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Skin Cancer - Science topic

Explore the latest questions and answers in Skin Cancer, and find Skin Cancer experts.
Questions related to Skin Cancer
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I am trying to culture NTERT immortalized human keratinocyte cells.
I found several suggested medias:
Keratinocyte serum-free medium (K-sfm) (GIBCO/BRL) plus 30 μg of bovine pituitary extract per ml, 0.1 ng of EGF per ml and additional CaCl2 to raise the [Ca2+] to 0.4 mM 
or
3:1 DMEM-Ham's F12 supplemented with 10% FBS, 10 ng/ml mouse epidermal growth factor (Serotec), 1 ng/ml cholera toxin (Sigma), 400 ng/ml hydrocortisone (Sigma), 5 mg/ml insulin (Sigma), 5 mg/ml transferrin (Sigma), 13 ng/ml liothyronine (Sigma), and 2 mM l-glutamine (Invitrogen)
or 
KGM-Gold complete medium from Lonza
Anyone who has them in culture and can suggest the best medium?
Thanks!
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Hi Mr. Roth,
for my PhD thesis I am about to purchase N/TERT immortalized keratinocytes, as well. I wonder, if you found an optimal formulation for your cells and would be glad, if you could share your experience.
Thanks in advance!
Best, Melanie
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Hi everyone, I'm working on skin cancer classification and I've extracted the feature from three pre-trained CNN models and concatenated all the features. Finally a dense layer with softmax function was used for classification.
But I encountered constant validation accuracy with lower training accuracy.
How can I solve this problem please. Despite this, I have tried many optimizer functions with different learning rate, regularizer, early_stopping, dropout, and also I used image augmentation
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Sahar Yousif Mohmmed Thank you for your answer
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What's the reason for the chosen choice of inferential statistics?
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Choosing the right inferential statistic for your UV exposure and skin cancer research depends on your data format:
  • Categorical Data (UV exposure & Skin Cancer): Use a Chi-Square test to see if there's a link between the two categories.
  • Continuous Data (UV exposure) & Binary Data (Skin Cancer): Use logistic regression to model the odds of getting skin cancer at different UV exposure levels, while accounting for other factors.
Remember, sample size and multiple comparisons can influence your choice. Consulting a statistician is recommended to pick the best test and interpret your results accurately.
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I am currently performing co-culture experiments with murine CD8 T cells isolated from mouse spleens and with skin cancer cells (PDV) in a 24-well plate. I first isolate the CD8 T cells from spleen which are around 70% alive at time of isolation, mix them together with CD3/CD28 T Cell activation beads to activate the CD8 T cells, and plate them 2x10^5 T cells on top of 2x10^5 skin cancer cells that were plated the night before. The cancer cells are treated with mitomycin C prior to plating the T cells in order to halt cancer cell proliferation. Then I let them incubate in a tissue culture incubator with standard parameters (37 degrees Celsius and 5% CO2) for 5 days. In addition to the wells where I co-culture the T cells with the plate cancer cells, I also plate some of the T cells with the activation beads in an empty well to act as a control. I then assess the viability of the T cells by staining with a live dead stain and running flow cytometry. However the results of the flow cytometry show show that most of my T cells are dead (<40% viability). The most problematic issue is that the T cell-only wells come up only 1% viability which render the rest of the experiment null since I would not have a T cell control to compare the T cell viability from the T cell/cancer cell co-culture wells.
The interesting observation is that the T cells co-cultured with cancer cells have greater viability compared to the control T cells cultured by themselves which makes me think that the cancer cells are stimulating the T cells and improving T cell viability that way. I was wondering if there are any adjustments I could make to improve the viability of my T cells especially for the T cells in the T cell only control wells?
Some adjustments I have made already:
1. Increase the speed of the T cell isolation from the spleen to improve baseline viability prior to seeding on the cancer cells
2. Utilize wide bore tips when pipetting T cells to decrease the shear force on the T cells
Thank you for any suggestions and apologies for the length of this question.
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Dear Matthew,
Your work seems interesting. Which type of cancer are you investigating? The results can be dependant on that too. What are the goals of your study?
Sincerely,
Amar, MSc in MLT, Researcher interested in breast cancer
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Hello everyone, I want to enhanced the medical image of skin cancer as well as feed the enhancement image to CNN for classification.
I wonder if generative adversarial network (GAN) is the best method? And how can I use GAN for the purpose of enhancement instead of generate a fake image.
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Using Generative Adversarial Networks (GANs) for medical image enhancement can be beneficial in various applications, such as improving image quality, denoising, super-resolution, or synthesizing missing information. Here's a general approach to utilizing GANs for medical image enhancement:
  1. Dataset Preparation: Gather a dataset of medical images relevant to your enhancement task. This dataset should include both high-quality images (possibly from experts) and corresponding lower-quality or noisy versions.
  2. Define the GAN Architecture:Generator: Design a generator network that takes low-quality images as input and aims to generate enhanced versions that resemble the high-quality images. The generator's architecture typically consists of convolutional layers, followed by up-sampling layers to increase the resolution of the output. Discriminator: Develop a discriminator network that distinguishes between the generated enhanced images and the original high-quality images. It aims to classify whether an image is real or fake. The discriminator can be a convolutional neural network (CNN) or a similar architecture.
  3. Training Process:Loss Functions: Define suitable loss functions for both the generator and discriminator. Common choices include adversarial loss (encouraging the generator to generate realistic images) and content loss (measuring the similarity between generated and high-quality images). Adversarial Training: Train the GAN in an adversarial manner. The generator aims to generate enhanced images that fool the discriminator, while the discriminator strives to accurately classify real and generated images. Optimization: Utilize optimization techniques like stochastic gradient descent (SGD) or adaptive algorithms to update the weights of the generator and discriminator networks iteratively.
  4. Evaluation and Testing:Validation: Use a separate validation set to monitor the performance of the GAN during training. Evaluate the quality of the generated images using quantitative metrics or by involving experts for subjective assessment. Testing: Apply the trained GAN to enhance new or unseen medical images. Feed the low-quality images into the generator to obtain their enhanced versions.
  5. Fine-tuning and Refinement:Fine-tuning: Fine-tune the GAN on specific tasks or datasets to further improve performance. Adjust the network architecture, hyperparameters, or loss functions as needed. Regularization Techniques: Consider using regularization techniques such as dropout, batch normalization, or data augmentation to enhance generalization and prevent overfitting.
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there any study connected between dermal filler and skin cancer .
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I am updating my earlier review on the role of Fluoride doped Hydroxyapatite in Cancer and my current focus is on Psammoma Bodies which have been found, and identifed as high risk, in a very wide range of Cancers. These include Cancers of the Bone, Spine, Brain, Choroid Plexus, Dura Mater, Gliofibroma, Medulloblastoma, Meningioma, Cervix and Endometrium, Ovary, Kidney, Lung, Mesothelioma, Pancreas, Skin, Hemangioendothelioma, Olfactory Neuroblastoma, Duodenal Somatostatinoma, Stomach and Thyroid. Early studies did not have the benefit of advanced analytical techniques, or did not even consider the Fluoride content or composition of the mineralization. Can anyone help by supplying analytical data based on Raman spectroscopy, neutron activation, x-ray or wet analysis?
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Hello, Dear Geoff.
We continue to work on the subject you mentioned. There are methods that can analyze this.
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Can anyone please share Skin cancer(melanoma) dataset please.
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I am working on a deep learning-based analysis to detect Melanoma Cancer. I want to use all types of algorithms to get the best possible solution.
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I hope this email finds you well.
I would like to invite you to have a look on the following links.
Thank you very much for your time and efforts.
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Basal cell carcinoma (BCC) is the most common form of skin cancer. An estimated 4.3 million cases of BCC are diagnosed in the U.S. each year. Squamous cell carcinoma (SCC) is the second most common form of skin cancer.
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Yes it does, and the most common classification used for this is Fitzpatrick scale.
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actually I searched the related web sites, but the quantity of samples are maximum 20 or 30 pictures, but I saw in articles that there are datasets from theses 2 sources with enough number of samples (more than 100).!!!
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The International Skin Imaging Collaboration: Melanoma Project is an academia and industry partnership designed to facilitate the application of digital skin imaging to help reduce melanoma mortality. When recognized and treated in its earliest stages, melanoma is readily curable. Digital images of skin lesions can be used to educate professionals and the public in melanoma recognition as well as directly aid in the diagnosis of melanoma through teledermatology, clinical decision support, and automated diagnosis. Currently, a lack of standards for dermatologic imaging undermines the quality and usefulness of skin lesion imaging. ISIC is developing proposed standards to address the technologies, techniques, and terminology used in skin imaging with special attention to the issues of privacy and interoperability (i.e., the ability to share images across technology and clinical platforms). In addition, ISIC has developed and is expanding an open source public access archive of skin images to test and validate the proposed standards. This archive serves as a public resource of images for teaching and for the development and testing of automated diagnostic systems.
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I am doing a research on Skin Cancer Detection. I have read a lot of redundant research papers about the problems which related to the same topic. Therefore, I wish to know the recent research directions of skin cancer detection.
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With no doubt, deep learning models have shown a great performance in terms of skin cancer detection. The highest results that have been achieved on skin cancer detection challenges were obtained by deep learning models.
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Hi, is there any dataset about occupational skin diseases (especially skin cancers) that contains skin lesions images (simple or dermoscopic or histologic) ,integrated with clinical data and occupational history (e.g. to see if they have had occupations with carcinogenic exposures particularly UV)
I want to use it to make a research on the contributions of these exposures in the development of skin cancers and the possibility of early detection of the malignancy of these lesions by data mining and image processing considering occupational exposure as an important parameter
any suggestion is appreciated
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I actually found a few dataset samples on https://www.kaggle.com/search?q=skin+diseases.
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I am working on skin cancer on female swiss albino mice. I am inducing skin cancer by topical treatment of DMBA and the other group DMBA+ cationic peptide treatment (Cationic peptide is given sc) I will be studying mainly the expression of apoptosis proteins bcl2,bax and cytochrome c. Want to know how can I preserve that for about 1 month this skin cancer tissues by liquid nitrogen and keeping in -20 degree deep freeze. whether it will be fine to preserve that way. plz help 
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what is the optimal concentration to induce cutaneous melanoma please ?
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How can we assess the presence and amount of T-cells in the freshly removed skin tissue after surgery or punch biopsy? Also, if we freeze the skin tissue at -20C for a long time, after thawing to warm PBS or water, how can we make sure we have T-cells especially CD4 and CD8 T cells in the extracted frozen skin tissue? Does skin have to go in a specific solution or it has to be assessed for the specific markers ?
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Attaching papers for your reference. It is quite common to look for lymphocytes (CD4,CD8) from fresh punch biopsy. Not much knowledge about frozen biopsies.
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A prospective study has been published by Wen-Qing Li (JAMA Intern Med. doi:10.1001/jamainternmed.2014.594, online April 7, 2014) raising an intriguing question, stating that Sildenafil use for ED showed a statistically significant elevated risk of melanoma. We´re really concerned about this. Any insight regarding this important subject?
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Use of viagra does not cause the development of melanoma.
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I am doing research on melanoma detection for dark skin people. so it's very difficult to identify the dark skin images, please tell me the idea to get the dark skins.
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Dear Ahmed do follow this link to a project i was involved in last year. There is a dermoscopy tool kit with links to lots of website, where you will find an abidance of images for every skin type and skin lesion:
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This question is defined in greater detail in my blogpost 
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I have the same problem. My skin seems to be burned under the watch. I'll set the watch into safe battery mode, which turns the sensor light off, and observe for a few days in order to see if the burns disappears.
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I am working on ISIC skin cancer image segmentation in my project i got high dice coefficient score, high recall, precision but when i evaluate the ROC and PR curve i do not get good result can any one explain this.
Thanks very much
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Skin bleaching ( whitening ) creams have a negative impact on the users, including the prospect of causing cancer, skin diseases ( dermatitis ) and even secondary bacterial infectiins. Did you agree? If yes what chemical contents in the creams cause the above mentioned impacts.
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As with skin bleaching, there are many risks involved with tanning. Evidence links UVA rays to malignant melanoma, the deadliest form of skin cancer. Overexposure to any Ultra violate rays can cause loss of skin elasticity, premature aging, and cancer; damage to the skin is irreversible.
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i can't find ground truth image for HAM10000 dataset.
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The question my project aims to answer includes ...Does providing skin cancer risk assessment questionnaires as an intake process before a patient examination, increase skin-related interventions by primary care providers? Patient questionnaires will be available for 30 clinical days with an estimated sample of a minimum of 50 completed questionnaires. The questions include the generic including; age, gender , and ethnicity as well as about ten yes/no questions with corresponding points to determine if a patient is 1) high-risk or 2)low-risk. The questions range from eye color, hair color, to history of sunburn. The main outcome I want to identify is if by conveying their risk status to their PCP, I want to determine if their risk status lead to corresponding interventions which will also be a check box with answers such as referral to dermatologies or provided full body skin assessment. There will be no comparison of provider interventions without the questionnaire nor will there be any pre or post tests. Any help would be beneficial.
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From what you have written it sounds that your outcome and exposure are binary, in which case logistic regression examining association between high or low risk on questionnaire and whether patient underwent skin related intervention (yes/no).
This would produce an odds ratio.
This is a useful paper to guide your statistical analysis:
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Papers related to Melanoma Skin cancer using Image processing and the latest methodology being Incorporated to identify the Cancerous cells?
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Dear Colleagues and Friends
I have faced a strange results in my previous experiment.
I had Melanoma cells in culture and after 4 days, I wondered when I saw that the melanoma cells were morphologically changed to a neuron like cells or more likely to melanoblast cells.
The most exciting part of this morphological changes, that prevent me to ignore, was that their growth have been stopped or significantly decreased without applying any specific/new chemicals.
So, I would like to know about any non-specific reason behind this phenomena.
Considering that, this morphological and metabolic changes were happened for a malignant/invasive type of skin cancer cells, the answer may results in a way to step forward in cancer treatment.
Best Regards
Behnaz Ghaemi
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A noticeable change in cell morphology that associated with a cell growth arrest often results due to sub-optimal cell culture conditions. These conditions include, a change in cell density, culture medium (growth factors), cell culture flask/plate (a change in extracellular matrix-induced signaling), and sub-optimal trypsinization of cells. Other conditions (the list is long) are also known to alter the cell morphology. Therefore, if you have notes from your cell culture conditions, it should be possible to identify potential factor(s) that might have contributed to your observations.
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I want to find out if skin tatoo has any effect in skin cancer
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Hello,
I wondered this; these papers might be of interest:
Kluger, N. (2016). Cutaneous and systemic complications associated with tattooing. La Presse Médicale, 45(6), 567-576.
This is the ResearchGate link:
I have not seen the full text of this 2008 paper, but it sounds relevant:
Kluger, N., Phan, A., Debarbieux, S., Balme, B., & Thomas, L. (2008). Skin cancers arising in tattoos: coincidental or not?. Dermatology, 217(3), 219-221.
Kluger, N. (2009). Skin tumors arising in tattoos: coincidental or upcoming public health issue?. Expert Review of Dermatology, 4(4), 313-315.
Very best wishes,
Mary
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Hello, 
I am planning to start a project on UVB induced skin cancer. For that I read articles and found the different methods used by the researchers for UVB, but I am unable to identify the design of the apparatus. It will be highly appreciable, if someone can guide me to the design of the chamber.
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Thank you Nobuyuki Hamada and Amit Kumar Srivastava.
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- low dose ASA is in discussion to increase skin cancer in male adults.
- ASA showed significant decreased thymus-size in animal studies.
- Should we create studies to clear this question ?
Is their any data in neonates or children after longterm low dose ASA in pregnancy?
In Germany we observe an uncritical use of low dose ASA in reproductive medicine and every kind of previous pregnancy complication.
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Melanomas and sun related skin damages occur exponentially in the last decades. Primary care providers are the perfect professional group to screen the skin of patients.
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"The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of visual skin examination by a clinician to screen for skin cancer in adults." (in asymptomatic adults)
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Recently, i've studied skin cancer. I used A431 and SK-Mel-28 both skin cancer cell line.
When i transfected "A" gene into two cell lines, but cell proliferation and migration were totally different.
I searched on the web what makes different results between two types of skin cancer.
Many papers showed effect of gene over-expression and knockdown in both skin cancer is almost the same. I did not found different effect on non-melanoma and melanoma.
Could you give me introduce some papers or explain why this results produced?
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Sorry, but it is a little bit hard, to understand your English. However, from what I understood, you were trying to transfect a certain gene in two different melanoma cell line and got different results for its effect.
Since you did not specify which gene I guess you are not asking about specific pathways or regulatory mechanisms it seems.
So the general answer is ever cancer has a different genetic and epigenetic mark-up. This is especially true for cell lines, which often changed much from the -in this case- tumour cells they originated from. It is thus not surprising, that different cells will react differently. Most likely one of the cell lines is lacking or overacting a specific pathway responsible for the suppression or activation of the gene you are investigating.
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Anti-pollution cosmetics is gaining lot of attention worldwide. The pollution can be from sunlight, air and electromagnetic or optical devices. Pollution can affect health particularly the skin, hairs and eye.
Pollution creates excess free radicals which can damages the skin microstructure and components such as lipids and initiate inflammation, hyperpigmentation, aging process and skin cancers.
Many cosmetic products claiming anti-pollution properties with some data. However, we do not know what are legit techniques and gold standards. As such regulatory agencies have so far quite on this issue and are not providing any guidance to consumers and cosmetic companies. This is dangerous as many un-safe cosmetics can be sold in the market. Therefore, we need to work together to find gold standards and help consumers. Hope this initiative will trigger more interest and participation worldwide. Thank you.
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Where can i find a good dataset of at least 200 images of melanoma
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Hi,
I'm looking for average skin tone data by country. I found one on target map but I couldn't find its resource. Does anyone have an idea?
Thanks
Dror
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Hi, I got the same question.
Did you find some dataset about skin tone?
Thank a lot!
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          I am researching the potential benefits and decreased health risks of providing man-made, cultivated, and/or natural shade for public playgrounds. Benefits may include increased participation in play and socialization, and decreased risks may include decreased exposure to excess sun and heat at outdoor public playgrounds, including: dehydration; heat injuries, including heat cramps, heat exhaustion, and heat stroke; thermal burns from overheated surfaces and equipment, including plastics and ground cover; and injuries from exposure to ultraviolet rays of the sun, including sunburn and skin cancers such as melanoma. 
          This question is related my Capstone for my Master in Occupational Therapy degree. I appreciate any feedback regarding search methods, existing research, and guidelines for pursuing the question further.
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Thank you for your opinion and feedback.
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I am developing a medical device (orthopedic prosthetic), during application I want to use UV curable adhesive for fixing and cavity filling. for that I am planing to use High power UV led light having peak wavelength of 365 nm and intensity is ~100mw/cm2. I coulden't find any confirmed data on safety study over skin. exposure is one time and it would last for 3-4 minutes.
Should I go ahead with above UV LED light ?
Would you please help me to find safety study for this ?
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for general and occupational UV exposure limits see ICNIRP:
there a monochromaltic exposure limit of 270 kJ/m2 to eyes and skin is set at 365 nm, but also an overall limit of 10 kJ/m2 to UVA irradiation (315-400 nm). Because of thermal effects the exposure rate should not exceed 10 kW/m2, especially for the eye.
All these exposure limits do not pertain to medical applications. The question apparently relates to fixation of a prosthetic, which to me is a borderline case. Considering UVA1 therapies in dermatology, there should not be a problem with a skin exposure of 240 kJ/m2  @ 365 nm for this application.
It is also not necessarily true that 405 nm would be any safer, e.g. if we consider oxidative effects
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Hello, I plan to start inducing skin cancer in Wistar rats, but since we do not have an absorbent hood in our lab, so I would like to know, please, if i can use a chemical mask that i bougth online from this site;
(N° 3 cartridge are Normally impermeable to organic chemical vapors such as acetone and several other organic chemicals)? and can I use safely this mask and work a dorsal applications of DMBA in outdoors so in the open air?
If this is not feasible, is the application of 1% DMBA / 1% croton oil on rats capable to causing skin cancer in wistar rats because I did not found a scientific article 'paper' that talks about?
thank you very mutch 
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Hello, this mask is good, yes, it is good to have an air extractor in the laboratory. When I did a review on cancer induction, I read that the wistar rat is not susceptible to DMBA and TPA, drugs I used, it is best to use mice, but I think it forms some papillomas.
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Thanks in advance for your replies.
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I've opened a repository in github with our script so it can be available to everyone :)
The link also includes instructions for using the script :)
Let us know if it's working for you, and on the other hand
If you experience any trouble using it, let us know in the issues section!
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It is quite easy to find databases with images of skin cancerous, non-typical moles. It is however, quite difficult to find images with normal moles.
Obviously you need both types to train your classifier.
Any suggestions are highly welcome.
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This question is specifically asked within the Project called "Treatment of Melanoma Brain Metastases."
Because neurological tissues as well as many forms of skin malignancies will tend to express at least some significant CB1 and CB2 receptors, perhaps using moderate dosing of a safe agonist like Delta 9-THC may be useful?  And consider including evaluation of equivalent to 100-300 mg or oral CBD for humans as well as this is becoming very common among patients.  
I work with both brain cancer patients (mostly Glioblastoma) and many breast cancer patients and they had already chosen to integrate cannabis extracts into their therapies. Because CBD and THC cross the BBB, and does not appear toxic to healthy normal cells, it may be reasonable to consider exploring this with research. I do have one interesting patient who reported using these compounds to treat her ER-PR-HER2+ brain metastases with tremendous success in only 3 months. The Herceptin and Perjeta she was on are too large to cross the BBB, so the situation is dire for her otherwise. Best wishes and thank you for your project!
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OK.  I think it is a good idea.
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I am trying to download the ISIC2017 training and testing data but I didn't find any link. I tried the ISIC2016 I found the Training data but there is no TEST data.
Regards,
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@Patrycja Thank you. :) got it.
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I would like to analyse proapoptotic activity of a compound to be used on Actinic keratosis. Is there any cell line that might represent early phases of photocarcinogenesis?
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Dear Vieri,
I suppose you can ask professor Jean Kanitakis from Lyon.
Regards,
Aldona
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Dear Scientific Community :)
A colleague recently tested his melanoma (ME1402) cells for mycoplasma and obtained some strange images of rod-like structures - quite different from the 'dot-like' beads on a string look of mycoplasma. Please a look at the attached image and provide some insight.
TIA
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Highly likely they are mycoplasma/PPLO, sorry to say.  They vary from spherical to filamentous.  (Try Googling "What shape are mycoplasma?")  I would just discard and go back to the freezer.    You only need a kit if the DNA stain shows nothing in the cytoplasm, or something faint and ambiguous, and you want to be more sure.
DAPI/bisbenzamide can stain mitochondria, but only at higher concentrations than used in the standard protocols for PPLO, and anyway those would be evenly in all cells, not patchy like this.
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I am extracting RNA from skin cancer samples. The pipette was contaminated with crystal violet (the undergrad might have sucked in crystal violet while working with it). 
Now I am facing a problem which is a less intense 28S band on the agarose gel for my samples. Is that because of crystal violet? and do you think this crystal violet intercalation with RNA would affect the RT step and PCR?
Thanks
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I hope you have more skin samples. Who knows what that pipette was contaminated with, and what's now contaminating your samples. At this point it doesn't matter much - you know they're contaminated and whatever you were doing with them is compromised. Sorry.
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I need melanoma skin cancer images dataset, kindly help me out, suggestions will be appreciated. 
Regards,
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Hello Atif.
I know the Project link below.
This Project has an iPad app called DERMOFIT that you can download in ==> http://www.dermofit.org/
Best regards.
Emilio.
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Hi,
I was performing MTT assay in my lab hood. Accidentally, I did not turn off germicidal lamp (UV-C 254 nm) in the hood and I worked for about 25 minutes. I was wearing latex gloves and my hands and arms were completely covered in my labcoat and also my winter coat. My face however was uncovered and I was wearing my glasses. There was hood glass between the lamp and myself and the distance between my face and lamp was as usual as in normal airflow hoods. 
This happened 4 days from writing this post. After overexposure, I did not see any symptoms like burns in my cornea or erythema so far. I am really scared as to what fate awaits me after 6-12 months as they say this can lead to skin cancer. 
I would be really grateful if anyone could suggest on what I should do and what fate awaits me in the next one or two years.
Regards,
Pratik
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Thank you Mr. Martin. I have not got any sunburns or any sorts of issues with my skin. The problem is skin cancer symptoms would not be seen until 6-8 months after exposure. So, I am worried on the same.
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Is there any benefit in irradiating a skin tumor that has necrosed after cetuximab and shows a solution of continuity with the subcutaneous cellular tissue, although it is still present (partial response) and it is associated with local lymphadenopathies? Will the wound ever heal?
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The patient is obviously having a T3/4 N2/3 tumour. Prognosis is poor. He will need chemoradiotherapy. Surgery may also have to be considred before or after chemoradiation depending on the practice of the Oncologists in your area and the age and general condition of the patient
Narayanan
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can I have the reference as well?
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Hi, below you can find what you're looking for. Good luck! There are many other papers which report this data; just le me know in case you need further details on this topic.
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Or does cobimetinib not work any more if a patient does not answer to vemurafenib/shows progresssive disease? Would you switch to a PD1 inhibitor?
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In my opinion, combination of different targeted molecules is the best option and should be always taken into account. Almost all tumors are heterogeneous and this is the reason why, in addiction to drug resistance, tumor progresses when treated with a single drug, because only the portion of tumor expressing that antigen will respond to that treatment, but the rest will keep progressing. Moreover, BRAF inhibitor resistance via MAPK-reactivating mechanisms develops after BRAF inhibitor monotherapy. For this reason, the combination of BRAF + MEK inhibitors is superior to the BRAF inhibitors monotherapy, in order to prevent future resistances. In the specific, clinical data showed that Dabrafenib+Trametinib is better than Vemurafrenib+Cobimetinib treatment, in terms of OS and side effects.
As regard to combination with a PD1 inhibitor, Ipilimumab+Nivolumab therapy is showing good results but, at the moment, can be used only in clinical trials.
Best regards, 
FM
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The European union is hearing evidence on whether the lower the amount of topical vitamin A that may be used in a cosmetic.   Vitamin A is almost completely locked in the skin because there are no transport mechanisms to take it form tissues into the blood stream so topical vitamin A can never be absorbed into the  blood and poses no risks, even at high topical doses.  We need to show that higher levels of topical vitamin A reduce skin cancers, and make skin healthy.  High doses of oral vitamin A may well reduce alzheimers.  Vitamin A in conjunction with vitamin D keeps bones healthy.  I have used 50,000 i.u. per day for 22 years and my bones are better than average for 26 year old people on scanning.  We know already that certain leukemias respond to vitamin A.    I am collecting evidence and would appreciate as much feedback as possible.
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The problem that oral Vitamin A in high doses for a long time may have some hazards , since it is fat soluble , and not water soluble, so it could be deposited in the fat and liver for a long time, and theoretically if the person taking this large dose loose weight in a short period , a condition like vitamin A toxicity could prevail.
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Hi everyone,
does anybody work with the melanoma cell line RPM-MC and knows whether they contain mutations in either BRAF (e.g. V600E) or NRAS (e.g. Q61R/K)?
Thanks a lot in advance!
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Have a look on the attached article.
Sorry, but I did not check for your cell line.
Best regards
Robert
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Dear All,
I'm using DMBA/TPA to induce the skin cancer in Balb/C mice, I would like to know how does my compound of interest in inhibiting the growth of tumors. What are the mechanisms that are involved in the inhibition of the cancer in the skin of Mice.
Please help me to get a clear concept of this phenomenon.
Thank You
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I do not understand well the question and the responses.
A "chemopreventive" agent is an agent that avoid growth development. Experimentally, a chemopreventive agent is given BEFORE grafting or inducing the tumor model in vivo.
A chemopreventive agent's purpose is therefore not to inhibit tumor growth but to limit / prevent tumor apparition.
A chemotherapeutic agent's purpose is to inhibit tumor growth. It is experimentally given AFTER tumor occurence.
Are we thus actually speaking about "chemopreventive agents" in the cancer field?
Best regards
Robert 
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The etiology of skin cancer is different in Black skin compared to White skin, and excess sun exposure is not the only risk factor. Black Africans do experience sunburn and cataracts, so a public health communication tool relevant to dark skin may be important.
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Hi Caradee, Melanoma is predominant in low-pigmented skin people. High-pigmented skin people experience Melanoma but the incidence is much lower. Furthermore, tumorigenesis tend to be different; in low-pigmented skin people melanoma often develops from precursor lesions while in high-pigmented skin people not. However, afro-american people basically experience BCC. I think that just a simple UV metric method is not appropriate.
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Hello to everybody,
 I want to isolate all the leukocyte populations (CD45) from B16F10 tumors (injected in mice subcutaneously). Can someone recommend a good dissociation media (like PBS or complete RPMI)? In particular, which enzymes would you use? I know that some of them can degrade surface antigens.
Thank you very much,
Michele
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Suggest that you look into the use of collagenase / DNAse digestion.  Smashing through a cell strainer kills a lot of cells and you loose frequency data.  Also the released DNA can aggregate cells.  We and many others have published the digestion approach.  Beads are of course one approach.  Alternatively, you can largely separate parenchymal cells from leukocytes by density gradient centrifugation.  Again see various papers on techniques.  You might then use beads for a final separation of specification cell types. 
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Is U.S. public health policy on sun protection based entirely on epidemiological evidence? Has there ever been an RCT on sun protection and skin cancer?
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Dear Tom:
I agree with Mark Farrar and those 2 studies -for me- are the most helpful and those who best address your question.
I also use those studies to show residents/students that daily sunscreen use prevents melanoma.
Have a nice week !
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As far as I am concerned, the standard coverage 50x for the analysis of highly heterogeneous tumor samples such as melanoma is insufficient and scientific literature recommends base coverage around 500x or even 1000x. However, with that coverage the cost of analysis increase enormously.
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There is no one coverage that is right or wrong, better or worse. The answer will almost solely depend on the question you are trying to ask of the data and what confidence level you require for detecting SNVs. You would likely require lower coverage if you were only interested in detecting more commonly mutated genes in melanoma, such as BRAF, vs. the much higher coverage required for discovering novel SNVs if for example one were interested in doing a study on tumour evolution or spatial/temporal heterogeneity.
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Hi Guys! i will appreciate if you can answer the following questions:
1- which cell line(s) is used to study keratinocytes and their potential UV-induced malignancy formation?
2- is there a mouse model for that? ✓
3- is there mouse line in which UV radiation causes visibil skin damage? 
Many thanks in advance.
Cheers!
Peter
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Hi Peter, 
Well, again. If you want to focus on melanomas induced by UV, you need to look at untransformed melanocytes and use melanoma cells lines (best to use both from human origin, as not all mouse data can be related directly to human disease). If you want to focus on non-melanoma skin cancers, such as BCC or SCC, induced by UV exposure, you need to work in a human keratinocyte line and compare to a transformed keratinocyte cell line isolated from an appropriate BCC or SCC. I would strongly encourage you to reconsider the HaCat keratinocyte line, as they have altered responses, due to their p53 deficiency. 
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Hi. Recently I used GeneChip® miRNA 3.0 Array - Part #902018 (Affymetrix) to make a microRNA profile of skin cancer cells. First of all, I transfected my cells with hs-miRNA-34-5p, and the transfection increased 327- fold change when compared to non-transfected cells. How can I find information about level of microRNA transfection? I want to know if this concentration of microRNA are toxic to cells, if inhibits another endogenous microRNA processing, or if this fold change is good.
All miRNAs found in high or low levels will be validated by qRT-PCR. However, I wonder if I could use some miRNA microarray database to compare my results with other cells types. Like in silico screening of frequency alteration of microRNAs expression in skin cancer lines. Could someone suggest a database to do this search? I really need help with Bioinformatics.
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here are some papers : 
I can give you the pdf of these articles , just send to me the related links . Good luck
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Background: Preventive and health promotion projects aim to induce healthy habits in children through education about sun exposure in order to protect against and reduce the incidence of skin cancer. Education about the prevention of skin cancer is most effective when it is taught as part of a health education curriculum.
Our program was named as "Sol, Amigo da Infância - Sun, Friend of Childhood". This program was established on January 2013 by SBD-RESP board. The program partner schools received materials to facilitate the classroom instruction, and the program also encouraged the implementation of structural measures (such
as planting trees) and individual measures (such as encouraging the use of hats, appropriated clothing, sunglasses and sunscreen).
The program is composed by flexible elements that can be used independently or as supplements to the curriculum of existing health promotion in school.
Aim: The program "Sun, Friend of Childhood" is a school health education and disease prevention project directed to instruct children and educators through activities in school that aim to encourage the adoption and maintenance of behaviours that ensure proper sun protection and the consequent prevention of skin cancer.
A total of 194,000 children and 800 teaching coordinators of public and private schools received lessons and activities about our Educational program on photoprotection between 2013 and 2014. HQ´s comics, DVD movie and teachers involvement have been showed effective to disseminate these informations.
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Here in Queensland where we have a very high incidence of melanoma, it is very important to educate children. Campaigns such as "slip, slap, slop" and "no hat no play" have been very effective over the years
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Hi everyone,
I am doing spheroids experiment in 96 ultra low attachment well plates. Unfortunately, I faced several problems when I use 96 low attachment plates, so I decided to go with the gel experiment. So how I can do gel experiment for 3D spheroid in skin cancer cell lines.
Thank you so much.
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We have developped an innovative hydrogel, based on hyaluronic acid, it s highly porous and provide a physiological environment much closer to the biological reality.
With this 96 well plate you won't have any problem to retrieve your 3D spheroid, please find more detail attached
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I am trying to compare x ray with UV radiation and was wondering if someone knows how much UV C is necessary to have the same cell killing as 1 Gy x ray? I searched the net but it wasn't really fruitful so far...
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It´s not only a strong depth dependence of dose, it´s above all a strong effect dependence with depth by different tisues and mechanisms. UV-C is at the limit to ionizing radiation and the absorption maximum for the DNA bases is at the lower energy limit (about 4 eV, production of dimers).
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Recent experiments revealed that both IR stress and DMBA treatment increase the stem cell factor (SCF) expression level at the secondary hair germ and dermal papillae. However, IR stress causes hair graying due to the damaged melanocytic stem cells (McSCs), while DMBA treatment causes the hyperpigmentation of coat hair in the dorsal skin. This result provokes two important questions;
1) SCF/c-KIT signal is the only signal pathway to maintain the differentiation of immature melanocytes also referred to as melanoblasts or McSCs?
2) What is responsible for the paradoxical phenotype between enhanced SCF expression level and coat hair color?
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Thank you for your helpful comments, Dr. Dorothy C Bennett.
This experimental data is under revised period now.
IR herein means ionizing radiation at the dose of 4-5 Gy.
1) Survival is the anti-apoptotic capacity due to Bcl-2 and I am also devoted in the normal differentiation of McSCs. I will check the Notch activity by performing q-PCR to reveal the transcription level of Hey and Hes. Also, I will try the F-IHC with Notch ICD antibody merged with SCF-GFP knock-in mice. Thank in advance for your comment!
2) According to q-PCR, both of IR and DMBA treatment increases SCF mRNA level up to two-fold as compared with control. I have already made the mating with Dct-Cre;p53(fx/fx); SCF-GFP-KI, but contrary to my expectations, there was no much difference depending on p53 expression. CDK such as p21 might not only induce cellular senescence (cell cycle arrest) but also influence on the paradoxical phenotype.
Anyway, I have to investigate into the molecular machinery why I cannot detect positive correlation of SCF expression and coat hair color between IR and DMBA treatment, both of which increases SCF expression, but induces hair graying and hyper-pigmentation, respetively.      
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there are a lots of micro RNAs effect in skin cancer but I need to know the most one that change in skin cancer.
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Thank you
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See above
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Dear Vladimir A. Kulchitsky 
Thank you for the information.
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Hi, Is it possible to induce keloid in skin of lab animal? If yes, Could you please introduce me any papers?
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Not that Im aware of unfortunately.
Some success with hypertrophic models but not yet with keloid models of scarring. This study nicely illustrates the different attempts made to create an ideal model - none of which have been fully successful.
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can someone tell me best Methods to transfect MCC cell lines. I tried Lipofacamine but it did not work .
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Dear Kashif,
We also had only low transfection efficancy with lipofectamine. Therefore, we now do everything with lentiviral transduction. That works fine. So if you have the possibility to work with lentivirus I would suggest giving that a try. 
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Hi! I wanted to know if melan-a cell lines are immortalized with hTERT and if they carry any other mutation (p53, CDK4...)? Thank you very much.
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Thank you very much for your response Dr. Bennett. 
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I'm looking for murine malignant melanoma cell lines which are BRAF wt and BRAF mut. We already have B16F10 (BRAF wt) in the lab and are in the process of procuring SM1 (BRAF mut.), but I would like to have at least one more BRAF wt and one BRAF mut. if possible. Does anyone know of any good cell lines? I've found it hard to find any commonly used murine cell lines in the literature with the exception of B16.
Thanks for the help!
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Thanks for the answer Dorothy, I appreciate it very much!
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I am working on hpv5 e6 oncoprotein expression in skin cancer biopsy  by RT PCR (not real time) and I get only smear bands, how could I ensure that my results are negative or do I have pcr problem
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Use a positive control to ensure that your PCR conditions are right. If the positive control band appears, do a Northern to check if the mRNA of gene-of-interest is present, and not because your cDNA procedure failed. Some genes only produce mRNA at a certain stage, and RT-PCR is based on the amplification of a specific cDNA which derived from its corresponding mRNA.
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I would like to read some pubblications about melanomapt1a prognosis and risk of recurrance
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Value and prognostic significance of mitotic rate in a retrospective series of pT1 cutaneous malignant melanoma patients.onti G, Pollio A, Cesinaro AM, Pellacani G, Magnoni C, Seidenari S. Cancer Epidemiol. 2012 Jun;36(3):303-5. doi: 10.1016/j.canep.2011.11.003. Epub 2011 Dec 5.
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Can anyone tell me one good buffer which works best to isolate type I collagen from murine skin samples to detect it through western blots?
I have homogenized skin tissue and lysed in NP40 (normal lysis buffer) and also boiled directly the skin homegenate in BSB, in both the cases i could not see Type I collagen bands. Please suggest.
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Wich conditions do you use for the transfer of proteins in your western?
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In such cases, one questions himself about his ability of early recognition of melanoma, which is of great importance in the right on time removing of the nevus (or melanoma).
In your opinion, is it more a question of ignorance (you do not see, because you do not know) or could it be attributable to the nature of the tumor that can appear so suddenly and abruptly?
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Sir,
True nodular melanomas NEVER arise in a nevus. They always arise de novo, which means they are nodular from the very beginning. This is the definition of nodular melanoma. However, vertical growth phase in already present superfitial spreading melanoma (SSM) is usually mistaken for nodular melanoma. Vertical growth phase looks like a nodule, but it is NOT a nodular melanoma since it has its horizontal phase of SSM.
 Chances to miss melanoma and to allow to develop into vertical growth phase are zero if regularly followed-up with dermatoscopy.
Of course,
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An elderly woman who complained of pain and progressive erosive lesion measuring 5cms * 4cms eroding the ear lobe. Duration 2-3 years. Complained of pain down the neck. urface was rough with erosion at places, margins elevated uniform with a distinct line of black color, soft to touch, tenderness was present.
No lymph nodes were palpable, hearing was good, no vertigo, no diabetes, mild hypertension was told.
History of moderate sun exposure noted.
Probable diagnosis of basal cell carcinoma was made.
She is poor, and single.
Can I get some inputs regarding the case? Open for any questions
les
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Surgery is option of choice if not invading into deeper structures, otherwise radiotherapy.
There is no establshed role for chemotherapy in the given case. Hedgehog inhibitors are a -however expensive- option in non-resectable cases which are not eligible or refractory to radiotherapy.
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I am using 5 FU liposomes for transdermal delivery but I am confused a little bit regarding how much formulation must be loaded into donor compartment of the Franz Diffusion Cells for 5 FU liposomes which must be cytotoxic to cancerous cells. I browsed the internet for weeks but didn't find a satisfactory answer since all topical available formulations of 5 FU state to "apply twice a day". But no answer to the question of exactly how much 5 FU must be applied.
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You can just put 1 ml in donor compartment and form your liposome study you know how much drug is there in donor compartment. Because in the end you are going to measure the concentration in receiving media which should be negligible and at the end of experiment you can perform mass balance experiment to find out actual amount of drug.
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Can anyone guide and help me to promote the growth of human melanoma cell line (SK-MEL-2) and murine melanoma cell line (B16). We bought both of them directly from ATCC 2 months ago. At begining they were grow very well (DMEM media + 10% FBS+ 1% antibiotic and antimycotic) and we prepared about 10 stocks from each. Now we want to thaw and regrow again, but we can not. The cells are not growing at all. TQ 
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Pigmentation of melanocytes, and of any melanoma cells that are able to differentiate, depends on the tyrosine concentration as Michael Z said, and also on the pH, and on the cell density. 
When the cells are highly pigmented they grow more slowly or not at all. 
So for fast growth, you can grow them at pH 6.9 to 7, which you can get with RPMI 1640 medium plus 10% CO2, and with 5-10% FCS.  Ham's F10 or F12 have very low tyrosine so that's good, but also have low concentrations of basic nutrients (these media are designed for cloning cells from very low density).  So you with Ham's you would need to change the medium almost every day for fast-growing cells like B16 sublines. We plate B16 cells at 1x10*4 cells/ml in RPMI/10% CO2  as above, and they will grow 20-30-fold in 3 days or 50-60-fold in 4 days *(change medium on day 3).
  You should even be able to rescue them from a low-viability frozen stock this way - just plate more cells to start with (like 10*6 cells per 3-cm dish or well), and after 4-16 hours wash away any that didn't attach (these are dead).
Human melanoma cells can be grown the same way except they generally don't grow as fast as mouse cells
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Estimation cyclooxygenases directly or by its products?
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There are generally three assay methods frequently employed for the assay of COX activity:
1. Detection/assay of the final product of the reaction, PGE2, by ELISA;
2. Direct oxygen uptake measurement resulting from the first step of the reaction using an oxygen sensor;
3. Spectrophotometric determination of the second reaction (peroxidase function)
James K. Gierse, Carol M. Koboldt. Cyclooxygenase Assays, Unit 3.1, Current Protocols in Pharmacology, DOI: 10.1002/0471141755.ph0301s00
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In order to cultivate keratinocytes with an air-liqiuid interface you have to de-epidermize human skin flaps in one step of the procedures. This is described by Prunieras M, Regneir M, and Woodley D.
To de-epidermize skin flaps you have to maintain the flaps in PBS at 37º for several days.
The PBS I used consists of NaCl, KCl, NaH2PO4, KH2PO4, Mg Ca Free. X1 concentration.
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I don't know if an answer is still required. Separating the epidermis with dispase can also be done in 30-60 min when incubating at 37C. We use this only in case of isolating keratinocytes for cell-culture. When De-Epidermized Dermis (DED) is used as a matrix, we want to get rid of all viable cells. To prepare DED we use 85% glycerol for 3 weeks (37C, shaking). After washing with PBS, DED is incubated in PBS (37C, shaking) for up to 2 weeks. The epidermis can be peeled or scraped off.
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My wife died less than three months ago due to complications in melanoma. Truly a sad day for my family. I wish there was some reliable way to detect it early since it progresses rather fast. And could anybody share some insights on what triggers it? All I could find are hormonal changes, etc... but could anybody more specific?
Thanks guys.
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check your skin regularly! Get your moles checked! Avoid excessive sun exposure and especially sun beds!
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There is no current evidence to support the use of aqueous cream versus any other moisturising brand or indeed using nothing whilst undergoing radiotherapy treatment. Has anyone looked into doing any form of trials to determine which works best?
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Two articles summarize the current, yet limited knowledge on this issue:
Ward et al., Cutaneous manifestations of acute radiation exposure: a review. Int. J. Dermatol. 2012, 51: 1282-91
Titaree Suwannalai, Prevention and management of acute radiation dermatitis by the topical agents: a literature review. J. Thai. Soc. Therap. Radiol. Oncol. 2010, 16 (1): 27-40
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I want to do FISH for two regions of chromosomes. One region can be variable in length, and I want to measure its length and length variation. Other region should be least prone to chromosomal rearrangements, so I could analyse fluorescent signal intensities ratio to estimate length of the region of interest. Which region is the least prone to chromosomal rearrangements in melanoma? Is using D2Z okay? What other region would you suggest, and which probe would you use?
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We just had a manuscript accepted in Environmental and Molecular Mutagenesis looking at chromosomal instability in about 40 melanoma lines using CGH. It is in the galley proof stage now. In a couple of weeks I should be able to give you a copy. Send me a private message if you are interested. We were looking for the most rearranged regions and common patterns. As Vincent wrote the centromeres are generally the least messed up. Melanoma's appear to be much more rearranged than other cancers.
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I am interested in polarimetry imaging of skin. I would like to use fuzzy logic on polarized images to extract information about skin cancer and its diagnosis.
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Unfortunately I have not used polarized images, yet. I refer the pathologic daignosis to the pathologist, who are interesed in sub-types and special stainings.
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