Special ointments can remove large birthmarks and prevent skin cancer

Skin Cream Ointment
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Researchers at Massachusetts General Hospital (MGH) have found that several drugs can be applied to the skin to remove moles and prevent skin cancer.

New treatment may help shrink giant congenital nevi

Skin cancer is the most common type of cancer in the United States. Every day, approximately 9,500 people in the United States are diagnosed with skin cancer. Skin cancer is classified into three types: basal cell carcinoma, squamous cell carcinoma and melanoma.

Melanoma, the deadliest form of skin cancer, develops in the cells that create melanin, the pigment that gives your skin its color. Although the exact cause of all melanomas is unknown, exposure to ultraviolet radiation, whether from the sun or elsewhere, increases the risk of developing melanoma. Also, people who have a lot of moles or abnormal moles are more likely to get skin cancer.

One in 20,000 newborn babies is born with a giant congenital nevus, which is a large, pigmented mole that can cover much of the face and body. Due to the appearance of the mole and the possibility of it turning into skin cancer in the future, many parents choose to have their children undergo major surgery to remove the entire lesion, which can lead to significant and permanent scarring. Researchers from Massachusetts General Hospital (MGH) developed several preclinical models of this condition and used them to demonstrate that several ointments can be applied to the skin to regress the lesions. A topical drug also protected against skin cancer. Their results were published in the journal Cell May 12, 2022.

“The objectives of our study were to develop a series of animal models designed to elucidate the main biological characteristics of these lesions and to test non-surgical drug treatments on the skin, aimed at causing nevus cells to recoil, thereby removing the need of surgical treatments. says lead author David E. Fisher, MD, Ph.D., director of the MGH Cancer Center’s Melanoma Program and director of MGH’s Cutaneous Biology Research Center.

The models included mice engineered to express a gene called NRAS, which contains a mutation known to cause most congenital giant moles in humans, as well as mice with transplanted skin grafts containing human congenital giant moles. Fisher and his colleagues used these models to examine the different stages of these nevi to better understand how they originate and grow. Additionally, when scientists used the animals to evaluate topical applications of single or combination drugs that inhibit signaling pathways known to be triggered by NRAS mutations, they found that several of the treatments resulted in significant nevus regressions. Additionally, after three treatments with a drug that triggers a type of inflammatory response after topical administration to the skin, the moles regressed completely. The treatment also provided complete protection against the formation of skin cancers in mice.

“We hope these findings will pave the way for further improvements aimed at directly testing these skin treatments on patients with congenital giant nevi,” says Fisher. “This work will include further safety studies, possible further improvements in efficacy and further analysis of the underlying mechanisms. The overall goals are to prevent melanoma in these patients and also to avoid the challenges of disfiguring these lesions.

Reference: “Topical Treatment for Melanoma Regression and Prevention of Congenital Giant Nevi” by Yeon Sook Choi, Tal H. Erlich, Max von Franque, Inbal Rachmin, Jessica L. Flesher, Erik B. Schiferle, Yi Zhang, Marcello Pereira da Silva, Alva Jiang, Allison S. Dobry, Mack Su, Sharon Germana, Sebastian Lacher, Orly Freund, Ezra Feder, Jose L. Cortez, Suyeon Ryu, Tamar Babila Propp, Yedidyah Leo Samuels, Labib R. Zakka, Marjan Azin, Christin E. Burd, Norman E. Sharpless, X. Shirley Liu, Clifford Meyer, William Gerald Austen Jr., Branko Bojovic, Curtis L. Cetrulo Jr., Martin C. Mihm, Dave S. Hoon, Shadmehr Demehri, Elena B. Hawryluk and David E. Fisher, May 12, 2022, Cell.
DOI: 10.1016/j.cell.2022.04.025

This work was supported by the National Institutes of Health and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation.

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