Goldberg MS, Doucette JT, Lim HW et al.Risk factors for presumptive melanoma in skin cancer screening: American Academy of Dermatology National Melanoma/Skin Cancer Screening Program experience 2001-2005. J Am Acad Dermatol 57:60-66
Since its inception in 1985, the American Academy of Dermatology (AAD) National Melanoma/Skin Cancer Screening Program has strived to enhance early detection of cutaneous malignant melanoma (MM) by providing nationwide skin cancer education campaigns in combination with free skin cancer screenings.
To analyze the AAD screening data from 2001 to 2005 in order to identify factors associated with MM detection, and thereby derive a model of increased likelihood for MM detection through visual skin examinations at screenings.
Patients completed a standardized AAD pre-screening form with historical and phenotypic information. Clinicians then recorded suspected clinical findings noted at visual skin examination. Statistical analyses were conducted using SPSS 14 (SPSS Inc., Chicago, Ill).
Five factors, which can be remembered with the acronym HARMM, independently increased the likelihood of suspected MM being found in the 362,804 persons screened: History of previous melanoma (odds ratio [OR] = 3.3; 95% confidence interval [CI], 2.9-3.8); Age over 50 (OR = 1.2; 95% CI, 1.1-1.3); Regular dermatologist absent (OR = 1.4; 95% CI, 1.3-1.5); Mole changing (OR = 2.0; 95% CI, 1.9-2.2); and Male gender (OR = 1.4; 95% CI, 1.3-1.5). Individuals at highest risk (4 or 5 factors) comprised only 5.8% of the total population, yet accounted for 13.6% of presumptive MM findings, and were 4.4 times (95% CI, 3.8-5.1) more likely to be diagnosed with suspected MM than individuals at lowest risk (0 or 1 factor). Receipt of a total skin examination at screening independently increased the likelihood for identifying suspected MM (OR = 1.4; 95% CI, 1.3-1.6). However, significantly fewer screenees in the highest risk group versus those in the lowest risk group underwent total skin examinations (53.7% vs 62.5%).
Risk factors studied limited to variables collected in screenee enrollment form.
A higher-risk subgroup of the skin cancer screening population can be identified through assessment of MM risk factors using the HARMM criteria. Refocusing efforts to provide a total skin examination to those individuals with multiple risk factors has the potential to both reduce costs and increase yields for suspected MM in future mass screening initiatives.
Available from: Wendan Yu
- "Melanoma is one of the most aggressive forms of skin cancer, which has been occurring with an increased incidence faster than that of any other cancer in the world –. Although melanoma in early stage is curable, the prognosis and overall survival for patients with metastasized melanoma is unfavourable. "
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ABSTRACT: Melatonin is a hormone identified in plants and pineal glands of mammals and possesses diverse physiological functions. Fisetin is a bio-flavonoid widely found in plants and exerts antitumor activity in several types of human cancers. However, the combinational effect of melatonin and fisetin on antitumor activity, especially in melanoma treatment, remains unclear. Here, we tested the hypothesis that melatonin could enhance the antitumor activity of fisetin in melanoma cells and identified the underlying molecular mechanisms. The combinational treatment of melanoma cells with fisetin and melatonin significantly enhanced the inhibitions of cell viability, cell migration and clone formation, and the induction of apoptosis when compared with the treatment of fisetin alone. Moreover, such enhancement of antitumor effect by melatonin was found to be mediated through the modulation of the multiply signaling pathways in melanoma cells. The combinational treatment of fisetin with melatonin increased the cleavage of PARP proteins, triggered more release of cytochrome-c from the mitochondrial inter-membrane, enhanced the inhibition of COX-2 and iNOS expression, repressed the nuclear localization of p300 and NF-κB proteins, and abrogated the binding of NF-κB on COX-2 promoter. Thus, these results demonstrated that melatonin potentiated the anti-tumor effect of fisetin in melanoma cells by activating cytochrome-c-dependent apoptotic pathway and inhibiting COX-2/iNOS and NF-κB/p300 signaling pathways, and our study suggests the potential of such a combinational treatment of natural products in melanoma therapy.
Available from: Mohammad Rais Mustafa
- "Melanoma is a skin cancer that arises from the malignant transformation of melanocytes. Epidemiological studies showed that the incidence of melanoma is increasing at a rate faster than that of any other cancers worldwide [1-3]. Moreover, although early stage melanoma is confined to epidermis and is curable, metastasized melanoma has an unfavourable prognosis, where the overall survival for patients with metastatic melanoma ranges from 4.7 to 11 months, with a median survival of 8.5 months . "
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ABSTRACT: Centratherum anthelminticum (L.) Kuntze (scientific synonyms: Vernonia anthelmintica; black cumin) is one of the ingredients of an Ayurvedic preparation, called "Kayakalp", commonly applied to treat skin disorders in India and Southeast Asia. Despite its well known anti-inflammatory property on skin diseases, the anti-cancer effect of C. anthelminticum seeds on skin cancer is less documented. The present study aims to investigate the anti-cancer effect of Centratherum anthelminticum (L.) seeds chloroform fraction (CACF) on human melanoma cells and to elucidate the molecular mechanism involved.
A chloroform fraction was extracted from C. anthelminticum (CACF). Bioactive compounds of the CACF were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Human melanoma cell line A375 was treated with CACF in vitro. Effects of CACF on growth inhibition, morphology, stress and survival of the cell were examined with MTT, high content screening (HSC) array scan and flow cytometry analyses. Involvement of intrinsic or extrinsic pathways in the CACF-induced A375 cell death mechanism was examined using a caspase luminescence assay. The results were further verified with different caspase inhibitors. In addition, Western blot analysis was performed to elucidate the changes in apoptosis-associated molecules. Finally, the effect of CACF on the NF-kappaB nuclear translocation ability was assayed.
The MTT assay showed that CACF dose-dependently inhibited cell growth of A375, while exerted less cytotoxic effect on normal primary epithelial melanocytes. We demonstrated that CACF induced cell growth inhibition through apoptosis, as evidenced by cell shrinkage, increased annexin V staining and formation of membrane blebs. CACF treatment also resulted in higher reactive oxygen species (ROS) production and lower Bcl-2 expression, leading to decrease mitochondrial membrane potential (MMP). Disruption of the MMP facilitated the release of mitochondrial cytochrome c, which activates caspase-9 and downstream caspase-3/7, resulting in DNA fragmentation and up-regulation of p53 in melanoma cells. Moreover, CACF prevented TNF-alpha-induced NF-kappaB nuclear translocation, which further committed A375 cells toward apoptosis.
Together, our findings suggest CACF as a potential therapeutic agent against human melanoma malignancy.
Available from: PubMed Central
- "The use of genetic risk information is likely to be persuasive for both patients and physicians. As we identify and evaluate such opportunities, we need to hold genomic risk information to the test of comparative effectiveness : for example, is a DNA-based test to identify increased risk for melanoma better than the 'simpler' genomic test of identifying individuals with pale skin prone to freckling , or than other commonly used methods of risk assessment, such as family history? "
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ABSTRACT: ABSTRACT : The recent flood of information about new gene variants associated with chronic disease risk from genome-wide association studies has understandably led to enthusiasm that genetic discoveries could reduce disease burdens and increase the availability of direct-to-consumer tests offering risk information. However, we suggest caution: if it is to be any benefit to health, genetic risk information needs to prompt individuals to pursue risk-reduction behaviors, yet early evidence suggests that genetic risk may not be an effective motivator of behavior change. It is not clear how genetic information will inform risk-based behavioral intervention, or what harms might occur. Research is needed that examines the behavioral consequences of genetic risk knowledge in the context of other motivators and social conditions, as well as research that determines the subgroups of people most likely to be motivated, in order to inform policy decisions about emerging genetic susceptibility tests. Without such research, it will not be possible to determine the appropriate health care uses for such tests, the impact on health care resources from consumer-initiated testing, or the criteria for truthful advertising of direct-to-consumer tests.
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