Keratoacanthoma: A benign, non-neoplastic, usually self-limiting epithelial lesion closely resembling squamous cell carcinoma clinically and histopathologically. It occurs in solitary, multiple, and eruptive forms. The solitary and multiple forms occur on sunlight exposed areas and are identical histologically; they affect primarily white males. The eruptive form usually involves both sexes and appears as a generalized papular eruption.Skin Neoplasms: Tumors or cancer of the SKIN.Skin: The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.Skin DiseasesSkin Aging: The process of aging due to changes in the structure and elasticity of the skin over time. It may be a part of physiological aging or it may be due to the effects of ultraviolet radiation, usually through exposure to sunlight.Pancreatic Neoplasms: Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Search of: 'Skin Neoplasms' - Results by Topic - ClinicalTrials.govIMPORTANT: Listing of a study on this site does not reflect endorsement by the National Institutes of Health. Talk with a trusted healthcare professional before volunteering for a study. Read more... ...
C44.101 UNSPECIFIED MALIGNANT NEOPLASM OF SKIN OF UNSPECIFIED EYELID, INCLUDING CANTHUSThis code is grouped under diagnosis codes for neoplasms. ... ICD-10 C44.101 is unspecified malignant neoplasm of skin of ... Neoplasms (C00-D48) *Melanoma and other malignant neoplasms of skin (C43-C44) *Other and unspecified malignant neoplasm of skin ... Other specified malignant neoplasm of skin of nose. 56. C44.399. Other specified malignant neoplasm of skin of other parts of ... Other specified malignant neoplasm of skin of scalp and neck. 62. C44.5. Other and unspecified malignant neoplasm of skin of ...
ICD-10 Diagnosis Code C44.40 Unspecified malignant neoplasm of skin of scalp and neckskin NOS. »scalp. C44.40. C79.2. D04.4. D23.4. D48.5. D49.2. »skin NOS. »supraclavicular region [See Also: Neoplasm, skin, neck ... Neoplasms (C00-D48) * Melanoma and other malignant neoplasms of skin (C43-C44) *Other and unspecified malignant neoplasm of ... Unspecified malignant neoplasm of skin of scalp and neck Long Description: Unspecified malignant neoplasm of skin of scalp and ... skin NOS. »cervical region [See Also: Neoplasm, skin, neck]. C44.40. C79.2. D04.4. D23.4. D48.5. D49.2. ...
Benign facial skin neoplasm. Plastic surgery: Diagnostic in Germany, Erlangen hospitals on BookingHealth.comBenign facial skin neoplasm. Plastic surgery: Diagnostic in Erlangen, Germany ✈. Prices on BookingHealth.com - booking ... Plastic surgery: Benign facial skin neoplasm. Diagnostic in Germany, Erlangen See also for benign facial skin neoplasm:. * ... Diagnosis of benign facial skin neoplasm #257071. The Department of Plastic and Hand Surgery offers the full range of modern ...
The Safety and Effectiveness of Ritonavir in the Treatment of HIV-Related Kaposi's Sarcoma - Full Text View -...Skin Neoplasms. Sarcoma, Kaposi. Acquired Immunodeficiency Syndrome. HIV Protease Inhibitors. Ritonavir. Additional relevant ... Neoplasms, Connective and Soft Tissue. Neoplasms by Histologic Type. Neoplasms. Herpesviridae Infections. DNA Virus Infections ... Neoplasms, Vascular Tissue. Ritonavir. HIV Protease Inhibitors. Protease Inhibitors. Enzyme Inhibitors. Molecular Mechanisms of ...
EARLY SKIN CANCER PICTURES : CANCER PICTURES - BEST CANCER FIGHTING FOODSEarly skin cancer pictures : Leukemia cancer research. Early Skin Cancer Pictures. skin cancer *a malignant neoplasm of the ... Skin neoplasms are growths on the skin which can have many causes. The three most common skin cancers are basal cell cancer, ... Skin cancer occurs when skin cells start growing abnormally, causing cancerous growths. Most skin cancers develop on the ... and that the puff of skin on her sides is caused by the surgery and the implants... nothing to worry about... and the puff will ...
Ryan J. Martinez, MD, FACS | Swedish Medical Center Seattle and Issaquahbenign neoplasm of colon. *benign neoplasm of skin. *bile duct cancer. *bile duct occlusion ...
swedish.org/swedish-physicians/profile.aspx?name=martinez ryan j&id=159783
Avaliação de 496 laudos anatomopatológicos de melanoma diagnosticados no município de Florianópolis, Santa Catarina, BrasilKeywords : Diagnosis; Melanoma; Melanoma [pathology]; Skin neoplasms. · abstract in Portuguese · text in Portuguese · ... BACKGROUND - Melanoma is the most lethal cutaneous neoplasm and its incidence has increased worldwide. Statistical knowledge ... The main metastasis sites were skin and subcutaneous tissue, lymph nodes and brain. CONCLUSIONS - In this study, the ...
Dermoscopic classification of atypical melanocytic nevi (Clark nevi).Skin Neoplasms / classification*, pathology*. Comments/Corrections. Comment In: Arch Dermatol. 2001 Dec;137(12):1641-4 [PMID: ... 15244227 - Randomized controlled trial of skin-to-skin contact from birth versus conventional incu.... 21642947 - A role of ... SETTING: Two pigmented skin lesion clinics. PATIENTS: We examined 829 Clark nevi on 23 individuals. MAIN OUTCOME MEASURE: A ... 2565367 - Evaporation and skin penetration characteristics of mosquito repellent formulations.. 17300657 - Precalcaneal ...
Anjela Galan, MD > Yale Cancer Center | Yale School of...Skin Diseases. *Skin Neoplasms. Patient Care. Accepts new patients? Yes. Patient Type: Adult; Adolescent; Child. Referrals: MD ...
Chemoprevention of Skin Cancer Program Project - David AlbertsSkin cancer is the most common malignancy in the world. One out of three new cancers is a skin cancer. More than 1 million cases of non-melanoma skin cancer (NM...
METHOD FOR PREVENTING OR TREATING SKIN TUMOR - GALDERMA RESEARCH & DEVELOPMENTMethods, compositions and products for preventing skin tumor formation or inhibiting the development of an existing skin tumor in a subject are described. The methods involve administering to the subject a composition containing an α adrenergic receptor agonist, such as brimonidine.
Skin Cancer by the Numbers: It's the Most Common Cancer of All | WHAMHere are some statistics about skin cancer and tips for staying safe.One in five Americans will be diagnosed with skin cancer at some point in life, according to skincancer.org.There are four common types of skin cancers, according to the American Academy
More melanoma deaths in areas without skin doctors | Lifescript.comNEW YORK (Reuters Health) - Fewer people die from the skin cancer melanoma in U.S. counties that have at least one dermatologist, according to a new study.It's...
Dermal equivalent: The dermal equivalent is an in vitro model of the dermal layer of skin. It is constructed by seeding dermal fibroblasts into a collagen gel.Actinic elastosis: Actinic elastosis, also known as solar elastosis is an accumulation of abnormal elastin (elastic tissue) in the dermis of the skin, or in the conjunctiva of the eye, which occurs as a result of the cumulative effects of prolonged and excessive sun exposure, a process known as photoaging.Pancreatoblastoma
(1/10127) Activation of telomerase and its association with G1-phase of the cell cycle during UVB-induced skin tumorigenesis in SKH-1 hairless mouse.
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)
(2/10127) L-[1-11C]-tyrosine PET to evaluate response to hyperthermic isolated limb perfusion for locally advanced soft-tissue sarcoma and skin cancer.
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)
(3/10127) Frequent nuclear/cytoplasmic localization of beta-catenin without exon 3 mutations in malignant melanoma.
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)
(4/10127) Interleukin-10-treated human dendritic cells induce a melanoma-antigen-specific anergy in CD8(+) T cells resulting in a failure to lyse tumor cells.
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)
(5/10127) Gardner's syndrome and steatocystoma multiplex. Two unusual genetically determined conditions occurring in same patient.
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)
(6/10127) MDM2 overexpression generates a skin phenotype in both wild type and p53 null mice.
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)
(7/10127) Tumor suppression in human skin carcinoma cells by chromosome 15 transfer or thrombospondin-1 overexpression through halted tumor vascularization.
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)
(8/10127) Glucocorticoid mediation of dietary energy restriction inhibition of mouse skin carcinogenesis.
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)
- Another type of skin cancer, melanoma, is more dangerous but less common. (icdlist.com)
- The three most common skin cancers are basal cell cancer, squamous cell cancer, and melanoma, each of which is named after the type of skin cell from which it arises. (google.com)
- BACKGROUND - Melanoma is the most lethal cutaneous neoplasm and its incidence has increased worldwide. (scielo.br)
- For each site there are six possible code numbers according to whether the neoplasm in question is malignant, benign, in situ, of uncertain behavior, or of unspecified nature. (icdlist.com)
- Benign facial skin neoplasm. (bookinghealth.com)
- The main metastasis sites were skin and subcutaneous tissue, lymph nodes and brain. (scielo.br)
- Patients who have multiple skin cancers because of xeroderma pigmentosum (XP). (clinicaltrials.gov)
- Other research includes studies of the p53 gene in skin cancer, epidemiology of skin cancer, and innovative diagnostic devices. (yale.edu)
- Well-differentiated neuroendocrine tumors in skin: Terminology and diagnostic utility of cytokeratin 5/6 and p63. (yale.edu)
- Patient must be available for and agreeable to regular follow up examinations in the clinic for clinical evaluation, blood tests, diagnostic x-rays and possibly skin biopsies. (clinicaltrials.gov)
- Most skin cancers develop on the visible outer layer of the skin (the epidermis), particularly in sun-exposed areas (face, head, hands, arms, and legs). (google.com)
- If not treated, some types of skin cancer cells can spread to other tissues and organs. (icdlist.com)
- Mastocytosis is a disorder characterized by presence of excessive numbers of mast cells in skin, bone marrow and internal organs. (clinicaltrials.gov)
- PTCH codon 1315 polymorphism and risk for nonmelanoma skin cancer. (yale.edu)
- Family history of skin cancer is associated with early-onset basal cell carcinoma independent of MC1R genotype. (yale.edu)
- Subsequent skin cancer in patients with early-onset basal cell carcinoma. (yale.edu)
- Mastocytosis in children is generally limited to the skin and follows a self limited course, while it is a disorder of the hematopoietic stem cell associated with somatic mutations of the c-kit gene in most patients with adult-onset of disease. (clinicaltrials.gov)
- Skin cancer is the most common form of cancer in the United States. (icdlist.com)
- Skin cancer occurs when skin cells start growing abnormally, causing cancerous growths. (google.com)
- Dr. Leffell and colleagues discovered the skin cancer gene, PTCH, in 1996 and have directed subsequent research towards understanding how skin cancer develops. (yale.edu)
- How likely is it for someone with a few atypical moles to develop skin cancer in the future? (healthcaremagic.com)
- If skin irritation results from the drug, then we will stop use of the drug. (clinicaltrials.gov)
- Because of the long-term storage of etretinate, a known teratogen, fertile women who may be treated in this protocol, must have skin disease that is severe and recalcitrant to all other standard modalities. (clinicaltrials.gov)
hair and eyes
- I am fair-skinned, and I have very dark hair and eyes. (healthcaremagic.com)
- They will then be prescribed 0.1% rapamune topical formulation to apply twice daily to their skin for the first two weeks and then once daily. (clinicaltrials.gov)
- and that the puff of skin on her sides is caused by the surgery and the implants. (google.com)
- You should have your doctor check any suspicious skin markings and any changes in the way your skin looks. (icdlist.com)