Keratoacanthoma
Skin
Skin Diseases
Skin Aging
Pancreatic Neoplasms
Neoplasms
Dictionaries, Medical
Malignant Atrophic Papulosis
Activation of telomerase and its association with G1-phase of the cell cycle during UVB-induced skin tumorigenesis in SKH-1 hairless mouse. (1/10127)
Telomerase is a ribonucleoprotein enzyme that adds hexanucleotide repeats TTAGGG to the ends of chromosomes. Telomerase activation is known to play a crucial role in cell-immortalization and carcinogenesis. Telomerase is shown to have a correlation with cell cycle progression, which is controlled by the regulation of cyclins, cyclin dependent kinases (cdks) and cyclin dependent kinase inhibitors (cdkis). Abnormal expression of these regulatory molecules may cause alterations in cell cycle with uncontrolled cell growth, a universal feature of neoplasia. Skin cancer is the most prevalent form of cancer in humans and the solar UV radiation is its major cause. Here, we investigated modulation in telomerase activity and protein expression of cell cycle regulatory molecules during the development of UVB-induced tumors in SKH-1 hairless mice. The mice were exposed to 180 mjoules/cm2 UVB radiation, thrice weekly for 24 weeks. The animals were sacrificed at 4 week intervals and the studies were performed in epidermis. Telomerase activity was barely detectable in the epidermis of non-irradiated mouse. UVB exposure resulted in a progressive increase in telomerase activity starting from the 4th week of exposure. The increased telomerase activity either persisted or further increased with the increased exposure. In papillomas and carcinomas the enzyme activity was comparable and was 45-fold higher than in the epidermis of control mice. Western blot analysis showed an upregulation in the protein expression of cyclin D1 and cyclin E and their regulatory subunits cdk4 and cdk2 during the course of UVB exposure and in papillomas and carcinomas. The protein expression of cdk6 and ckis viz. p16/Ink4A, p21/Waf1 and p27/Kip1 did not show any significant change in UVB exposed skin, but significant upregulation was observed both in papillomas and carcinomas. The results suggest that telomerase activation may be involved in UVB-induced tumorigenesis in mouse skin and that increased telomerase activity may be associated with G1 phase of the cell cycle. (+info)L-[1-11C]-tyrosine PET to evaluate response to hyperthermic isolated limb perfusion for locally advanced soft-tissue sarcoma and skin cancer. (2/10127)
PET with L-[1-11C]-tyrosine (TYR) was investigated in patients undergoing hyperthermic isolated limb perfusion (HILP) with recombinant tumor necrosis factor alpha (rTNF-alpha) and melphalan for locally advanced soft-tissue sarcoma and skin cancer of the lower limb. METHODS: Seventeen patients (5 women, 12 men; age range 24-75 y; mean age 52 y) were studied. TYR PET studies were performed before HILP and 2 and 8 wk afterwards. The protein synthesis rates (PSRs) in nanomoles per milliliter per minute were calculated. After final PET studies, tumors were resected and pathologically examined. Patients with pathologically complete responses (pCR) showed no viable tumors after treatment. Those with pathologically partial responses (pPR) showed various amounts of viable tumors in the resected tumor specimens. RESULTS: Six patients (35%) showed a pCR and 11 patients (65%) showed a pPR. All tumors were depicted as hot spots on PET studies before HILP. The PSR in the pCR group at 2 and 8 wk after perfusion had decreased significantly (P < 0.05) in comparison to the PSR before HILP. A significant difference was found in PSR between the pCR and pPR groups at 2 and at 8 wk (P < 0.05). Median PSR in nonviable tumor tissue was 0.62 and ranged from 0.22 to 0.91. With a threshold PSR of 0.91, sensitivity and specificity of TYR PET were 82% and 100%, respectively. The predictive value of a PSR > 0.91 for having viable tumor after HILP was 100%, whereas the predictive value of a PSR < or = 0.91 for having nonviable tumor tissue after HILP was 75%. The 2 patients in the pPR groups with a PSR < 0.91 showed microscopic islets of tumor cells surrounded by extensive necrosis on pathological examination. CONCLUSION: Based on the calculated PSR after HILP, TYR PET gave a good indication of the pathological outcome. Inflammatory tissue after treatment did not interfere with viable tumor on the images, suggesting that it may be worthwhile to pursue TYR PET in other therapy evaluation settings. (+info)Frequent nuclear/cytoplasmic localization of beta-catenin without exon 3 mutations in malignant melanoma. (3/10127)
Beta-Catenin has a critical role in E-cadherin-mediated cell-cell adhesion, and it also functions as a downstream signaling molecule in the wnt pathway. Mutations in the putative glycogen synthase kinase 3beta phosphorylation sites near the beta-catenin amino terminus have been found in some cancers and cancer cell lines. The mutations render beta-catenin resistant to regulation by a complex containing the glycogen synthase kinase 3beta, adenomatous polyposis coli, and axin proteins. As a result, beta-catenin accumulates in the cytosol and nucleus and activates T-cell factor/ lymphoid enhancing factor transcription factors. Previously, 6 of 27 melanoma cell lines were found to have beta-catenin exon 3 mutations affecting the N-terminal phosphorylation sites (Rubinfeld B, Robbins P, Elgamil M, Albert I, Porfiri E, Polakis P: Stabilization of beta-catenin by genetic defects in melanoma cell lines. Science 1997, 275:1790-1792). To assess the role of beta-catenin defects in primary melanomas, we undertook immunohistochemical and DNA sequencing studies in 65 melanoma specimens. Nuclear and/or cytoplasmic localization of beta-catenin, a potential indicator of wnt pathway activation, was seen focally within roughly one third of the tumors, though a clonal somatic mutation in beta-catenin was found in only one case (codon 45 Ser-->Pro). Our findings demonstrate that beta-catenin mutations are rare in primary melanoma, in contrast to the situation in melanoma cell lines. Nonetheless, activation of beta-catenin, as indicated by its nuclear and/or cytoplasmic localization, appears to be frequent in melanoma, and in some cases, it may reflect focal and transient activation of the wnt pathway within the tumor. (+info)Interleukin-10-treated human dendritic cells induce a melanoma-antigen-specific anergy in CD8(+) T cells resulting in a failure to lyse tumor cells. (4/10127)
Dendritic cells (DC) are critically involved in the initiation of primary immune processes, including tumor rejection. In our study, we investigated the effect of interleukin-10 (IL-10)-treated human DC on the properties of CD8(+) T cells that are known to be essential for the destruction of tumor cells. We show that IL-10-pretreatment of DC not only reduces their allostimulatory capacity, but also induces a state of alloantigen-specific anergy in both primed and naive (CD45RA+) CD8(+) T cells. To investigate the influence of IL-10-treated DC on melanoma-associated antigen-specific T cells, we generated a tyrosinase-specific CD8(+) T-cell line by several rounds of stimulation with the specific antigen. After coculture with IL-10-treated DC, restimulation of the T-cell line with untreated, antigen-pulsed DC demonstrated peptide-specific anergy in the tyrosinase-specific T cells. Addition of IL-2 to the anergic T cells reversed the state of both alloantigen- or peptide-specific anergy. In contrast to optimally stimulated CD8(+) T cells, anergic tyrosinase-specific CD8(+) T cells, after coculture with peptide-pulsed IL-10-treated DC, failed to lyse an HLA-A2-positive and tyrosinase-expressing melanoma cell line. Thus, our data demonstrate that IL-10-treated DC induce an antigen-specific anergy in cytotoxic CD8(+) T cells, a process that might be a mechanism of tumors to inhibit immune surveillance by converting DC into tolerogenic antigen-presenting cells. (+info)Gardner's syndrome and steatocystoma multiplex. Two unusual genetically determined conditions occurring in same patient. (5/10127)
A 43-year-old man is described who had Gardner's syndrome and steatocystoma multiplex. These two unusual genetically determined conditions were associated because he had inherited the Gardner's syndrome from his father and the steatocystoma multiplex from his mother. (+info)MDM2 overexpression generates a skin phenotype in both wild type and p53 null mice. (6/10127)
The MDM2 proto-oncogene is overexpressed in human tumours and regulates the activities of the tumour suppressors p53 and pRB. We created mice that overexpress MDM2 under the control of the CMV promoter. These mice did not display an increased tumour incidence, but rather a specific skin phenotype, characterized by desquamation and hyperkeratosis. Transgenic MDM2 was found to be overexpressed in the epidermis, a tissue that normally expresses high levels of MDM2. The phenotype appeared during the first week after birth and then lessened with age, closely following the level of expression of the transgene. MDM2 overexpression was associated with an increase in proliferation in the basal layer, thickening of the epidermis, altered expression of the differentiation markers cytokeratin CK14, CK10 and CK1, and a decrease in the size and the number of granules that contain products of differentiation. Transgenic mice on a p53 null background displayed similar although not identical changes, showing that the effects of MDM2 are to a certain degree p53 independent. The skin is a major site of MDM2 expression in mice, raising the possibility that MDM2 overexpression perturbs the normal pattern of MDM2 expression and inhibits differentiation of the epidermis. (+info)Tumor suppression in human skin carcinoma cells by chromosome 15 transfer or thrombospondin-1 overexpression through halted tumor vascularization. (7/10127)
The development of skin carcinomas presently is believed to be correlated with mutations in the p53 tumor suppressor and ras gene as well as with the loss of chromosome 9. We now demonstrate that, in addition, loss of chromosome 15 may be a relevant genetic defect. Reintroduction of an extra copy of chromosome 15, but not chromosome 4, into the human skin carcinoma SCL-I cells, lacking one copy of each chromosome, resulted in tumor suppression after s.c. injection in mice. Transfection with thrombospondin-1 (TSP-1), mapped to 15q15, induced the same tumor suppression without affecting cell proliferation in vitro or in vivo. Halted tumors remained as small cysts encapsulated by surrounding stroma and blood vessels. These cysts were characterized by increased TSP-1 matrix deposition at the tumor/stroma border and a complete lack of tumor vascularization. Coinjection of TSP-1 antisense oligonucleotides drastically reduced TSP-1 expression and almost completely abolished matrix deposition at the tumor/stroma border. As a consequence, the tumor phenotype reverted to a well vascularized, progressively expanding, solid carcinoma indistinguishable from that induced by the untransfected SCL-I cells. Thus, these data strongly suggest TSP-1 as a potential tumor suppressor on chromosome 15. The data further propose an unexpected mechanism of TSP-1-mediated tumor suppression. Instead of interfering with angiogenesis in general, in this system TSP-1 acts as a matrix barrier at the tumor/stroma border, which, by halting tumor vascularization, prevents tumor cell invasion and, thus, tumor expansion. (+info)Glucocorticoid mediation of dietary energy restriction inhibition of mouse skin carcinogenesis. (8/10127)
Dietary energy restriction (DER) inhibits carcinogenesis in numerous animal models. DER is a potent and reproducible inhibitor of two-stage mouse skin carcinogenesis when administered during the promotion phase. Previous research demonstrated that adrenalectomy abolished cancer prevention by food restriction. Several lines of evidence suggest that glucocorticoid elevation in the DER mouse mediates the prevention of skin cancer. Our research tested the hypothesis that elevated glucocorticoid hormone activates the glucocorticoid receptor (GR) and that this activated receptor interferes with the activator protein-1 (AP-1) transcription factor. Induction of AP-1 by the phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is essential to tumor promotion. We have been unable to demonstrate elevated activated GR in the epidermis of the DER mouse, perhaps because only indirect strategies have been possible with the use of epidermis from DER mice. However, DER blocked the induction of AP-1 and c-jun, a constituent protein of AP-1, in the epidermis of mice. Current studies are focused on the inhibition of signaling down the MAP-1/Raf-1 kinase pathway that leads to induction of constituent proteins of AP-1, including c-Jun. Although several pathways lead to the induction of AP-1 transcriptional activity, the MAP-1/Raf-1 pathway can be activated by protein kinase C (PKC); previous studies from our laboratory demonstrated an inhibition of PKC activity and a reduction in selected isoforms of PKC in the epidermis of the DER mouse. Our current working hypothesis is that elevated glucocorticoid hormone in the DER mouse reduces the amount and activity of PKC isoforms important in the activation of MAP-1/Raf-1 kinase pathway. We propose that this results in attenuation in the induction of the AP-1 transcription factor by TPA. Because AP-1 induction by TPA is obligatory for mouse skin promotion, we propose this as an essential component of the mechanism of DER prevention of mouse skin carcinogenesis. (+info)Keratoacanthoma is a rapidly growing, dome-shaped, skin tumor that typically arises on sun-exposed areas such as the face, arms, and legs. It is considered a low-grade squamous cell carcinoma (a type of skin cancer) because it shares some characteristics with both benign and malignant tumors.
Keratoacanthomas usually develop over a period of several weeks to months, growing rapidly in size before eventually stabilizing and then gradually regressing on their own within a few months to a year. However, the regression process can take years, and some lesions may not regress completely, leading to cosmetic concerns or even local invasion.
Histologically, keratoacanthomas are characterized by a central keratin-filled crater surrounded by a well-differentiated layer of squamous epithelial cells. The tumor's growth pattern and histological features can make it difficult to distinguish from other types of skin cancer, such as squamous cell carcinoma.
Treatment options for keratoacanthomas include surgical excision, cryosurgery, curettage and electrodesiccation, and topical therapies like imiquimod or 5-fluorouracil. The choice of treatment depends on various factors such as the size, location, and number of lesions, as well as patient preferences and overall health status.
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.
In medical terms, the skin is the largest organ of the human body. It consists of two main layers: the epidermis (outer layer) and dermis (inner layer), as well as accessory structures like hair follicles, sweat glands, and oil glands. The skin plays a crucial role in protecting us from external factors such as bacteria, viruses, and environmental hazards, while also regulating body temperature and enabling the sense of touch.
Skin diseases, also known as dermatological conditions, refer to any medical condition that affects the skin, which is the largest organ of the human body. These diseases can affect the skin's function, appearance, or overall health. They can be caused by various factors, including genetics, infections, allergies, environmental factors, and aging.
Skin diseases can present in many different forms, such as rashes, blisters, sores, discolorations, growths, or changes in texture. Some common examples of skin diseases include acne, eczema, psoriasis, dermatitis, fungal infections, viral infections, bacterial infections, and skin cancer.
The symptoms and severity of skin diseases can vary widely depending on the specific condition and individual factors. Some skin diseases are mild and can be treated with over-the-counter medications or topical creams, while others may require more intensive treatments such as prescription medications, light therapy, or even surgery.
It is important to seek medical attention if you experience any unusual or persistent changes in your skin, as some skin diseases can be serious or indicative of other underlying health conditions. A dermatologist is a medical doctor who specializes in the diagnosis and treatment of skin diseases.
Skin aging, also known as cutaneous aging, is a complex and multifactorial process characterized by various visible changes in the skin's appearance and function. It can be divided into two main types: intrinsic (chronological or natural) aging and extrinsic (environmental) aging.
Intrinsic aging is a genetically determined and time-dependent process that results from internal factors such as cellular metabolism, hormonal changes, and genetic predisposition. The primary features of intrinsic aging include gradual thinning of the epidermis and dermis, decreased collagen and elastin production, reduced skin cell turnover, and impaired wound healing. Clinically, these changes present as fine wrinkles, dryness, loss of elasticity, and increased fragility of the skin.
Extrinsic aging, on the other hand, is caused by external factors such as ultraviolet (UV) radiation, pollution, smoking, alcohol consumption, and poor nutrition. Exposure to these environmental elements leads to oxidative stress, inflammation, and DNA damage, which accelerate the aging process. The main features of extrinsic aging are coarse wrinkles, pigmentary changes (e.g., age spots, melasma), irregular texture, skin laxity, and increased risk of developing skin cancers.
It is important to note that intrinsic and extrinsic aging processes often interact and contribute to the overall appearance of aged skin. A comprehensive approach to skincare should address both types of aging to maintain healthy and youthful-looking skin.
Pancreatic neoplasms refer to abnormal growths in the pancreas that can be benign or malignant. The pancreas is a gland located behind the stomach that produces hormones and digestive enzymes. Pancreatic neoplasms can interfere with the normal functioning of the pancreas, leading to various health complications.
Benign pancreatic neoplasms are non-cancerous growths that do not spread to other parts of the body. They are usually removed through surgery to prevent any potential complications, such as blocking the bile duct or causing pain.
Malignant pancreatic neoplasms, also known as pancreatic cancer, are cancerous growths that can invade and destroy surrounding tissues and organs. They can also spread (metastasize) to other parts of the body, such as the liver, lungs, or bones. Pancreatic cancer is often aggressive and difficult to treat, with a poor prognosis.
There are several types of pancreatic neoplasms, including adenocarcinomas, neuroendocrine tumors, solid pseudopapillary neoplasms, and cystic neoplasms. The specific type of neoplasm is determined through various diagnostic tests, such as imaging studies, biopsies, and blood tests. Treatment options depend on the type, stage, and location of the neoplasm, as well as the patient's overall health and preferences.
Neoplasms are abnormal growths of cells or tissues in the body that serve no physiological function. They can be benign (non-cancerous) or malignant (cancerous). Benign neoplasms are typically slow growing and do not spread to other parts of the body, while malignant neoplasms are aggressive, invasive, and can metastasize to distant sites.
Neoplasms occur when there is a dysregulation in the normal process of cell division and differentiation, leading to uncontrolled growth and accumulation of cells. This can result from genetic mutations or other factors such as viral infections, environmental exposures, or hormonal imbalances.
Neoplasms can develop in any organ or tissue of the body and can cause various symptoms depending on their size, location, and type. Treatment options for neoplasms include surgery, radiation therapy, chemotherapy, immunotherapy, and targeted therapy, among others.
An acanthoma is a benign skin tumor characterized by the proliferation of epidermal cells, specifically the pickle cell layer (stratum spinosum). The term "acanthoma" comes from the Greek word "akantha," which means "thorn" or "spine."
There are several types of acanthomas, including:
1. Seborrheic keratosis: Also known as seborrheic warts, these are common benign growths that appear as rough, scaly patches on the skin. They can be tan, brown, or black and may have a waxy or greasy appearance.
2. Benign lichenoid keratosis: These are small, flat lesions with a scaly surface that typically occur on sun-exposed areas of the skin. They are usually asymptomatic but may occasionally itch.
3. Psoriasiform acanthoma: This is a rare type of acanthoma that resembles psoriasis, a chronic skin condition characterized by red, scaly patches.
4. Clear cell acanthoma: This is a distinctive type of acanthoma that appears as a solitary, dome-shaped nodule with a smooth surface and a central crust. It typically occurs on the lower legs of older adults.
Acanthomas are generally harmless and do not require treatment unless they become irritated or unsightly. In such cases, they can be removed through various methods, including cryosurgery (freezing), curettage (scraping), or excision (cutting).
A medical dictionary is a reference book that contains definitions and explanations of medical terms and jargon. It serves as a useful tool for healthcare professionals, students, patients, and anyone else who needs to understand medical terminology. Medical dictionaries can include definitions of diseases, conditions, treatments, procedures, drugs, equipment, anatomy, and more. They may also provide pronunciation guides, etymologies, and abbreviations.
Medical dictionaries can be found in print or digital form, and some are specialized to cover specific areas of medicine, such as oncology, psychiatry, or surgery. Some medical dictionaries are also bilingual, providing translations of medical terms between different languages. Overall, a medical dictionary is an essential resource for anyone who needs to communicate effectively in the field of medicine.
Malignant atrophic papulosis (MAP), also known as Kohlmeier-Degos disease, is a rare and progressive cutaneous vasculopathy of unknown etiology. It is characterized by the development of porcelain-white atrophic macules, which evolve into papules with a central necrotic depression or ulceration, surrounded by an erythematous halo. The lesions typically appear on the trunk and extremities, but may also affect mucous membranes, gastrointestinal tract, and other organs.
MAP is considered to be a chronic inflammatory disorder that affects small-sized blood vessels, leading to tissue ischemia and necrosis. The disease can have a variable clinical course, ranging from self-limited cutaneous involvement to systemic manifestations with potentially life-threatening complications.
The diagnosis of MAP is based on the clinical presentation, histopathological findings, and exclusion of other similar conditions. Treatment options for MAP are limited, and there is no cure for this disease. The management typically involves a multidisciplinary approach to address the various organ manifestations and prevent complications.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.