FROM MELANOCYTES TO MELANOMA
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JAMA , — Because of the controversy surrounding dysplastic naevi, the NIH held a consensus conference and attempted to explicitly define the features of dysplastic naevi. Tucker, M. Clinically recognized dysplastic nevi. A central risk factor for cutaneous melanoma. This study established that dysplastic naevi, as defined clinically, represent an independent melanoma risk factor.
Arumi-Uria, M. Grading of atypia in nevi: correlation with melanoma risk. Elder, D. Clemente, C. Histopathologic diagnosis of dysplastic nevi: concordance among pathologists convened by the World Health Organization Melanoma Programme. De Wit, P. Validity of the histopathological criteria used for diagnosing dysplastic naevi: an interobserver study by the pathology subgroup of the EORTC Malignant Melanoma Cooperative Group. Cancer 29 , — Shea, C. Correlating architectural disorder and cytologic atypia in Clark dysplastic melanocytic nevi.
Clinical decision making based on histopathologic grading and margin status of dysplastic nevi. Robles-Espinoza, C. POT1 loss-of-function variants predispose to familial melanoma. Shi, J. Rare missense variants in POT1 predispose to familial cutaneous malignant melanoma. Goldstein, A. Zuo, L.
Lebe, B. The significance of Ki proliferative index and cyclin D1 expression of dysplastic nevi in the biologic spectrum of melanocytic lesions. Florell, S. Proliferation, apoptosis, and survivin expression in a spectrum of melanocytic nevi. Rigel, D. Dysplastic nevi. Markers for increased risk for melanoma. Cancer 63 , — Shors, A. Dysplastic naevi with moderate to severe histological dysplasia: a risk factor for melanoma. Halpern, A. A cohort study of melanoma in patients with dysplastic nevi. A natural history of melanomas and dysplastic nevi: an atlas of lesions in melanoma-prone families.
Cancer 94 , — Balch, C. Final version of AJCC melanoma staging and classification. This study is the current basis for the staging of primary melanomas based on their thickness, ulceration and mitoses, and of metastatic melanomas based on the sites involved.
Odom, R. Andrews' Diseases of the Skin: Clinical Dermatology. Guerry, D. Lessons from tumor progression: the invasive radial growth phase of melanoma is common, incapable of metastasis, and indolent. Okamoto, N. A melanocyte—melanoma precursor niche in sweat glands of volar skin. Pigment Cell. Yazdi, A. Mutations of the BRAF gene in benign and malignant melanocytic lesions. Dong, J. BRAF oncogenic mutations correlate with progression rather than initiation of human melanoma. Omholt, K. Screening of N-ras codon 61 mutations in paired primary and metastatic cutaneous melanomas: mutations occur early and persist throughout tumor progression.
Stadelmeyer, E. Cancer Genome Atlas Network. Genomic classification of cutaneous melanoma. This Cancer Genome Atlas TCGA project represents the most comprehensive genomic and transcriptomic characterization of cutaneous melanoma to date. Weinstock, M. The risk of progression of lentigo maligna to lentigo maligna melanoma.
Kath, R. Growth factor independence in vitro of primary melanoma cells from advanced but not early or intermediate lesions. Cancer Ther. Control 1 , — Development of invasive and growth factor-independent cell variants from primary human melanomas. Satyamoorthy, K. Melanoma cell lines from different stages of progression and their biological and molecular analyses.
Hall, B. Suprabasal spread of melanocytes in dysplastic nevi and melanoma in situ : Kilabeling rate of junctional melanocytes and suprabasal cells may be a helpful clue to the diagnosis. Talve, L. Cancer 74 , — Reed, J. Pavey, S. Loss of p16 expression is associated with histological features of melanoma invasion. Ackermann, J. Wang, X. Hodges, C.
The genetic evolution of melanoma. Chromosomal gains and losses in primary cutaneous melanomas detected by comparative genomic hybridization. Distinguishing melanocytic nevi from melanoma by DNA copy number changes: comparative genomic hybridization as a research and diagnostic tool. Castresana, J. Lack of allelic deletion and point mutation as mechanisms of p53 activation in human malignant melanoma. Cancer 55 , — Absence of p53 gene mutations in cutaneous melanoma. Papp, T. Lack of p53 mutations and loss of heterozygosity in non-cultured human melanocytic lesions.
Stretch, J. Expression of mutant p53 in melanoma. Grant, S. Mutant p53 correlates with reduced expression of thrombospondin-1, increased angiogenesis, and metastatic progression in melanoma. Cancer Detect. Sparrow, L. Lassam, N. Overexpression of p53 is a late event in the development of malignant melanoma. Birck, A. Reifenberger, J. Virchows Arch. Goel, V.follow site
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Nuclear PTEN expression and clinicopathologic features in a population-based series of primary cutaneous melanoma. Cancer 99 , 63—67 Dankort, D. Pasquali, S. Surgeons' opinions on lymphadenectomy in melanoma patients with positive sentinel nodes: a worldwide web-based survey.
Efficacy of an elective regional lymph node dissection of 1 to 4 mm thick melanomas for patients 60 years of age and younger. Morton, D. Final trial report of sentinel-node biopsy versus nodal observation in melanoma. This clinical trial showed that patients with melanoma who had a positive sentinel lymph node biopsy have a worse prognosis than those without. Contrary to expectations, complete lymphadenectomy in these patients did not prolong overall survival, questioning the model of a phased metastatic dissemination from primary site, to regional lymph nodes, to distant sites.
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Cytotoxic T lymphocyte responses against melanocytes and melanoma
Reid, A. Markers of circulating tumour cells in the peripheral blood of patients with melanoma correlate with disease recurrence and progression. Fisher, B. Twenty-five-year follow-up of a randomized trial comparing radical mastectomy, total mastectomy, and total mastectomy followed by irradiation. International Breast Cancer Study Group. Randomized trial comparing axillary clearance versus no axillary clearance in older patients with breast cancer: first results of International Breast Cancer Study Group Trial Veronesi, U. The dissection of internal mammary nodes does not improve the survival of breast cancer patients.
Cancer 35 , — Lancet , — Sanborn, J. Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination. Natl Acad. USA , — This phylogenetic analysis of matched primary melanomas and their regional and distant metastases showed patterns of parallel metastatic dissemination and reseeding among different tumour deposits.
The Progression to Malignancy
Benign melanocytic nevus cells in axillary lymph nodes. A prospective incidence and immunohistochemical study with literature review. A study on the frequency of nodal naevi and a discussion of their pathogenesis, including the concept of benign metastasis in which nodal naevi are melanocytes derived from a nearby naevus. Carson, K. Nodal nevi and cutaneous melanomas. Holt, J. Nodal melanocytic nevi in sentinel lymph nodes.
Correlation with melanoma-associated cutaneous nevi. Taube, J. Dalton, S. Use of fluorescence in situ hybridization FISH to distinguish intranodal nevus from metastatic melanoma. Tietze, L. Benign metastasizing leiomyoma: a cytogenetically balanced but clonal disease. Schreibstein, J.
Benign metastasizing pleomorphic adenoma. Head Neck Surg. Colome-Grimmer, M. Metastasizing cellular dermatofibroma. A report of two cases. Nadelman, C. Pramesh, C. Benign metastasizing meningioma. Jpn J. Anbari, K. Melanoma of unknown primary site: presentation, treatment, and prognosis—a single institution study. Cancer 79 , — Dutton-Regester, K. Melanomas of unknown primary have a mutation profile consistent with cutaneous sun-exposed melanoma. This study demonstrated that MUPs have a high mutation burden and show signs of UV radiation- induced DNA damage, suggesting that they originate from the skin.
Ding, L. Clonal architectures and driver mutations in metastatic melanomas. Turajlic, S. Whole genome sequencing of matched primary and metastatic acral melanomas. Genome Res. Gartner, J. Comparative exome sequencing of metastatic lesions provides insights into the mutational progression of melanoma. BMC Genomics 13 , Nikolaev, S. Damsky, W.
Cancer Cell 20 , — Straume, O. Loss of nuclear p16 protein expression correlates with increased tumor cell proliferation Ki and poor prognosis in patients with vertical growth phase melanoma.
Wagle, N. Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling. Kim, M. Tumor self-seeding by circulating cancer cells. This study reports a mouse model of breast cancer that experimentally supports the reseeding hypothesis of metastatic dissemination. Gundem, G. The evolutionary history of lethal metastatic prostate cancer. Farmer, E. Discordance in the histopathologic diagnosis of melanoma and melanocytic nevi between expert pathologists. Download references. Correspondence to Boris C. A degenerative change of the elastic fibres of the dermis induced by long-term exposure to UV radiation.
Clinically enlarged flat naevi, or naevi that show atypical cellular or architectural features microscopically. The most common form of benign naevus, which tends to arise on the skin during childhood or adolescence as a brown flat or raised mole. The pattern of intra-epidermal growth of naevi and melanomas in which melanocytes are arranged mainly as individual units rather than as nests within the basilar epidermis.
The pattern of intra-dermal growth of naevi in which melanocytes are in the deeper dermis around appendages such as hair follicles, sweat glands and neurovascular bundles. A fibrotic change in the superficial dermis, which often has a lamellated appearance microscopically.
The most superficial part of the dermis immediately beneath the epidermis. The papillae are dermal protrusions that reach towards the epidermis, between individual rete ridges. A growth pattern of melanoma in which enlarged melanocytes, singly or in nests, are scattered throughout all layers of the epidermis. Invasive melanomas can be subclassified by their thickness, measured as the distance in millimetres between the granular layer of the epithelium and its base.
The term thin melanoma usually refers to stage T1 melanomas, which are less than 1 mm thick. To obtain permission to re-use content from this article visit RightsLink. Nutrients Proceedings of the National Academy of Sciences The American Journal of Dermatopathology Australasian Journal of Dermatology Article metrics.
Advanced search. Skip to main content. Abstract Melanomas on sun-exposed skin are heterogeneous tumours, which can be subtyped on the basis of their cumulative levels of exposure to ultraviolet UV radiation. Key points Melanomas on the non-glabrous skin skin outside the palms and soles can be broadly classified into those that arise on skin with chronic sun-induced damage CSD melanomas or those that arise on skin without such damage non-CSD melanomas. Rent or Buy article Get time limited or full article access on ReadCube. References 1. PubMed Article Google Scholar 6.
Google Scholar PubMed Article Google Scholar PubMed Google Scholar Article Google Scholar Bastian Authors Search for A. Glossary Solar elastosis A degenerative change of the elastic fibres of the dermis induced by long-term exposure to UV radiation. Precursor lesions Melanocytic neoplasms that have an increased risk of progressing to melanoma. Dysplastic naevi Clinically enlarged flat naevi, or naevi that show atypical cellular or architectural features microscopically. Melanoma in situ A proliferation of atypical melanocytes confined to the epithelial layer.
Basilar epidermis The lower-most level of the epidermis. Common acquired naevus The most common form of benign naevus, which tends to arise on the skin during childhood or adolescence as a brown flat or raised mole. Lentiginous growth pattern The pattern of intra-epidermal growth of naevi and melanomas in which melanocytes are arranged mainly as individual units rather than as nests within the basilar epidermis.
Congenital growth pattern The pattern of intra-dermal growth of naevi in which melanocytes are in the deeper dermis around appendages such as hair follicles, sweat glands and neurovascular bundles. Rete ridges The 'pegs' of the epidermis that protrude into the underlying dermis. A diagnosis of melanoma is supported by the presence of the S protein marker. HMB is a monoclonal antibody that reacts against an antigen present in melanocytic tumors such as melanomas. It is used in anatomic pathology as a marker for such tumors. The antibody was generated to an extract of melanoma.
It reacts positively against melanocytic tumors but not other tumors, thus demonstrating specificity and sensitivity. The antibody also reacts positively against junctional nevus cells but not intradermal nevi, and against fetal melanocytes but not normal adult melanocytes. HMB is nonreactive with almost all non-melanoma human malignancies, with the exception of rare tumors showing evidence of melanogenesis e. Further context on cancer staging is available at TNM. Also of importance are the " Clark level " and " Breslow's depth ", which refer to the microscopic depth of tumor invasion.
Melanoma stages  and 5-year survival rates:. Minimizing exposure to sources of ultraviolet radiation the sun and sunbeds ,  following sun protection measures and wearing sun protective clothing long-sleeved shirts, long trousers, and broad-brimmed hats can offer protection. Using artificial light for tanning was once believed to help prevent skin cancers, but it can actually lead to an increased incidence of melanomas.
From Melanocytes to Melanoma. The progression to malignancy : Melanoma Research
UV nail lamps, which are used in nail salons to dry nail polish, are another common and widespread source of UV radiation that could be avoided. The body uses UV light to generate vitamin D so there is a need to balance getting enough sunlight to maintain healthy vitamin D levels and reducing the risk of melanoma; it takes around a half hour of sunlight for the body to generate its vitamin D for the day and this is about the same amount of time it takes for fair-skinned people to get a sunburn.
Exposure to sunlight can be intermittent instead of all at one time. Sunscreen appears to be effective in preventing melanoma. Sunscreen also protects against squamous cell carcinoma , another skin cancer. Concerns have been raised that sunscreen might create a false sense of security against sun damage. A review found tentative evidence that statin and fibrate medication may decrease the risk of melanoma. Confirmation of the clinical diagnosis is done with a skin biopsy.
This is usually followed up with a wider excision of the scar or tumor. Depending on the stage, a sentinel lymph node biopsy may be performed. Controversy exists around trial evidence for sentinel lymph node biopsy;  with unclear evidence of benefit as of Excisional biopsies may remove the tumor, but further surgery is often necessary to reduce the risk of recurrence. Complete surgical excision with adequate surgical margins and assessment for the presence of detectable metastatic disease along with short- and long-term followup is standard.
Melanoma-in-situ and lentigo malignas are treated with narrower surgical margins, usually 0. Many surgeons consider 0. The wide excision aims to reduce the rate of tumor recurrence at the site of the original lesion. This is a common pattern of treatment failure in melanoma. Considerable research has aimed to elucidate appropriate margins for excision with a general trend toward less aggressive treatment during the last decades. Melanomas that spread usually do so to the lymph nodes in the area of the tumor before spreading elsewhere.
Attempts to improve survival by removing lymph nodes surgically lymphadenectomy were associated with many complications, but no overall survival benefit. Recently, the technique of sentinel lymph node biopsy has been developed to reduce the complications of lymph node surgery while allowing assessment of the involvement of nodes with tumor. Biopsy of sentinel lymph nodes is a widely used procedure when treating cutaneous melanoma. Further precision is provided using a blue tracer dye , and surgery is performed to biopsy the node s.
Polymerase chain reaction PCR tests on nodes, usually performed to test for entry into clinical trials, now demonstrate that many patients with a negative sentinel lymph node actually had a small number of positive cells in their nodes. Alternatively, a fine-needle aspiration biopsy may be performed and is often used to test masses. If a lymph node is positive, depending on the extent of lymph node spread, a radical lymph node dissection will often be performed.
If the disease is completely resected, the patient will be considered for adjuvant therapy. Excisional skin biopsy is the management of choice. The biopsy should include the epidermal, dermal, and subcutaneous layers of the skin. This enables the histopathologist to determine the thickness of the melanoma by microscopic examination. This is described by Breslow's thickness measured in millimeters. However, for large lesions, such as suspected lentigo maligna, or for lesions in surgically difficult areas face, toes, fingers, eyelids , a small punch biopsy in representative areas will give adequate information and will not disrupt the final staging or depth determination.
In no circumstances should the initial biopsy include the final surgical margin 0. A large initial excision will disrupt the local lymphatic drainage and can affect further lymphangiogram-directed lymphnode dissection. A small punch biopsy can be used at any time where for logistical and personal reasons a patient refuses more invasive excisional biopsy. Small punch biopsies are minimally invasive and heal quickly, usually without noticeable scarring.
High-risk melanomas may require adjuvant treatment , although attitudes to this vary in different countries. In the United States, most patients in otherwise good health will begin up to a year of high-dose interferon treatment, which has severe side effects, but may improve the patient's prognosis slightly. The unpleasant side effects also greatly decrease quality of life. In Europe, interferon is usually not used outside the scope of clinical trials. Chemotherapy drugs such as Dacarbazine have been the backbone of metastatic melanoma treatment since FDA approval in however, its efficacy in terms of survival has never been proven in an RCT.
In people with locally advanced cutaneous malignancies and sarcoma, isolated limb infusion ILI has been found to be a minimally invasive and well-tolerated procedure for delivering regional chemotherapy. Melanoma cells have mutations that allow them to survive and grow indefinitely in the body. A number of treatments improve survival over traditional chemotherapy. Immunotherapy is aimed at stimulating the person's immune system against the tumor, by enhancing the body's own ability to recognize and kill cancer cells.
Ongoing research is looking at treatment by adoptive cell transfer. Standard excision is still being done by most surgeons. This is due to the ill-defined visible surgical margin, and the facial location of the lesions often forcing the surgeon to use a narrow surgical margin. The narrow surgical margin used, combined with the limitation of the standard "bread-loafing" technique of fixed tissue histology — result in a high "false negative" error rate, and frequent recurrences.
Margin control peripheral margins is necessary to eliminate the false negative errors. If bread loafing is used, distances from sections should approach 0. A meta-analysis of the literature in found no randomized controlled trials of surgical interventions to treat lentigo maligna or melanoma in-situ, even though surgery is the most widely used treatment. Some melanocytic nevi, and melanoma-in-situ lentigo maligna have resolved with an experimental treatment, imiquimod Aldara topical cream, an immune enhancing agent. Some dermasurgeons are combining the 2 methods: surgically excising the cancer and then treating the area with Aldara cream postoperatively for three months.
While some studies have suggested the adjuvant use of topical tazarotene, the current evidence is insufficient to recommend it and suggests that it increases topical inflammation, leading to lower patient compliance. Radiation therapy is often used after surgical resection for patients with locally or regionally advanced melanoma or for patients with unresectable distant metastases. Kilovoltage x-ray beams are often used for these treatments and have the property of the maximum radiation dose occurring close to the skin surface.
Radiotherapy has a role in the palliation of metastatic melanoma. Certain types of melanoma have worse prognoses but this is explained by their thickness. Less invasive melanomas even with lymph node metastases carry a better prognosis than deep melanomas without regional metastasis at time of staging. When melanomas have spread to the lymph nodes , one of the most important factors is the number of nodes with malignancy.
Extent of malignancy within a node is also important; micrometastases in which malignancy is only microscopic have a more favorable prognosis than macrometastases. In some cases micrometastases may only be detected by special staining, and if malignancy is only detectable by a rarely employed test known as the polymerase chain reaction PCR , the prognosis is better.
Macrometastases in which malignancy is clinically apparent in some cases cancer completely replaces a node have a far worse prognosis, and if nodes are matted or if there is extracapsular extension, the prognosis is worse still. In addition to these variables, expression levels and copy number variations of a number of relevant genes may be used to support assessment of malignant melanoma prognosis.
When there is distant metastasis, the cancer is generally considered incurable. Treatment is palliative , focusing on life extension and quality of life. In some cases, patients may live many months or even years with metastatic melanoma depending on the aggressiveness of the treatment. Metastases to skin and lungs have a better prognosis. Metastases to brain, bone and liver are associated with a worse prognosis.
Survival is better with metastasis in which the location of the primary tumor is unknown. There is not enough definitive evidence to adequately stage, and thus give a prognosis for, ocular melanoma and melanoma of soft parts, or mucosal melanoma e. Even though regression may increase survival, when a melanoma has regressed, it is impossible to know its original size and thus the original tumor is often worse than a pathology report might indicate.
About genes are prognostic in melanoma, with both unfavorable genes where high expression is correlated to poor survival and favorable genes where high expression is associated with longer survival times. Globally, in , melanoma occurred in , people and resulted in 55, deaths. The rate of melanoma has increased in the recent years, but it is not clear to what extent changes in behavior, in the environment, or in early detection are involved. Australia has a very high — and increasing — rate of melanoma. In , deaths from melanoma occurred in 7.
In Australia, melanoma is the third most common cancer in either sex; indeed, its incidence is higher than for lung cancer , although the latter accounts for more deaths. It is estimated that in , more than 12, Australians were diagnosed with melanoma: given Australia's modest population, this is better expressed as In the United States about 9, people die from melanoma a year.
Melanoma is more than 20 times more common in whites than in African Americans. Overall, the lifetime risk of getting melanoma is about 2. The risk of melanoma increases as people age. The average age of people when the disease is diagnosed is Although melanoma is not a new disease, evidence for its occurrence in antiquity is rather scarce. However, one example lies in a s examination of nine Peruvian mummies, radiocarbon dated to be approximately years old, which showed apparent signs of melanoma: melanotic masses in the skin and diffuse metastases to the bones.
John Hunter is reported to be the first to operate on metastatic melanoma in Although not knowing precisely what it was, he described it as a "cancerous fungous excrescence". It was not until that microscopic examination of the specimen revealed it to be an example of metastatic melanoma. The first English-language report of melanoma was presented by an English general practitioner from Stourbridge, William Norris in Norris was also a pioneer in suggesting a link between nevi and melanoma and the possibility of a relationship between melanoma and environmental exposures, by observing that most of his patients had pale complexions.
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The first formal acknowledgment of advanced melanoma as untreatable came from Samuel Cooper in He stated that the only chance for a cure depends upon the early removal of the disease i. The word melanoma has a long history of being used in a broader sense to refer to any melanocytic tumor , benign or malignant but usually malignant,   but today the narrower sense referring only to malignant types has become so dominant that benign tumors are usually not called melanomas anymore and the word melanoma is now usually taken to mean malignant melanoma unless otherwise specified.
Terms such as "benign melanocytic tumor " unequivocally label the benign types, and modern histopathologic tumor classifications used in medicine do not use the word for benign tumors. Pharmacotherapy research for unresectable or metastatic malignant melanoma is ongoing. In clinical research, adoptive cell therapy and gene therapy , are being tested. Two kinds of experimental treatments developed at the National Cancer Institute NCI , have been used in metastatic melanoma with tentative success. The first treatment involves adoptive cell therapy ACT using TILs immune cells tumor-infiltrating lymphocytes isolated from a person's own melanoma tumor.
TIL therapy following lymphodepletion can result in durable complete response in a variety of setups. The second treatment, adoptive transfer of genetically altered autologous lymphocytes, depends on delivering genes that encode so called T cell receptors TCRs , into patient's lymphocytes. A cancer vaccine showed modest benefit in late-stage testing in against melanoma. Early clinical trials suggested that B-Raf inhibitors including Plexxicon's vemurafenib could lead to substantial tumor regression in a majority of patients if their tumor contain the B-Raf mutation.
Some researchers believe that combination therapies that simultaneously block multiple pathways may improve efficacy by making it more difficult for the tumor cells to mutate before being destroyed. In October a study reported that combining Dabrafenib with a MEK inhibitor trametinib led to even better outcomes. Some side effects were, however, increased in the combined study. At the American Society of Clinical Oncology Conference in June , the Bristol-Myers Squibb pharmaceutical company reported the clinical findings of their drug ipilimumab. The study found an increase in median survival from 6.
Ipilimumab was approved by the FDA in March to treat patients with late-stage melanoma that has spread or cannot be removed by surgery. In June , a clinical trial of ipilimumab plus dacarbazine combined this immune system booster with the standard chemotherapy drug that targets cell division. It showed an increase in median survival for these late stage patients to 11 months instead of the 9 months normally seen. Researchers were also hopeful of improving the five year survival rate, though serious adverse side-effects were seen in some patients.
The drug's brandname is Yervoy. Advances in high resolution ultrasound scanning have enabled surveillance of metastatic burden to the sentinel lymph nodes. In some countries oncolytic virotherapy methods are studied and used to treat melanoma. Oncolytic virotherapy is a promising branch of virotherapy , where oncolytic viruses are used to treat diseases; viruses can increase metabolism, reduce anti-tumor immunity and disorganize vasculature.
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