent in lesions of psoralen ultraviolet A-treated patients (p < 0.001). Our data strongly argue for infections with epidermodysplasia verruciformis-specific papillomaviruses being an almost consistent feature of the lesional psoriatic skin and substantiate the importance of further studies to elucidate a possible involvement of human papillomaviruses in psoriasis pathology.  (+info)

Evidence for a nonallelic heterogeneity of epidermodysplasia verruciformis with two susceptibility loci mapped to chromosome regions 2p21-p24 and 17q25. (3/60)

Epidermodysplasia verruciformis is a rare genodermatosis associated with a high risk of skin cancer. This condition is characterized by an abnormal susceptibility to specific related human papillomavirus genotypes, including the oncogenic HPV5. Epidermodysplasia verruciformis is usually considered as an autosomal recessive disease. We recently mapped a susceptibility locus for epidermodysplasia verruciformis (EV1) to chromosome 17qter within the 1 cM interval between markers D17S939 and D17S802. We report here the genotyping for 10 microsatellite markers spanning 29 cM around EV1 in two consanguineous epidermodysplasia verruciformis families from Colombia (C2) and France (F1) comprising five patients and two patients, respectively. Using homozygosity mapping, linkage with 17qter markers was observed for family C2 only. Multipoint linkage analysis yielded maximum multipoint LOD-score values above 10 between markers D17S1839 and D17S802 encompassing the EV1 locus. A genome-wide search performed in family F1 yielded evidence for linkage between epidermodysplasia verruciformis and the chromosomal 2p marker D2S365. Nine additional microsatellite markers spanning 15 cM in this region were analyzed. Assuming an autosomal recessive inheritance with a complete penetrance, the expected maximum two-point LOD-score value of 1.8 was obtained for three markers and multipoint linkage analysis yielded a maximum LOD-score value of 3. 51 between markers D2S2144 and D2S392. Haplotype analysis allowed to map a candidate region for a second epidermodysplasia verruciformis susceptibility locus (EV2) within the 8 cM interval between markers D2S171 and D2S2347 of the 2p21-p24 region. In contrast, linkage with 2p markers was excluded for family C2 and for the three families in which we mapped EV1 previously. The disclosure of two susceptibility loci for epidermodysplasia verruciformis provides evidence for a nonallelic heterogeneity in this disease.  (+info)

Mutation and abnormal expression of the p53 gene in the viral skin carcinogenesis of epidermodysplasia verruciformis. (4/60)

Patients suffering from epidermodysplasia verruciformis are prone to nonmelanoma skin cancers, due to an inherited abnormal susceptibility to the oncogenic human papillomavirus type 5. Genotoxic sunlight ultraviolet B radiations are likely to be a cofactor. Lesions of two human-papillomavirus-type-5-infected epidermodysplasia verruciformis patients collected during an 8 y period were retrospectively studied for p53 mutations in exons 5 through 8 by a polymerase chain reaction single-strand conformation polymorphism technique and/or by DNA sequencing of amplified exons. Mutations were detected in 11 of 26 (42.3%) specimens, including five (62.5%) squamous cell carcinomas, three (33.3%) Bowen's carcinomas in situ, two (40%) actinic keratoses, and one (33%) benign lesion. The nine mutations characterized by sequencing were shown to be missense and to affect mutational hotspots in human cancers. Five were C-->T transitions at dicytidine sites considered as ultraviolet signature mutations. Two were transversions (C-->G and C-->A) at dicytidine sites and two were C-->T transitions at nondipyrimidine sites. A marked p53 immunoreactivity was disclosed in 72.7% of 11 invasive carcinomas, 55.6% of nine carcinomas in situ, 37.5% of eight actinic keratoses, and one of three benign lesions. This includes 81.8% of 11 specimens with a p53 mutation but also 50% of 14 specimens with no mutation detected. A dysfunction of the p53 gene is thus likely to play a part in epidermodysplasia verruciformis carcinogenesis, either due to ultraviolet-B-induced p53 mutations, as in nonmelanoma skin cancers in the general population, or involving other mutagens or mechanisms. The part played by human papillomavirus type 5 proteins expressed in epidermodysplasia verruciformis keratinocytes remains to be determined.  (+info)

Association between epidermodysplasia verruciformis-associated human papillomavirus DNA in plucked eyebrow hair and solar keratoses. (5/60)

Epidermodysplasia-verruciformis-associated human papillomavirus DNA has been demonstrated in squamous cell carcinomas and plucked hair from immunocompetent patients and renal transplant recipients. This study investigated the association between infection with epidermodysplasia-verruciformis-associated human papillomavirus, identified by the detection of viral DNA in plucked eyebrow hairs, and solar keratoses. These lesions are strongly predictive of squamous cell carcinoma. In a cross-sectional study 518 individuals were enrolled from a randomly selected sample of a subtropical Australian community. Epidermodysplasia-verruciformis-associated human papillomavirus DNA in eyebrow hair was detected using a nested polymerase chain reaction specific for epidermodysplasia-verruciformis-associated human papillomavirus types. Epidermo dysplasia-verruciformis-associated human papillomavirus DNA was present in 121 (49%) of 245 men and 116 (44%) of 262 women. There was a strongly significant increase in epidermodysplasia-verruciformis-associated human papillomavirus infection with age (p < 0.00001), with prevalences of 29% in the 25-39 y age group, 42% at 40-59 y and 65% in the 60-79 y age group. Among men there was a strong association between epidermodysplasia-verruciformis-associated human papillomavirus and solar keratoses with an odds ratio, adjusted for age, skin color, and occupational sun exposure, of 3.40 (95% confidence interval, 1.77-6.53). No such association was found among women [odds ratio 1.03 (95% confidence interval 0.59-1.77, after adjustment for the same factors)]. Differences in occupational sun exposure and smoking histories could not explain these apparently different associations between epidermodysplasia-verruciformis-associated human papillomavirus infection and solar keratoses in men and women. In conclusion, epidermodysplasia-verruciformis-associated human papillomavirus infection is associated with solar keratoses in men suggesting that epidermodysplasia-verruciformis-associated human papillomavirus infection, in conjunction with sex specific factors (like androgens), may be involved in neoplastic changes of keratinocytes.  (+info)

Transduction of the E6 and E7 genes of epidermodysplasia-verruciformis-associated human papillomaviruses alters human keratinocyte growth and differentiation in organotypic cultures. (6/60)

Epidermodysplasia-verruciformis-associated human papilloma virus DNA has been detected in skin cancers, in premalignant and benign skin lesions, and in plucked hairs from immunocompetent and immunosuppressed patients. The role of epidermodysplasia-verruciformis-associated human papilloma virus in the pathogenesis of nonmelanoma skin cancer is still enigmatic. In organotypic cultures we investigated the effects of retroviral transduction of the E6 and E7 genes of epidermodysplasia-verruciformis-associated human papilloma virus types 5, 12, 15, 17, 20, and 38 on the growth and differentiation of human keratinocytes. Differentiation was disturbed to different degrees as revealed by histology and by the expression patterns of differentiation markers keratin 10 and small proline rich protein 2. Conversely, proliferating cell nuclear antigen was induced in some of the suprabasal, differentiated cells to varying extent. No unscheduled DNA synthesis was detected in these cells, however, as probed by 5'-bromo-2'-deoxyuridine incorporation. Most intriguingly, when the E6 and E7 genes of epidermodysplasia-verruciformis-associated human papilloma virus types 15 and 17 were transduced, a broadening layer of basal cells and an accelerated differentiation were observed. In addition, "papilla-like structures" comprising basal-like keratinocytes arose from the basal layer into the differentiated layers. These cells did not express the differentiation markers keratin 10 and small proline rich protein 2, but did actively replicate DNA. These observations warrant further research by using this system to elucidate the replication strategy of epidermodysplasia-verruciformis-associated human papilloma virus types in keratinocytes and to shed light on the role of these human papilloma virus types in the pathogenesis of skin cancer.  (+info)

Dual role of tumor suppressor p53 in regulation of DNA replication and oncogene E6-promoter activity of epidermodysplasia verruciformis-associated human papillomavirus type 8. (7/60)

Human papillomavirus 8 (HPV8) is a representative of Epidermodysplasia verruciformis (EV)-associated viruses. Transient assays in the human skin keratinocyte cell line RTS3b have shown that its replication depends in trans on expression of the viral proteins E1 and E2, similarly to other HPVs. Using deletion mutants and cloned subfragments of the noncoding region (NCR) of HPV8 we identified a 65-bp sequence in the 3' part of the NCR to be necessary and sufficient to support replication in cis. The origin of replication (ori) of HPV8 is composed of the sequence motifs "CCAAC" (nt 57-73) and M29 (nt 84-112), which are highly conserved among the majority of EV HPVs. Analysis of M29 revealed an unconventional binding site of the E2 protein and an overlapping DNA recognition site of the tumor suppressor protein p53. Both these factors competitively bind to M29. In transient replication assays p53 acted as a potent inhibitor of ori activity, most probably in a DNA-binding-dependent fashion. The minimal ori sequences are also functionally critical for the E6 oncogene promoter P(175). In contrast to its effect on replication, p53 stimulated promoter activity depending on its interaction with M29. Our observations suggest that p53 is involved in controlling the balance between DNA replication and gene expression of HPV8.  (+info)

Seroreactivity to epidermodysplasia verruciformis-related human papillomavirus types is associated with nonmelanoma skin cancer. (8/60)

DNA from epidermodysplasia verruciformis-related human papillomavirus (EV-HPV) types is frequently found in nonmelanoma skin cancer (squamous and basal cell carcinoma). Epidemiological studies that investigate the relation between EV-HPV infection and nonmelanoma skin cancer are scarce. We designed a case-control study in which we looked for HPV infection in 540 cases with a history of skin cancer and 333 controls. By measuring seroreactivity to L1 virus-like particles of EV-HPV types 5, 8, 15, 20, 24, and 38 and the genital type HPV16 and by estimating the skin cancer relative risk among HPV seropositives, we analyzed whether EV-HPV serorecognition is associated with nonmelanoma skin cancer. Seroreactivity to five of the six EV-HPV types tested (HPV5, 8, 15, 20, and 24) was significantly increased in the squamous cell carcinoma cases. After adjusting for age and sex, the estimated squamous cell carcinoma relative risk was significantly increased in HPV8 and HPV38 seropositives [odds ratio (OR) = 14.7 (95% confidence interval (CI), 1.6-135) and OR = 3.0 (95% CI, 1.1-8.4), respectively]. The estimated relative risk for nodular and superficial multifocal basal cell carcinoma was also significantly increased in the HPV8 seropositives [OR = 9.2 (95% CI, 1.1-78.2) and OR = 17.3 (95% CI, 2.1-143), respectively] and in the HPV20 seropositives [OR = 3.2 (95% CI 1.3-7.9) and OR = 3.4 (95% CI 1.2-9.5), respectively]. The relative risk of developing malignant melanoma was not increased among HPV seropositives, and no associations were found for HPV16. Restricted analyses among the HPV seropositives only, to exclude distortion by interindividual differences in seroresponsiveness, underscored the significance of our findings. Restricted analyses among patients with skin cancer only, however, revealed that EV-HPV seropositivity was not significantly more present in patients with nonmelanoma skin cancer than in those with melanoma skin cancer. Taken together, our results indicate that EV-HPV serorecognition is nonspecifically associated with nonmelanoma skin cancer and suggest that EV-HPV-directed seroresponses are induced upon skin cancer formation, rather than upon infection.  (+info)

Epidermodysplasia verruciformis (EV) is a rare genetic skin disorder characterized by the development of scaly macules and papules that can progress to malignant lesions. It is caused by mutations in the EVER1 or EVER2 genes, which lead to an increased susceptibility to human papillomavirus (HPV) infection. The condition typically presents in childhood or early adulthood and affects both sexes equally.

The skin abnormalities associated with EV are often described as "wart-like" and can appear anywhere on the body, but they most commonly affect sun-exposed areas such as the hands, arms, and face. The lesions may be flat or slightly raised, and they can vary in color from white to brown or gray. In some cases, the lesions may become thickened and crusted, and they can be pruritic (itchy) or painful.

People with EV are at an increased risk of developing skin cancer, particularly squamous cell carcinoma (SCC). The SCCs associated with EV tend to occur at a younger age than those that develop in the general population, and they often arise within existing EV lesions. Regular skin examinations and sun protection measures are recommended for individuals with EV to help prevent the development of skin cancer.

Treatment options for EV include topical therapies such as retinoids, immunomodulators, and chemotherapeutic agents, as well as systemic therapies such as antiviral medications and interferon. Surgical excision may be necessary for the treatment of malignant lesions.

Warts are small, rough growths on the skin or mucous membranes caused by one of several types of human papillomavirus (HPV). They can appear anywhere on the body but most often occur on the hands, fingers, and feet. Warts are benign, non-cancerous growths, but they can be unsightly, uncomfortable, or painful, depending on their location and size.

Warts are caused by HPV infecting the top layer of skin, usually through a small cut or scratch. The virus triggers an overproduction of keratin, a protein in the skin, leading to the formation of a hard, rough growth. Warts can vary in appearance depending on their location and type, but they are generally round or irregularly shaped, with a rough surface that may be flat or slightly raised. They may also contain small black dots, which are actually tiny blood vessels that have clotted.

Warts are contagious and can spread from person to person through direct skin-to-skin contact or by sharing personal items such as towels or razors. They can also be spread by touching a wart and then touching another part of the body. Warts may take several months to develop after exposure to HPV, so it may not always be clear when or how they were contracted.

There are several types of warts, including common warts, plantar warts (which occur on the soles of the feet), flat warts (which are smaller and smoother than other types of warts), and genital warts (which are sexually transmitted). While most warts are harmless and will eventually go away on their own, some may require medical treatment if they are causing discomfort or are unsightly. Treatment options for warts include topical medications, cryotherapy (freezing the wart with liquid nitrogen), and surgical removal.

Betapapillomavirus is a type of human papillomavirus (HPV) that primarily infects the skin, particularly the flat, dry areas known as the cutaneous epithelium. This genus of HPV is not typically associated with cancers or genital warts, unlike other high-risk HPV types. However, some betapapillomavirus types have been linked to benign skin growths called epidermodysplasia verruciformis (EV) lesions, which can develop into squamous cell carcinomas in immunocompromised individuals.

It is important to note that there are more than 200 known types of HPV, and they are classified into different genera based on their genetic similarities. Betapapillomaviruses belong to the genus Beta-Papillomavirus, which includes at least 49 distinct types. Some common examples of betapapillomaviruses include HPV types 5, 8, 17, 20, 23, and 41.

Research into the epidemiology, risk factors, and clinical implications of various HPV types is ongoing, as understanding the role of these viruses in human health and disease can help inform prevention strategies and treatment approaches.

Papillomaviridae is a family of small, non-enveloped DNA viruses that primarily infect the epithelial cells of mammals, birds, and reptiles. The name "papillomavirus" comes from the Latin word "papilla," which means nipple or small projection, reflecting the characteristic wart-like growths (papillomas) that these viruses can cause in infected host tissues.

The family Papillomaviridae includes more than 200 distinct papillomavirus types, with each type being defined by its specific DNA sequence. Human papillomaviruses (HPVs), which are the most well-studied members of this family, are associated with a range of diseases, from benign warts and lesions to malignant cancers such as cervical, anal, penile, vulvar, and oropharyngeal cancers.

Papillomaviruses have a circular, double-stranded DNA genome that is approximately 8 kbp in size. The viral genome encodes several early (E) proteins involved in viral replication and oncogenesis, as well as late (L) proteins that form the viral capsid. The life cycle of papillomaviruses is tightly linked to the differentiation program of their host epithelial cells, with productive infection occurring primarily in the differentiated layers of the epithelium.

In summary, Papillomaviridae is a family of DNA viruses that infect epithelial cells and can cause a variety of benign and malignant diseases. Human papillomaviruses are a significant public health concern due to their association with several cancer types.

Infectious skin diseases are conditions characterized by an infection or infestation of the skin caused by various microorganisms such as bacteria, viruses, fungi, or parasites. These organisms invade the skin, causing inflammation, redness, itching, pain, and other symptoms. Examples of infectious skin diseases include:

1. Bacterial infections: Cellulitis, impetigo, folliculitis, and MRSA (methicillin-resistant Staphylococcus aureus) infections are examples of bacterial skin infections.
2. Viral infections: Herpes simplex virus (HSV), varicella-zoster virus (VZV), human papillomavirus (HPV), and molluscum contagiosum are common viruses that can cause skin infections.
3. Fungal infections: Tinea pedis (athlete's foot), tinea corporis (ringworm), candidiasis (yeast infection), and pityriasis versicolor are examples of fungal skin infections.
4. Parasitic infestations: Scabies, lice, and bed bugs are examples of parasites that can cause infectious skin diseases.

Treatment for infectious skin diseases depends on the underlying cause and may include topical or oral antibiotics, antiviral medications, antifungal treatments, or insecticides to eliminate parasitic infestations. Proper hygiene, wound care, and avoiding contact with infected individuals can help prevent the spread of infectious skin diseases.

Bowen's disease is a skin condition that is characterized by the growth of abnormal cells on the outermost layer of the skin (the epidermis). It is also known as squamous cell carcinoma in situ. The affected area often appears as a red, scaly patch or plaque, and it can develop anywhere on the body, but it is most commonly found on sun-exposed areas such as the face, hands, arms, and legs.

Bowen's disease is considered a precancerous condition because there is a risk that the abnormal cells could eventually develop into invasive squamous cell carcinoma, a type of skin cancer. However, not all cases of Bowen's disease will progress to cancer, and some may remain stable or even regress on their own.

The exact cause of Bowen's disease is not known, but it is thought to be associated with exposure to certain chemicals, radiation, and human papillomavirus (HPV) infection. Treatment options for Bowen's disease include cryotherapy, topical chemotherapy, photodynamic therapy, curettage and electrodessication, and surgical excision. Regular follow-up with a healthcare provider is recommended to monitor the condition and ensure that it does not progress to cancer.

Skin neoplasms refer to abnormal growths or tumors in the skin that can be benign (non-cancerous) or malignant (cancerous). They result from uncontrolled multiplication of skin cells, which can form various types of lesions. These growths may appear as lumps, bumps, sores, patches, or discolored areas on the skin.

Benign skin neoplasms include conditions such as moles, warts, and seborrheic keratoses, while malignant skin neoplasms are primarily classified into melanoma, squamous cell carcinoma, and basal cell carcinoma. These three types of cancerous skin growths are collectively known as non-melanoma skin cancers (NMSCs). Melanoma is the most aggressive and dangerous form of skin cancer, while NMSCs tend to be less invasive but more common.

It's essential to monitor any changes in existing skin lesions or the appearance of new growths and consult a healthcare professional for proper evaluation and treatment if needed.

Papillomavirus infections are a group of diseases caused by various types of human papillomaviruses (HPVs). These viruses infect the skin and mucous membranes, and can cause benign growths such as warts or papillomas, as well as malignant growths like cervical cancer.

There are more than 100 different types of HPVs, and they can be classified into low-risk and high-risk types based on their potential to cause cancer. Low-risk HPV types, such as HPV-6 and HPV-11, commonly cause benign genital warts and respiratory papillomas. High-risk HPV types, such as HPV-16 and HPV-18, are associated with an increased risk of developing cancer, including cervical, anal, penile, vulvar, and oropharyngeal cancers.

HPV infections are typically transmitted through sexual contact, and most sexually active individuals will acquire at least one HPV infection during their lifetime. In many cases, the immune system is able to clear the virus without any symptoms or long-term consequences. However, persistent high-risk HPV infections can lead to the development of cancer over time.

Prevention measures for HPV infections include vaccination against high-risk HPV types, safe sex practices, and regular screening for cervical cancer in women. The HPV vaccine is recommended for both boys and girls aged 11-12 years old, and can also be given to older individuals up to age 45 who have not previously been vaccinated or who have not completed the full series of shots.

Viral DNA refers to the genetic material present in viruses that consist of DNA as their core component. Deoxyribonucleic acid (DNA) is one of the two types of nucleic acids that are responsible for storing and transmitting genetic information in living organisms. Viruses are infectious agents much smaller than bacteria that can only replicate inside the cells of other organisms, called hosts.

Viral DNA can be double-stranded (dsDNA) or single-stranded (ssDNA), depending on the type of virus. Double-stranded DNA viruses have a genome made up of two complementary strands of DNA, while single-stranded DNA viruses contain only one strand of DNA.

Examples of dsDNA viruses include Adenoviruses, Herpesviruses, and Poxviruses, while ssDNA viruses include Parvoviruses and Circoviruses. Viral DNA plays a crucial role in the replication cycle of the virus, encoding for various proteins necessary for its multiplication and survival within the host cell.

A tumor virus infection is a condition in which a person's cells become cancerous or transformed due to the integration and disruption of normal cellular functions by a viral pathogen. These viruses are also known as oncoviruses, and they can cause tumors or cancer by altering the host cell's genetic material, promoting uncontrolled cell growth and division, evading immune surveillance, and inhibiting apoptosis (programmed cell death).

Examples of tumor viruses include:

1. DNA tumor viruses: These are double-stranded DNA viruses that can cause cancer in humans. Examples include human papillomavirus (HPV), hepatitis B virus (HBV), and Merkel cell polyomavirus (MCV).
2. RNA tumor viruses: Also known as retroviruses, these single-stranded RNA viruses can cause cancer in humans. Examples include human T-cell leukemia virus type 1 (HTLV-1) and human immunodeficiency virus (HIV).

Tumor virus infections are responsible for approximately 15-20% of all cancer cases worldwide, making them a significant public health concern. Prevention strategies, such as vaccination against HPV and HBV, have been shown to reduce the incidence of associated cancers.

Oncogene proteins, viral, are cancer-causing proteins that are encoded by the genetic material (DNA or RNA) of certain viruses. These viral oncogenes can be acquired through infection with retroviruses, such as human immunodeficiency virus (HIV), human T-cell leukemia virus (HTLV), and certain types of papillomaviruses and polyomaviruses.

When these viruses infect host cells, they can integrate their genetic material into the host cell's genome, leading to the expression of viral oncogenes. These oncogenes may then cause uncontrolled cell growth and division, ultimately resulting in the formation of tumors or cancers. The process by which viruses contribute to cancer development is complex and involves multiple steps, including the alteration of signaling pathways that regulate cell proliferation, differentiation, and survival.

Examples of viral oncogenes include the v-src gene found in the Rous sarcoma virus (RSV), which causes chicken sarcoma, and the E6 and E7 genes found in human papillomaviruses (HPVs), which are associated with cervical cancer and other anogenital cancers. Understanding viral oncogenes and their mechanisms of action is crucial for developing effective strategies to prevent and treat virus-associated cancers.

Squamous cell carcinoma is a type of skin cancer that begins in the squamous cells, which are flat, thin cells that form the outer layer of the skin (epidermis). It commonly occurs on sun-exposed areas such as the face, ears, lips, and backs of the hands. Squamous cell carcinoma can also develop in other areas of the body including the mouth, lungs, and cervix.

This type of cancer usually develops slowly and may appear as a rough or scaly patch of skin, a red, firm nodule, or a sore or ulcer that doesn't heal. While squamous cell carcinoma is not as aggressive as some other types of cancer, it can metastasize (spread) to other parts of the body if left untreated, making early detection and treatment important.

Risk factors for developing squamous cell carcinoma include prolonged exposure to ultraviolet (UV) radiation from the sun or tanning beds, fair skin, a history of sunburns, a weakened immune system, and older age. Prevention measures include protecting your skin from the sun by wearing protective clothing, using a broad-spectrum sunscreen with an SPF of at least 30, avoiding tanning beds, and getting regular skin examinations.

Darier Disease is a genetic skin disorder, also known as Keratosis Follicularis. It is characterized by the formation of greasy, crusted, keratotic papules and plaques that typically appear on the upper arms, torso, and scalp. The lesions may also affect the nasolabial folds, central face, and mucous membranes. Darier Disease is caused by mutations in the ATP2A2 gene, which encodes a calcium pump protein involved in keratinization. It is an autosomal dominant disorder, meaning that a person has a 50% chance of inheriting the disease if one of their parents is affected. The onset of symptoms typically occurs during adolescence or early adulthood. Treatment options include topical medications, oral retinoids, and photodynamic therapy.

A precancerous condition, also known as a premalignant condition, is a state of abnormal cellular growth and development that has a higher-than-normal potential to progress into cancer. These conditions are characterized by the presence of certain anomalies in the cells, such as dysplasia (abnormal changes in cell shape or size), which can indicate an increased risk for malignant transformation.

It is important to note that not all precancerous conditions will eventually develop into cancer, and some may even regress on their own. However, individuals with precancerous conditions are often at a higher risk of developing cancer compared to the general population. Regular monitoring and appropriate medical interventions, if necessary, can help manage this risk and potentially prevent or detect cancer at an early stage when it is more treatable.

Examples of precancerous conditions include:

1. Dysplasia in the cervix (cervical intraepithelial neoplasia or CIN)
2. Atypical ductal hyperplasia or lobular hyperplasia in the breast
3. Actinic keratosis on the skin
4. Leukoplakia in the mouth
5. Barrett's esophagus in the digestive tract

Regular medical check-ups, screenings, and lifestyle modifications are crucial for individuals with precancerous conditions to monitor their health and reduce the risk of cancer development.

Skin diseases of viral origin are conditions that affect the skin caused by viral infections. These infections can lead to various symptoms such as rashes, blisters, papules, and skin lesions. Some common examples of viral skin diseases include:

1. Herpes Simplex Virus (HSV) infection: This causes cold sores or genital herpes, which are characterized by small, painful blisters on the skin.
2. Varicella-zoster virus (VZV) infection: This causes chickenpox and shingles, which are characterized by itchy, fluid-filled blisters on the skin.
3. Human Papillomavirus (HPV) infection: This causes warts, which are small, rough growths on the skin.
4. Molluscum contagiosum: This is a viral infection that causes small, raised, and pearly white bumps on the skin.
5. Measles: This is a highly contagious viral disease characterized by fever, cough, runny nose, and a rash that spreads all over the body.
6. Rubella: Also known as German measles, this viral infection causes a red rash on the face and neck that spreads to the rest of the body.

Viral skin diseases can be spread through direct contact with an infected person or contaminated objects, such as towels or bedding. Some viral skin diseases can be prevented through vaccination, while others can be treated with antiviral medications or other therapies.

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EPX Epidermodysplasia verruciformis; 226400; TMC6 Epidermodysplasia verruciformis; 226400; TMC8 Epidermolysis bullosa ... SLC39A4 Acrokeratosis verruciformis; 101900; ATP2A2 Acromesomelic dysplasia, Hunter-Thompson type; 201250; GDF5 Acromesomelic ...
2006). "Four mutations in Epidermodysplasia verruciformis 1 (EVER1) gene are not contributors to susceptibility in RRP". Int. J ... 2000). "Evidence for a nonallelic heterogeneity of epidermodysplasia verruciformis with two susceptibility loci mapped to ... 1999). "A susceptibility locus for epidermodysplasia verruciformis, an abnormal predisposition to infection with the oncogenic ... "Novel mutations of EVER1/TMC6 gene in a Japanese patient with epidermodysplasia verruciformis". J. Hum. Genet. 49 (4): 223-5. ...
2008). "Identification of defective Fas function and variation of the perforin gene in an epidermodysplasia verruciformis ... Mutations in the TMC8 gene are associated with epidermodysplasia verruciformis (EV), an autosomal recessive dermatosis ... 2000). "Evidence for a nonallelic heterogeneity of epidermodysplasia verruciformis with two susceptibility loci mapped to ... 2007). "Novel homozygous nonsense TMC8 mutation detected in patients with epidermodysplasia verruciformis from a Brazilian ...
In 1972, she theorized the association of human papilloma viruses with skin cancer in epidermodysplasia verruciformis. In 1978 ...
... functional clues from hearing loss and epidermodysplasia verruciformis". Genomics. 82 (3): 300-8. doi:10.1016/S0888-7543(03) ...
... in 1972 Jabłońska proposed the association of the human papilloma viruses with skin cancer in epidermodysplasia verruciformis; ...
... in 1972 Jabłońska proposed the association of the human papilloma viruses with skin cancer in epidermodysplasia verruciformis; ...
The first human IEI described was epidermodysplasia verruciformis in 1946, with the first primary immunodeficiency (X-linked ...
"Isolation of a human papillomavirus from a patient with epidermodysplasia verruciformis: Presence of related viral DNA genomes ...
... its anatomic distribution should facilitate distinction from widespread common warts and from epidermodysplasia verruciformis.[ ...
... filaggrin and e-cadherin in plane warts and epidermodysplasia verruciformis plane wart-type lesions". J. Cutan. Pathol. 36 (6 ...
TGF beta-1 and TNF alpha expression in the epidermis of patients with epidermodysplasia verruciformis. J Invest Dermatol. 1991 ... Natural cell-mediated cytotoxicity against various target cells in patients with epidermodysplasia verruciformis. J Am Acad ...
... filaggrin and e-cadherin in plane warts and epidermodysplasia verruciformis plane wart-type lesions". J. Cutan. Pathol. 36 (6 ...
Just prior to his death, he described epidermodysplasia verruciformis, a rare skin disorder sometimes known as "Lewandowsky- ...
A short video which shows the effects of papillomavirus on the skin of an Indonesian man with epidermodysplasia verruciformis, ...
... epidermodysplasia verruciformis) which causes tree-like growths Florence "Flo" & Katherine "Kay" Lyman, identical twin female ...
Eczema vaccinatum Epidermodysplasia verruciformis Eruptive pseudoangiomatosis Erythema infectiosum (fifth disease, slapped ... 18q deletion syndrome Acrodermatitis enteropathica Acrogeria (Gottron syndrome) Acrokeratosis verruciformis (acrokeratosis ... verruciformis of Hopf) Adams-Oliver syndrome Adducted thumbs syndrome Albright's hereditary osteodystrophy Angelman syndrome ...
... epidermodysplasia verruciformis The list continues at List of MeSH codes (C05). (Wikipedia articles in need of updating from ...
Epiderma Epidermal nevus vitamin D resistant rickets Epidermo Epidermod-Epidermoi Epidermodysplasia verruciformis Epidermoid ...
... was an Indonesian carpenter with epidermodysplasia verruciformis (EV), a rare disease that causes the human papillomavirus (HPV ...
Levi Becket of Atlantic City, New Jersey, 1870 Wart Actinic keratosis Epidermodysplasia verruciformis List of cutaneous ...
... in patients with epidermodysplasia verruciformis) Hydrochlorothiazide 1-Hydroxyanthraquinone Indeno[1,2,3-cd]pyrene Indium tin ...
... epidermodysplasia verruciformis) (17q25.3) WT4: encoding protein Wilms tumor-4 The following diseases are related to genes on ... tp53 Corticobasal degeneration Cystinosis Depression Ehlers-Danlos syndrome Epidermodysplasia verruciformis Frontotemporal ...
... deficiency of with ataxia Lutz-Richner-Landolt syndrome Lutz-Lewandowsky epidermodysplasia verruciformis Lyell's syndrome ...
... epidermodysplasia verruciformis The list continues at List of MeSH codes (C03). (Articles with short description, Short ... epidermodysplasia verruciformis MeSH C02.256.700.091 - aleutian mink disease MeSH C02.256.700.300 - erythema infectiosum MeSH ... epidermodysplasia verruciformis MeSH C02.928.313.165 - burkitt lymphoma MeSH C02.928.914.217 - condylomata acuminata MeSH ...
Epidermodysplasia verruciformis », Clin Dermatol, (1985) 3(4), p. 83-96 Orth G, « Epidermodysplasia verruciformis : a model for ... Epidermodysplasia verruciformis: a model for the role of papillomaviruses in human cancer », Cold Spring Harbor Conf. Cell ... Genetics of epidermodysplasia verruciformis: insight into host defense against papillomaviruses », Semin Immunol, (2006) 18, p ... Characterization of two types of human papillomaviruses in lesions of epidermodysplasia verruciformis », Proc Natl Acad Sci USA ...
IRAK4 deficiency IRAK1 deficiency MyD88 deficiency TIRAP deficiency MDA5 deficiency Epidermodysplasia verruciformis WHIM ...
... epidermodysplasia verruciformis MeSH C17.800.849.077 - adiposis dolorosa MeSH C17.800.849.391 - lipodystrophy MeSH C17.800. ...
Epidermodysplasia verruciformis (EV) is a skin condition characterised by warty skin lesions. It results from an abnormal ... Viral diseases: epidermodysplasia verruciformis". Andrews Diseases of the Skin: Clinical Dermatology (13th ed.). Edinburgh: ... His treatment seemed to have worked better.[citation needed] In 2013, one case of epidermodysplasia verruciformis was reported ... Emsen, IM; Kabalar, ME (2010). "Epidermodysplasia verruciformis: An early and unusual presentation". The Canadian Journal of ...
Although epidermodysplasia verruciformis is most commonly inherited in an autosomal recessive manner, sporadic, sex-linked, and ... Epidermodysplasia verruciformis (EV) is a rare, inherited disorder that predisposes patients to widespread human papillomavirus ... encoded search term (Epidermodysplasia Verruciformis) and Epidermodysplasia Verruciformis What to Read Next on Medscape ... The term acquired epidermodysplasia verruciformis (AEV), also referred to as secondary epidermodysplasia verruciformis or ...
Perianal warts and the development of squamous cell carcinoma in epidermodysplasia verruciformis ... Epidermodysplasia verruciformis (EV) is a rare, inherited disorder that predisposes patients to chronic widespread human ... Clinical aspects of epidermodysplasia verruciformis and review of the literature. Int J Dermatol 2007;46:1069-72. ... Al Rubaie S, Breuer J, Inshasi J, Al Saady S, Fathi I. Epidermodysplasia verruciformis with neurological manifestations. Int J ...
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epidermodysplasia verruciformis answers are found in the Tabers Medical Dictionary powered by Unbound Medicine. Available for ... "Epidermodysplasia Verruciformis." Tabers Medical Dictionary, 24th ed., F.A. Davis Company, 2021. Nursing Central, nursing. ... verruciformis. Epidermodysplasia verruciformis. In: Venes DD, ed. Tabers Medical Dictionary. F.A. Davis Company; 2021. https ... Epidermodysplasia verruciformis. (2021). In Venes, D. (Ed.), Tabers Medical Dictionary (24th ed.). F.A. Davis Company. https ...
HomeDictionaryWhat is Epidermodysplasia Verruciformis used for?. What is Epidermodysplasia Verruciformis used for?. By fun-wiki ... What is epidermodysplasia verruciformis?. According to POLYHOBBIES, epidermodysplasia verruciformis is synonymous with Lutz- ... When Epidermodysplasia verruciformis is a disease which is present in the patients from birth to the skin. In the context of ... Epidermodysplasia verruciformis occurs very rarely and is one of the so-called genodermatoses, i.e. congenital diseases of the ...
Acquired Epidermodysplasia Verruciformis During Highly Active Antiretroviral Therapy.. Abheek Sil, Dibyendu B Bhanja, Avik ...
My partner has a genetic condition called Epidermodysplasia verruciformis. She has previously had sqarsquamous cell carcinoma ...
Epidermodysplasia Verruciformis. Epidermodysplasia Verruciformis : Introduction. Epidermodysplasia Verruciformis : Clinical. ... Epidermodysplasia Verruciformis : Microscopic. Epidermodysplasia Verruciformis : Molecular. Epidermodysplasia Verruciformis : ...
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Epidermodysplasia verruciformis. A retrospective study by Ahadiat et al suggested that an association exists between ...
The patient had epidermodysplasia verruciformis, suggesting a clinically important intrinsic T cell function defect. Like the ... The patient had epidermodysplasia verruciformis, suggesting a clinically important intrinsic T cell function defect. Like the ... Combined immunodeficiency with EBV positive B cell lymphoma and epidermodysplasia verruciformis due to a novel homozygous ... Combined immunodeficiency with EBV positive B cell lymphoma and epidermodysplasia verruciformis due to a novel homozygous ...
... characteristics were late clinical debut with an unusual mucocutaneous syndrome of epidermodysplasia verruciformis-human ... heterozygous CORO1A mutations in siblings with a mucocutaneous-immunodeficiency syndrome of epidermodysplasia verruciformis-HPV ...
Cloning of mucosal and cutaneous HPV sequences in a metastatic squamous cell carcinoma from an epidermodysplasia verruciformis ... Cloning of mucosal and cutaneous HPV sequences in a metastatic squamous cell carcinoma from an epidermodysplasia verruciformis ...
... dan 47 untuk Penyakit Epidermodysplasia verruciformis dengan Metode In Silico. *Friend, Usman Sumo (PI) ...
9 Clinical Trend: Epidermodysplasia Verruciformis A rare disease, epidermodysplasia verruciformis was named one of the "10 ...
HPV Diseases: From Cutaneous to Anogenital to Epidermodysplasia Verruciformis Expert Commentary. * Primary Care Clinicians ...
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People with epidermodysplasia verruciformis typically have mutations in two genes, called EVER1 and EVER2. Its not exactly ... "Finding ways to address skin lesions in epidermodysplasia verruciformis patients is a constant struggle," the paper said. ... Bajandar has a rare genetic condition called epidermodysplasia verruciformis, according to news reports. People with this ... Currently, there is no definitive cure for epidermodysplasia verruciformis, according to the 2010 paper. ...
Epidermodysplasia verruciformis. *Syringomelia hyperkeratosis. *Leukocyte adhesion deficiency syndrome. *Polyneuropathy hand ...
Carlson J, Rohwedder A. Genital and epidermodysplasia verruciformis-associated HPV types are frequently found in lichen ...
However, by polymerase chain reaction no HPV or epidermodysplasia verruciformis Discussion. virus DNA could be detected in 8 ... In our case no HPV or epidermodysplasia verruciformis virus DNA could be detected using PCR technique. ...
HPV Diseases: From Cutaneous to Anogenital to Epidermodysplasia Verruciformis Recommendations. * 2001/viewarticle/piroxicam- ...
... these include epidermodysplasia verruciformis (EV), an autosomal recessive disorder with mutations in EVER1 or EVER2 genes on ... The presence of antibodies against virus-like particles of epidermodysplasia verruciformis-associated humanpapillomavirus type ...
Additional Information: Lewandowsky-Lutz dysplasia (also known as Epidermodysplasia verruciformis) is a hereditary disorder ...
Differentiation-Dependent Transcription of the Epidermodysplasia Verruciformis-Associated Human Papillomavirus Type 5 in Benign ...
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Epidermodysplasia verruciformis after cutaneous T-cell lymphoma: Periungual presentation. Dermatol Online J 16(8):12, 2010. e- ... Condyloma and coincidental epidermodysplasia verruciformis (EDV) acanthoma positive for human papillomavirus-14 and -21. (* ... Unique Viral Cytopathic Changes to be Associated with Epidermodysplasia Verruciformis and Human Papillomavirus Type 49. J Cutan ...
  • Epidermodysplasia verruciformis (EV) is a rare, inherited disorder that predisposes patients to widespread human papillomavirus (HPV) infection and cutaneous squamous cell carcinomas . (medscape.com)
  • HPV-5 and HPV-8 have been isolated in more than 90% of epidermodysplasia verruciformis-associated squamous cell carcinomas. (medscape.com)
  • [ 12 ] A report also described a 19-year-old with an autosomal recessive MST1 (or STK4, serine/threonine kinase 4) deficiency who exhibited the epidermodysplasia verruciformis phenotype as well as a global immune deficiency with susceptibility to other bacterial and viral infections. (medscape.com)
  • Scaly patches of skin, warts and papules are typical of Epidermodysplasia verruciformis. (fun-wiki.com)
  • Patients with epidermodysplasia verruciformis are usually infected with multiple types of HPV, including common types that affect individuals without epidermodysplasia verruciformis (eg, HPV types 3 and 10) and those unique to epidermodysplasia verruciformis, the so called epidermodysplasia verruciformis-associated HPVs (EV-HPVs). (medscape.com)
  • Some EV-HPVs are detected in up to 20% of the non-epidermodysplasia verruciformis population, but they are only pathogenic in epidermodysplasia verruciformis patients. (medscape.com)
  • It has been suggested that the human papillomaviruses (HPVs) associated with epidermodysplasia verruciformis (EV), including the oncogenic HPV5, may contribute to the pathogenesis of psoriasis. (keyopinionleaders.com)
  • 2014) Epidermodysplasia Verruciformis.Curr Probl Dermatol. (unibas.ch)
  • The pathophysiology of epidermodysplasia verruciformis is linked to defective cell-mediated immunity, with elucidation of mutations in EVER1 ( TMC6 ) and EVER2 ( TMC8 ) genes (band 17q25). (medscape.com)
  • However, an estimated 25% of patients with epidermodysplasia verruciformis lack mutations in EVER1 and EVER2 , with the genetic defect in these patients not yet elucidated. (medscape.com)
  • [ 11 ] Sporadic reports have described patients with the epidermodysplasia verruciformis phenotype who exhibit mutations in other genes. (medscape.com)
  • Compound heterozygous CORO1A mutations in siblings with a mucocutaneous-immunodeficiency syndrome of epidermodysplasia verruciformis-HPV, molluscum contagiosum and granulomatous tuberculoid leprosy. (telomerescience.com)
  • People with epidermodysplasia verruciformis typically have mutations in two genes, called EVER1 and EVER2. (livescience.com)
  • For more in-depth clinical information, see Epidermodysplasia Verruciformis . (medscape.com)
  • Acquired epidermodysplasia verruciformis: clinical presentation and treatment update. (amedeo.com)
  • Epidermodysplasia verruciformis versus disseminated verrucae planae: is epidermodysplasia verruciformis a generalized infection with wart virus? (ncds.sk)
  • Although the role of EVER1 and EVER2 genes in the pathogenesis of epidermodysplasia verruciformis remains unclear, one hypothesis is that they are involved in the control of HPV infection within keratinocytes, or they play a role in the immune response to the infection itself. (medscape.com)
  • In 2012, two siblings who were homozygous for a mutation that created a stop codon in the Ras homolog gene family member H ( RHOH ) gene exhibited an epidermodysplasia verruciformis phenotype and their T cells exhibited impaired T-cell receptor (TCR) signaling. (medscape.com)
  • Epidermodysplasia verruciformis is extremely rare and increases the risk of developing skin cancer. (fun-wiki.com)
  • A rare disease, epidermodysplasia verruciformis was named one of the "10 strangest conditions you never knew existed" in an online article that was picked up by various medical outlets and circulated last month. (medscape.com)
  • Bajandar has a rare genetic condition called epidermodysplasia verruciformis, according to news reports. (livescience.com)
  • Abul Bajandar, 28, has undergone 25 operations since 2016 in an effort to treat a rare genetic condition, called epidermodysplasia verruciformis, that causes a wooden-like growths on his hands and feet. (rt.com)
  • Epidermodysplasia verruciformis (EV) is a rare genodermatosis associated with a high risk of skin cancer. (nih.gov)
  • The patient had epidermodysplasia verruciformis, suggesting a clinically important intrinsic T cell function defect. (umassmed.edu)
  • In non-epidermodysplasia verruciformis patients, the absence of E5 protects against EV HPV infections. (medscape.com)
  • When Epidermodysplasia verruciformis is a disease which is present in the patients from birth to the skin. (fun-wiki.com)
  • Finding ways to address skin lesions in epidermodysplasia verruciformis patients is a constant struggle," the paper said. (livescience.com)
  • Genetic defects in two genes called EVER1 and EVER2, which are located in the area of ​​the 17th chromosome, lead to the development of epidermodysplasia verruciformis. (fun-wiki.com)
  • Epidermodysplasia verruciformis is a genetic skin disease that is present in those affected from birth. (fun-wiki.com)
  • Other types of human papillomavirus can also trigger epidermodysplasia verruciformis. (fun-wiki.com)
  • In contrast, various types of skin cancer can be found in the malignant variant of Epidermodysplasia verruciformis. (fun-wiki.com)
  • Haller, K., Stubenrauch, F. and Pfister, H. (1995) Differentiation-Dependent Transcription of the Epidermodysplasia Verruciformis-Associated Human Papillomavirus Type 5 in Benign Lesions. (scirp.org)
  • Nursing Central , nursing.unboundmedicine.com/nursingcentral/view/Tabers-Dictionary/750546/all/epidermodysplasia_verruciformis. (unboundmedicine.com)
  • A CIB1 Splice-Site Founder Mutation in Families with Typical Epidermodysplasia Verruciformis. (medscape.com)
  • 1. Whole transcriptome-based skin virome profiling in typical epidermodysplasia verruciformis reveals α-, β-, and γ-HPV infections. (nih.gov)
  • Patel T, Morrison LK, Rady P, Tyring S. Epidermodysplasia verruciformis and susceptibility to HPV. (medscape.com)
  • Patients suffering from epidermodysplasia verruciformis are prone to nonmelanoma skin cancers, due to an inherited abnormal susceptibility to the oncogenic human papillomavirus type 5. (hal.science)
  • Four mutations in Epidermodysplasia verruciformis 1 (EVER1) gene are not contributors to susceptibility in RRP. (cdc.gov)
  • Abstract: Epidermodysplasia verruciformis (EV) is an extremely rare hereditary skin disease characterized by an abnormal susceptibility to the human papilloma virus (HPV) with an increased risk of cutaneous malignancy. (mbru.ac.ae)
  • An ANKRD26 nonsense somatic mutation in a female with epidermodysplasia verruciformis (Tree Man Syndrome). (medscape.com)
  • 5. Recalcitrant Warts, Epidermodysplasia Verruciformis, and the Tree-Man Syndrome: Phenotypic Spectrum of Cutaneous Human Papillomavirus Infections at the Intersection of Genetic Variability of Viral and Human Genomes. (nih.gov)
  • Dr. Michael Chernofsky, an orthopedist and plastic surgeon at Hadassah University Medical Center in Ein Kerem, said the Palestinian, Muhammad Taluli, 42, suffered from an extremely rare condition known as epidermodysplasia verruciformis or "tree man syndrome" that had no documentation in medical books. (jewishbreakingnews.com)
  • KaliÅ„ska-Bienias A, Kowalewski C, Majewski S. The EVER genes - the genetic etiology of carcinogenesis in epidermodysplasia verruciformis and a possible role in non-epidermodysplasia verruciformis patients. (medscape.com)
  • A dysfunction of the p53 gene is thus likely to play a part in epidermodysplasia verruciformis carcinogenesis, either due to ultraviolet-B-induced p53 mutations, as in nonmelanoma skin cancers in the general population, or involving other mutagens or mechanisms. (hal.science)
  • 1 The majority of the warts, papillomas, leukoplakias, or hyperplasias are benign, but some lesions, particularly dysplasias of the cervix uteri, macules of patients with epidermodysplasia verruciformis (EV), and laryngeal papillomas in adults, may progress to squamous cell carcinomas. (jamanetwork.com)
  • 4. TMC8 mutation in a Turkish family with epidermodysplasia verruciformis including laryngeal papilloma and recurrent skin carcinoma. (nih.gov)
  • Novel homozygous frameshift mutation of EVER1 gene in an epidermodysplasia verruciformis patient. (medscape.com)
  • Autosomal dominant epidermodysplasia verruciformis lacking a known EVER1 or EVER2 mutation. (medscape.com)
  • Epidermodysplasia Verruciformis: Genetic Heterogeneity and EVER1 and EVER2 Mutations Revealed by Genome-Wide Analysis. (medscape.com)
  • Scientists have identified a molecular pathway by which some types of human papilloma virus (HPV) might increase the risk of skin cancer, particularly in people with the rare genetic disorder epidermodysplasia verruciformis (EV). (sciencedaily.com)
  • Epidermodysplasia Verruciformis-A Genetic Disorder. (scholarena.co)
  • Identification of the LCK mutation in an atypical epidermodysplasia verruciformis family with T cell defects and virus-induced squamous cell carcinoma. (medscape.com)
  • Epidermodysplasia Verruciformis: Inborn Errors of Immunity to Human Beta-Papillomaviruses. (medscape.com)
  • A homozygous nonsense mutation in the EVER2 gene leads to epidermodysplasia verruciformis. (medscape.com)
  • 17. Epidermodysplasia verruciformis in a HIV-positive patient homozygous for the c917A-->T polymorphism in the TMC8/EVER2 gene. (nih.gov)
  • 2. Novel TMC8 splice site mutation in epidermodysplasia verruciformis and review of HPV infections in patients with the disease. (nih.gov)
  • A novel homozygous DOCK8 mutation associated with unusual coexistence of gross molluscum contagiosum and epidermodysplasia verruciformis in a DOCK8 deficiency patient. (medscape.com)
  • Epidermodysplasia verruciformis (EV) is a skin condition characterised by warty skin lesions. (wikipedia.org)