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1. Dai DL, Martinka M, Bush JA, Li G: Reduced Apaf-1 expression in human cutaneous melanomas. Br J Cancer; 2004 Sep 13;91(6):1089-95
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  • [Title] Reduced Apaf-1 expression in human cutaneous melanomas.
  • Malignant melanoma is a life-threatening skin cancer due to its highly metastatic character and resistance to radio- and chemotherapy.
  • However, the exact mechanism for failure in the apoptotic pathway in melanoma cells is unclear. p53, the most frequently mutated tumour suppressor gene in human cancers, is a key apoptosis inducer.
  • However, p53 mutation is only found in 15-20% of melanoma biopsies.
  • Recently, it was found that Apaf-1, a downstream target of p53, is inactivated in metastatic melanoma.
  • Specifically, loss of heterozygosity (LOH) of the Apaf-1 gene was found in 40% of metastatic melanoma.
  • To determine if loss of Apaf-1 expression is indeed involved in melanoma progression, we employed the tissue microarray technology and examined Apaf-1 expression in 70 human primary malignant melanoma biopsies by immunohistochemistry.
  • Our data showed that Apaf-1 expression is significantly reduced in melanoma cells compared with normal nevi (chi(2)=6.02, P=0.014).
  • In addition, our in vitro apoptosis assay revealed that overexpression of Apaf-1 can sensitise melanoma cells to anticancer drug treatment.
  • Taken together, our data indicate that Apaf-1 expression is significantly reduced in human melanoma and that Apaf-1 may serve as a therapeutic target in melanoma.
  • [MeSH-major] Melanoma / genetics. Proteins / genetics. Skin Neoplasms / genetics
  • [MeSH-minor] Apoptosis. Apoptotic Protease-Activating Factor 1. Cell Line, Tumor. Cell Survival. Enzyme-Linked Immunosorbent Assay. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Nevus / genetics. Nevus / pathology. Oligonucleotide Array Sequence Analysis. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 15305193.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / APAF1 protein, human; 0 / Apoptotic Protease-Activating Factor 1; 0 / Proteins
  • [Other-IDs] NLM/ PMC2747705
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2. Hiscutt EL, Hill DS, Martin S, Kerr R, Harbottle A, Birch-Machin M, Redfern CP, Fulda S, Armstrong JL, Lovat PE: Targeting X-linked inhibitor of apoptosis protein to increase the efficacy of endoplasmic reticulum stress-induced apoptosis for melanoma therapy. J Invest Dermatol; 2010 Sep;130(9):2250-8
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  • [Title] Targeting X-linked inhibitor of apoptosis protein to increase the efficacy of endoplasmic reticulum stress-induced apoptosis for melanoma therapy.
  • Melanoma remains notoriously resistant to current chemotherapeutics, leaving an acute need for novel therapeutic approaches.
  • The aim of this study was to determine the prognostic and therapeutic significance of X-linked inhibitor of apoptosis protein (XIAP) in melanoma through correlation of XIAP expression with disease stage, RAS/RAF mutational status, clinical outcome, and susceptibility to endoplasmic reticulum (ER) stress-induced cell death.
  • XIAP expression and N-RAS/B-RAF mutational status were retrospectively determined in a cohort of 55 primary cutaneous melanocytic lesions selected and grouped according to the American Joint Committee on Cancer staging system.
  • However, XIAP knockdown significantly increased ER stress-induced apoptosis of melanoma cells in a caspase-dependant manner.
  • The correlation of XIAP expression with disease stage, as well as data showing that XIAP knockdown significantly increases fenretinide and bortezomib-induced apoptosis of metastatic melanoma cells, suggests that XIAP may prove to be an effective therapeutic target for melanoma therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Boronic Acids / pharmacology. Fenretinide / pharmacology. Melanoma / drug therapy. Pyrazines / pharmacology. Skin Neoplasms / drug therapy. X-Linked Inhibitor of Apoptosis Protein / antagonists & inhibitors
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Bortezomib. Drug Resistance, Neoplasm. Endoplasmic Reticulum / physiology. Female. Gene Expression Regulation, Neoplastic. Genes, ras / physiology. Humans. In Vitro Techniques. Male. Middle Aged. Mutation / genetics. Nevus, Pigmented / drug therapy. Nevus, Pigmented / metabolism. Nevus, Pigmented / pathology. Proto-Oncogene Proteins B-raf / genetics. RNA, Small Interfering. Stress, Physiological / physiology

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  • [CommentIn] J Invest Dermatol. 2011 Mar;131(3):797 [21068753.001]
  • [CommentIn] J Invest Dermatol. 2010 Sep;130(9):2169-72 [20711206.001]
  • (PMID = 20520630.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 0 / RNA, Small Interfering; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; 187EJ7QEXL / Fenretinide; 69G8BD63PP / Bortezomib; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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3. Alessi SS, Sanches JA, Oliveira WR, Messina MC, Pimentel ER, Festa Neto C: Treatment of cutaneous tumors with topical 5% imiquimod cream. Clinics (Sao Paulo); 2009;64(10):961-6
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  • [Title] Treatment of cutaneous tumors with topical 5% imiquimod cream.
  • INTRODUCTION: There are various approaches to the treatment of cutaneous tumors; one of them is treatment with imiquimod, a synthetic toll-like receptor agonist with a low molecular weight that offers a topical, noninvasive, and non-surgical therapeutic option.
  • The main objective of our study was to provide data on 89 patients who used a 5% imiquimod cream for the treatment of cutaneous tumors at the Cutaneous Oncology Group of the Dermatology Department of Hospital das Clinicas from 2003 to 2008.
  • MATERIALS AND METHODS: Here, we present our experience in the treatment of 123 cutaneous tumors of various types, including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), Bowen's disease, erythroplasia of Queyrat, Paget's disease, and trichoepithelioma, with 5% imiquimod cream from 2003 to 2008 in the Cutaneous Oncology Group of the Dermatology Department of Hospital das Clinicas.
  • Patients were divided into two separate groups according to their diagnosis and comorbidities; these comorbidities included epidermodysplasia verruciformis, xeroderma pigmentosum, albinism, basal cell nevus syndrome, Brooke-Spiegler syndrome, HIV, chronic lymphocytic leukemia, B-cell lymphoma, and kidney transplantation.
  • Treatment duration, response to imiquimod, follow-up, recurrence, and local and systemic reactions associated with use of the drug were analyzed.
  • Aggressive BCC and superficial and nodular BCC did not present a good response to treatment.
  • One SCC lesion demonstrated a complete response, and tumors caused by Paget's disease and erythroplasia of Queyrat presented a partial response.
  • We demonstrate that patients with no response to imiquimod, even when they demonstrated no local reaction, can undergo another cycle of six weeks of imiquimod treatment and show a complete response.
  • CONCLUSIONS: Our experience confirms imiquimod as an effective treatment option for several types of cutaneous tumors, especially in patients without the cutaneous comorbidities cited above and with low-risk tumors.
  • Imiquimod has a relatively low cost compared to other therapeutic options and can be delivered via ambulatory care to patients with surgery contraindications, and its side effects are tolerable.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Skin Neoplasms / drug therapy

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  • (PMID = 19841702.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
  • [Other-IDs] NLM/ PMC2763070
  • [Keywords] NOTNLM ; Basal cell carcinoma / Imiquimod / Immunomodulator / Immunotherapy / Non-melanoma skin cancer
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4. Bogenrieder T, Weitzel C, Schölmerich J, Landthaler M, Stolz W: Eruptive multiple lentigo-maligna-like lesions in a patient undergoing chemotherapy with an oral 5-fluorouracil prodrug for metastasizing colorectal carcinoma: a lesson for the pathogenesis of malignant melanoma? Dermatology; 2002;205(2):174-5
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  • [Title] Eruptive multiple lentigo-maligna-like lesions in a patient undergoing chemotherapy with an oral 5-fluorouracil prodrug for metastasizing colorectal carcinoma: a lesson for the pathogenesis of malignant melanoma?
  • Induction of multiple eruptive dermal and atypical melanocytic naevi has frequently been reported in children with malignant haematological diseases and chemotherapy-induced immunosuppression.
  • This is the first report of an adult patient to develop multiple eruptive melanocytic skin lesions while undergoing chemotherapy with an oral 5-fluorouracil prodrug for metastasizing cancer.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Carcinoma / drug therapy. Carcinoma / secondary. Colorectal Neoplasms / pathology. Deoxycytidine / adverse effects. Deoxycytidine / analogs & derivatives. Drug Eruptions / etiology. Hutchinson's Melanotic Freckle / chemically induced. Prodrugs / adverse effects. Skin Neoplasms / diagnosis
  • [MeSH-minor] Administration, Oral. Capecitabine. Fluorouracil. Humans. Male. Melanoma / physiopathology. Middle Aged. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / pathology. Nevus, Pigmented / chemically induced. Nevus, Pigmented / diagnosis. Nevus, Pigmented / pathology. Skin / pathology

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  • [Copyright] Copyright 2002 S. Karger AG, Basel
  • (PMID = 12218237.001).
  • [ISSN] 1018-8665
  • [Journal-full-title] Dermatology (Basel, Switzerland)
  • [ISO-abbreviation] Dermatology (Basel)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Prodrugs; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; U3P01618RT / Fluorouracil
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5. Karbowniczek M, Spittle CS, Morrison T, Wu H, Henske EP: mTOR is activated in the majority of malignant melanomas. J Invest Dermatol; 2008 Apr;128(4):980-7
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  • [Title] mTOR is activated in the majority of malignant melanomas.
  • The objective of this study was to determine whether activation of the kinase mammalian target of rapamycin (mTOR) is associated with human melanoma.
  • We found moderate or strong hyperphosphorylation of ribosomal protein S6 in 78/107 melanomas (73%).
  • In contrast, only 3/67 benign nevi (4%) were moderately positive, and none were strongly positive.
  • These data indicate that mTOR activation is very strongly associated with malignant, compared to benign, melanocytic lesions.
  • Next, we tested six melanoma-derived cell lines for evidence of mTOR dysregulation.
  • The proliferation of three melanoma-derived lines was blocked by the mTOR inhibitor rapamycin, indicating that mTOR activation is a growth-promoting factor in melanoma-derived cells. mTOR is directly activated by the small guanosine triphosphatase Ras homolog enriched in brain (Rheb), in a farnesylation-dependent manner.
  • Therefore, to investigate the mechanism of mTOR activation, we used the farnesyl transferase inhibitor FTI-277, which partially blocked the growth of three of the six melanoma cell lines.
  • Together, these data implicate activation of mTOR in the pathogenesis of melanoma, and suggest that Rheb and mTOR may be targets for melanoma therapy.
  • [MeSH-major] Melanoma / enzymology. Melanoma / pathology. Protein Kinases / metabolism. Skin Neoplasms / enzymology. Skin Neoplasms / pathology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. DNA Mutational Analysis. Humans. Nevus / enzymology. Nevus / pathology. Phosphorylation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins p21(ras) / genetics. Ribosomal Protein S6 / metabolism. Sirolimus / pharmacology. TOR Serine-Threonine Kinases

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  • (PMID = 17914450.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 51052
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Ribosomal Protein S6; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); W36ZG6FT64 / Sirolimus
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6. Ha L, Merlino G, Sviderskaya EV: Melanomagenesis: overcoming the barrier of melanocyte senescence. Cell Cycle; 2008 Jul 1;7(13):1944-8
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  • Although melanoma ultimately progresses to a highly aggressive and metastatic disease that is typically resistant to currently available therapy, it often begins as a benign nevus consisting of a clonal population of hyperplastic melanocytes that cannot progress because they are locked in a state of cellular senescence.
  • Once senescence is overcome, the nevus can exhibit dysplastic features and readily progress to more lethal stages.
  • Recent advances have convincingly demonstrated that senescence represents a true barrier to the progression of many types of cancer, including melanoma.
  • Thus, understanding the mechanism(s) by which melanoma evades senescence has become a priority in the melanoma research community.
  • However, differences discovered among various tumor types, some subtle and others quite profound, have revealed that senescence frequently operates in a context-dependent manner.

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  • (PMID = 18604170.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / Z01 BC008756-20; United Kingdom / Wellcome Trust / / 078327
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.7.49 / Telomerase; EC 3.6.5.2 / ADP-Ribosylation Factors; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Number-of-references] 65
  • [Other-IDs] NLM/ NIHMS104222; NLM/ PMC2678050
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7. Wang W, Edington HD, Rao UN, Jukic DM, Wang H, Shipe-Spotloe JM, Kirkwood JM: STAT3 as a biomarker of progression in atypical nevi of patients with melanoma: dose-response effects of systemic IFNalpha therapy. J Invest Dermatol; 2008 Aug;128(8):1997-2002
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  • [Title] STAT3 as a biomarker of progression in atypical nevi of patients with melanoma: dose-response effects of systemic IFNalpha therapy.
  • Atypical nevi are nonobligate risk markers of melanoma, affording investigators a target for evaluation of progression biomarkers in vivo. pSTAT1tyr701 (pSTAT1) and pSTAT3tyr705 (pSTAT3) oppose one another in biological function.
  • Therefore, an analysis of phosphorylated STAT1 (pSTAT1) and pSTAT3 signaling was performed simultaneously using double-immunohistochemistry in biopsies of 168 atypical nevi from 42 patients receiving high- or low-dose IFNalpha (HDI and LDI).
  • With maturation of melanocytes from junctional into dermal components of nevi, pSTAT1 expression increased, whereas pSTAT3 expression decreased.
  • The percentage of pSTAT3-positive melanocytes was positively associated with the atypical degree of nevi (P<0.0001).
  • It is suggested that the relative balance of pSTAT1/pSTAT3 may be associated with melanocyte differentiation in vivo. pSTAT3 is a potential biomarker of melanocytic transformation and progression and is modulated by IFNalpha dose-dependently.
  • STAT3 is a potential target for chemoprevention of melanoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Interferon-alpha / therapeutic use. Melanoma / metabolism. Nevus / metabolism. STAT3 Transcription Factor / metabolism. Skin Neoplasms / drug therapy. Skin Neoplasms / metabolism
  • [MeSH-minor] Biopsy. Disease Progression. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic. Humans. Immunologic Factors / therapeutic use. STAT1 Transcription Factor / genetics. STAT1 Transcription Factor / metabolism

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  • (PMID = 18305569.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor
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8. Damato B, Coupland SE: Management of conjunctival melanoma. Expert Rev Anticancer Ther; 2009 Sep;9(9):1227-39
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  • [Title] Management of conjunctival melanoma.
  • Invasive conjunctival melanoma can arise de novo, from nevus or from melanoma in situ.
  • The literature reports that after treatment of invasive conjunctival melanoma more than 50% of patients develop local tumor recurrence, with 20% eventually requiring orbital exenteration and 20-30% developing fatal metastasis.
  • Our results have improved since we replaced adjuvant cryotherapy with radiotherapy and topical chemotherapy.
  • We have devised a clinical system for mapping conjunctival melanocytic lesions and a system for scoring the histological grade of atypia of conjunctival melanocytic intra-epithelial neoplasia/melanoma in situ.
  • We anticipate that these measures will improve outcomes after treatment of conjunctival melanoma in situ and invasive melanoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Conjunctival Neoplasms / therapy. Melanoma / therapy
  • [MeSH-minor] Administration, Topical. Clinical Trials as Topic. Combined Modality Therapy. Cryotherapy / methods. Humans. Neoplasm Invasiveness. Neoplasm Recurrence, Local. Treatment Outcome

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  • (PMID = 19761427.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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9. Murakami M, Wada T, Kashiwagi T, Ishida-Yamamoto A, Iizuka H: Nodular malignant melanoma with Spitz nevus-like pathological features finally confirmed by the pathological feature of the sentinel lymph node. J Dermatol; 2007 Dec;34(12):821-8
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  • [Title] Nodular malignant melanoma with Spitz nevus-like pathological features finally confirmed by the pathological feature of the sentinel lymph node.
  • The clinical and histopathological similarities of nodular melanoma and Spitz nevus currently still make a definitive diagnosis difficult.
  • We report here a case of nodular melanoma that was extremely difficult to diagnose both clinically and histopathologically.
  • Although our first impression was malignant melanoma, we asked two dermatopathologists for second opinions; however, one diagnosed a melanoma and the other a Spitz nevus.
  • Histopathological diagnosis to establish whether it was a melanoma metastasis or nodal nevi was also difficult, and we again asked for second opinions from another dermatopathologist in the USA.
  • According to its clinical course and the histopathology of the sentinel lymph node with additional immunohistochemistry, this case was finally diagnosed as a nodular melanoma (T4aN1aM0, stage IIIA).
  • To date, the patient has been given five courses of chemotherapy at 6-month intervals, with no local recurrence or distant metastases so far.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Melanoma / pathology. Scalp. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Humans. Male. Nevus, Epithelioid and Spindle Cell / pathology. Sentinel Lymph Node Biopsy


10. Schmid-Wendtner MH, Berking C, Baumert J, Schmidt M, Sander CA, Plewig G, Volkenandt M: Cutaneous melanoma in childhood and adolescence: an analysis of 36 patients. J Am Acad Dermatol; 2002 Jun;46(6):874-9
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  • [Title] Cutaneous melanoma in childhood and adolescence: an analysis of 36 patients.
  • Analysis of data of 6931 patients with cutaneous melanoma seen at the Department of Dermatology and Allergology at the Ludwig-Maximilians-University of Munich between 1977 and 1998 identified 36 patients in whom cutaneous melanomas developed during childhood or adolescence (age <18 years).
  • Thirty-one patients presented with nonmetastatic primary melanomas and 5 patients presented with metastatic melanoma.
  • Forty-seven percent of the primary lesions were associated with a nevus (22% with congenital nevi and 25% with acquired nevi).
  • Tumor thickness ranged from 0.24 to 7.0 mm, with a median of 1.29 mm (mean, 1.67 mm).
  • All patients with primary melanomas received surgical therapy; patients with metastatic disease received chemotherapy, radiation therapy, or both.
  • Similar to experience in adult patients, survival strongly correlated with tumor thickness and clinical stage at the time of diagnosis.
  • The data emphasize that a high index of suspicion for cutaneous melanoma is needed by clinicians assessing melanocytic lesions in children and adolescents for early diagnosis.
  • Reduction of the melanoma mortality rate in children and adolescents will be achieved through identification of patients at increased risk.
  • [MeSH-major] Melanoma / epidemiology. Melanoma / etiology. Neoplasm Recurrence, Local / epidemiology. Skin Neoplasms / epidemiology. Skin Neoplasms / etiology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Combined Modality Therapy. Female. Germany / epidemiology. Humans. Lymphatic Metastasis. Male. Medical Records. Nevus / congenital. Nevus / epidemiology. Retrospective Studies. Severity of Illness Index. Survival Analysis

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  • (PMID = 12063484.001).
  • [ISSN] 0190-9622
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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11. Lommatzsch PK, Werschnik C: [Malignant conjunctival melanoma. Clinical review with recommendations for diagnosis, therapy and follow-up]. Klin Monbl Augenheilkd; 2002 Oct;219(10):710-21
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  • [Title] [Malignant conjunctival melanoma. Clinical review with recommendations for diagnosis, therapy and follow-up].
  • [Transliterated title] Das maligne Melanom der Bindehaut - Klinische Ubersicht mit Empfehlungen zur Diagnose, Therapie und Nachsorge.
  • BACKGROUND: Malignant conjunctival melanoma is a rare disease with an incidence of 0.03 - 0.08.
  • This tumour is potentially lethal, even after prompt and proper treatment, especially after delayed onset of therapy.
  • Conjunctival melanoma arises from primary acquired melanosis (PAM), from a preexisting nevus or "de novo" without any precursor at all.
  • In contrast to uveal melanomas, conjunctival melanoma metastasizes via the ipsilateral lymph nodes and in rare cases through the lacrimal duct into the nasal cavities.
  • RESULTS: Removing the local tumour with preservation of visual functions and avoidance of metastases is the therapy of choice.
  • To minimize local recurrence rate surgical excision should be combined with an additional procedure such as cryotherapy, irradiation, or local chemotherapy with MMC.
  • The behaviour of conjunctival melanomas is individually unpredictable.
  • In our own patients the 5-year, 10-year, and 15-year cumulative melanoma-specific survival rate was 84.4 %, 77.7 %, and 75.0 %, respectively.
  • Up to now there is no effective treatment of the metastatic disease.
  • CONCLUSION: In all cases with pigmented lesions of the conjunctiva exclusion of a malignant melanoma has to be the first aim.
  • A patient suffering from a conjunctival melanoma should be referred to an ophthalmo-oncological center for proper treatment.
  • An international prospective study would be worthwhile to answer open questions and to develop new kinds of treatment of this potentially fatal tumour.
  • [MeSH-major] Conjunctival Neoplasms / diagnosis. Melanoma / diagnosis
  • [MeSH-minor] Combined Modality Therapy. Conjunctiva / pathology. Humans. Neoplasm Staging. Prognosis

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  • (PMID = 12447715.001).
  • [ISSN] 0023-2165
  • [Journal-full-title] Klinische Monatsblätter für Augenheilkunde
  • [ISO-abbreviation] Klin Monbl Augenheilkd
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 45
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12. Reutter JC, Long EM, Morrell DS, Thomas NE, Groben PA: Eruptive post-chemotherapy in situ melanomas and dysplastic nevi. Pediatr Dermatol; 2007 Mar-Apr;24(2):135-7
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  • [Title] Eruptive post-chemotherapy in situ melanomas and dysplastic nevi.
  • A 22-year-old white man without a personal or family history of atypical nevi had received chemotherapy for pre-B-cell acute lymphocytic leukemia at age 17 that included L-asparaginase, prednisone, methotrexate, mercaptopurine, daunorubicin, and cytoxan.
  • Two to three months after completing maintenance chemotherapy, the patient reports he developed many moles, which remained stable for approximately 2 years.
  • Histology of specimens of both types of lesions revealed three moderately atypical compound dysplastic melanocytic nevi and three in situ melanomas.
  • The lesions with only features of dysplastic nevi exhibited dermal fibrosis, cytologic atypia, junctional shoulders, lentiginous spread, and focal pigmentation.
  • The lesions with in situ melanomas in addition demonstrated pagetoid spread, extension down adnexal structures, and more severe cytologic atypia.
  • Malignant melanoma has been associated with chronic immunosuppression, and benign nevi have been reported to erupt after chemotherapy.
  • We report an occurrence of multiple eruptive dysplastic nevi and in situ melanomas appearing shortly after completion of chemotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Drug Eruptions / etiology. Dysplastic Nevus Syndrome / chemically induced. Immunosuppressive Agents / adverse effects. Melanoma / chemically induced. Skin Neoplasms / chemically induced

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  • (PMID = 17461808.001).
  • [ISSN] 0736-8046
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents
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13. McKenna DB, Doherty VR, McLaren KM, Hunter JA: Malignant melanoma and lymphoproliferative malignancy: is there a shared aetiology? Br J Dermatol; 2000 Jul;143(1):171-3
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  • [Title] Malignant melanoma and lymphoproliferative malignancy: is there a shared aetiology?
  • We report seven patients who developed malignant melanoma either coincident with or before the diagnosis of non-Hodgkin's lymphoma or chronic lymphatic leukaemia.
  • One patient died secondary to leukaemia, and chemotherapy-induced immunosuppression may have contributed to the development of metastatic melanoma in another patient.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / etiology. Lymphoma, Non-Hodgkin / etiology. Melanoma / etiology. Neoplasms, Multiple Primary / etiology. Skin Neoplasms / etiology
  • [MeSH-minor] Aged. Dysplastic Nevus Syndrome / complications. Female. Humans. Immune System / radiation effects. Immunosuppressive Agents / adverse effects. Male. Middle Aged. T-Lymphocytes, Regulatory / immunology. Ultraviolet Rays / adverse effects

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  • (PMID = 10886155.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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14. Requena L, de la Cruz A, Moreno C, Sangüeza O, Requena C: Animal type melanoma: a report of a case with balloon-cell change and sentinel lymph node metastasis. Am J Dermatopathol; 2001 Aug;23(4):341-6
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  • [Title] Animal type melanoma: a report of a case with balloon-cell change and sentinel lymph node metastasis.
  • Animal type melanoma is a rare histopathologic variant of melanoma characterized by sheets and nodules of heavily pigmented epithelioid melanocytes that involve the entire thickness of the dermis.
  • This human neoplasm mimics melanocytic neoplasms seen in gray horses and laboratory animals; thus, is termed animal type melanoma.
  • We report an example of animal type melanoma on the back of a 27-year-old man.
  • The lesion showed areas of melanoma in situ, which ruled out the possibility of metastatic melanoma.
  • In some areas, neoplastic melanocytes exhibited a balloon-cell appearance; in others the neoplasm was composed of sheets and fascicles of heavily pigmented epithelioid melanocytes that permeated the entire dermis and extended into the dermal-subcutaneous interface, mimicking a cellular blue nevus.
  • The neoplastic cells did not show evidence of maturation in deeper areas of the lesion.
  • In some sections, a nodule of heavily pigmented epithelioid melanocytes was seen far from the main bulk of the lesion, at the dermal-subcutaneous interface, raising the possibility of a satellite lesion.
  • A lymphoscintigraphy showed a sentinel lymph node in the right axilla and a subsequent axillary lymphadenectomy demonstrated that the architecture of the sentinel lymph node was effaced by metastatic melanoma.
  • The patient received adjuvant chemotherapy with inteferon alfa-2b and four months after this treatment the patient is alive and well, without evidence of recurrences or additional metastases.
  • [MeSH-major] Lymph Nodes / pathology. Melanoma. Skin Neoplasms
  • [MeSH-minor] Adult. Humans. Male. Melanoma, Experimental / pathology. Neoplasm Metastasis

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  • (PMID = 11481528.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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15. Mu XC, Tran TA, Ross JS, Carlson JA: Topoisomerase II-alpha expression in melanocytic nevi and malignant melanoma. J Cutan Pathol; 2000 May;27(5):242-8
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  • [Title] Topoisomerase II-alpha expression in melanocytic nevi and malignant melanoma.
  • Malignant melanoma (MM) is considered to be a chemotherapy-refractory tumor.
  • New anti-cancer drugs (e.g. etoposide) that target DNA topoisomerases (e.g. topoisomerase II-alpha (topo IIalpha)) show activity against a wide variety of solid tumors.
  • In this study, we investigated the frequency and rate of labeling for topo IIalpha in 163 MMs (primary and metastatic) and 67 melanocytic nevi to determine whether topo IIalpha expression is elevated in MM.
  • Primary MM exhibited significantly more frequent topo IIalpha expression compared to benign nevi (86% vs. 56%, p=0.0001).
  • The rate of topo IIalpha labeling in dysplastic melanocytic nevi, radial growth phase MM, vertical growth phase MM and metastatic MM revealed significant differences amongst groups and a positive covariance with advancing stage (means: 0.3, 0.5, 5, and 8 '+' cells/hpf, respectively; r=0.3, all p < or = 0.02).
  • These findings indicate topo IIalpha as a potential therapeutic target and marker for MM.
  • Immunohistochemical analysis of disseminated MM may allow for correlation with clinical response and enable selection of candidates sensitive for specific chemotherapy.
  • [MeSH-major] Antigens, Neoplasm / metabolism. DNA Topoisomerases, Type II / metabolism. Isoenzymes / metabolism. Melanoma / enzymology. Nevus, Pigmented / enzymology. Skin Neoplasms / enzymology

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  • (PMID = 10847549.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] DENMARK
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Isoenzymes; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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16. von Moos R, Schaffner R, Cathomas R, Grimm B: Intratumoral therapy with interferon-alpha in a locoregional advanced malignant blue nevus: a brief communication. J Immunother; 2010 Jan;33(1):92-5
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  • [Title] Intratumoral therapy with interferon-alpha in a locoregional advanced malignant blue nevus: a brief communication.
  • Malignant blue nevi are a rare variant of cutaneous melanoma often associated with metastatic disease and poor prognosis.
  • Information on the treatment of this condition is limited.
  • This case study reports the use of intralesional interferon -alpha2b (IFN-alpha2b) as a salvage option in a male patient with a congenital blue nevus on the right buttock.
  • After initial diagnosis, the primary lesion (lesion 1) was partially resected and the patient received aggressive treatment with radiotherapy and concomitant polychemotherapy (cisplatin, vinblastine, and dacarbazine).
  • However, the lesion progressed and the patient was treated second-line with carboplatin, paclitaxel, and sorafenib.
  • Although this treatment stabilized the primary lesion, at cycle 6, the patient developed a measurable locoregional metastasis (lesion 2).
  • At this stage, the patient was treated with intralesional IFN-alpha2b twice weekly at lesion 2, followed by weekly intralesional IFN-alpha2b therapy to both lesions, which resulted in partial disease regression.
  • Biweekly maintenance therapy with IFN-alpha2b administered to both lesions maintained a partial response (ongoing at 23+ mo) and allowed complete occupational rehabilitation.
  • Thus, intralesional therapy with IFN-alpha2b may be a viable treatment option in patients with locally advanced melanoma who have progressed on prior radiotherapy, polychemotherapy, and/or multikinase antiangiogenic-based therapy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Interferon-alpha / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Nevus, Blue / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 19952952.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha
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17. Andreani V, Richard MA, Blaise D, Gouvernet J, Grob JJ: Naevi in allogeneic bone marrow transplantation recipients: the effect of graft-versus-host disease on naevi. Br J Dermatol; 2002 Sep;147(3):433-41
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  • [Title] Naevi in allogeneic bone marrow transplantation recipients: the effect of graft-versus-host disease on naevi.
  • BACKGROUND: Non-melanoma skin carcinoma is more common in transplant recipients, probably because of immunosuppression.
  • An increased risk of developing melanoma could be a late effect of transplantation.
  • The number of naevi, which is a risk marker for melanoma, is increased in renal transplant recipients of all ages and may be related to immunosuppression.
  • The risk of melanoma has been suspected to be particularly high after bone marrow transplantation.
  • Cutaneous graft-versus-host disease (GVHD) might be an interesting model for the study of interactions between naevi and the immune system.
  • OBJECTIVE: To assess whether aBMT exposes an individual to a particularly high risk of melanoma, using naevi as a surrogate measure of the risk.
  • To improve our knowledge of the effect of the immune system on naevi, using GVHD as a model.
  • RESULTS: The number of naevi was not significantly increased in aBMT patients, as compared with controls, although there was a significant excess on the palms and legs.
  • In exploratory subgroup case-control comparisons and with the general linear model, patients who were conditioned with a combination of two alkylating drugs at high doses, and patients who had an aBMT before the age of 20 years tended to have a higher count of naevi (P = 0.002 and P = 0.06, respectively).
  • Conversely, there was a trend in favour of a lower count of naevi in patients with diffuse skin lesions of chronic GVHD (P = 0.01).
  • These data were corroborated by multivariate analysis, which showed that conditioning with high-dose chemotherapy, the absence of severe chronic cutaneous GVHD and a young age at transplantation were the main variables that independently predicted an excess of naevi.
  • CONCLUSIONS: This study of aBMT patients confirms that chemotherapy stimulates naevus growth.
  • It also suggests for the first time that diffuse lesions of chronic cutaneous GVHD are associated with a decreased number of naevi.
  • Whether allo-immunity, chronic skin inflammation or the masking of naevi by pigmentation and fibrosis is responsible for the decreased number of naevi requires further investigation.
  • With respect to the long-term risk of melanoma in aBMT recipients, our results support an increased risk particularly when aBMT is performed at a young age, and when conditioning is with high doses of alkylating drugs.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Graft vs Host Disease / complications. Nevus / etiology. Skin Neoplasms / etiology

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  • (PMID = 12207581.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
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18. Marnet D, Vinchon M, Mostofi K, Catteau B, Kerdraon O, Dhellemmes P: Neurocutaneous melanosis and the Dandy-Walker complex: an uncommon but not so insignificant association. Childs Nerv Syst; 2009 Dec;25(12):1533-9
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for dandy-walker complex .

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  • BACKGROUND: Neurocutaneous melanosis represents a rare congenital but nonheritable phakomatosis defined as the association of giant or multiple congenital nonmalignant melanocytic nevi with leptomeningeal melanosis or melanoma of the central nervous system.
  • METHODS: We describe the case of an adolescent with a giant congenital bathing trunk melanocytic nevus who developed progressive intracranial hypertension due to leptomeningeal melanosis confirmed by surgical biopsy.
  • Shunt placement, corticotherapy, and chemotherapy were attempted leading to transient relief but the boy died 12 months after the onset of primary neurological symptoms.

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  • (PMID = 19711088.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 48
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19. Soikkeli J, Lukk M, Nummela P, Virolainen S, Jahkola T, Katainen R, Harju L, Ukkonen E, Saksela O, Hölttä E: Systematic search for the best gene expression markers for melanoma micrometastasis detection. J Pathol; 2007 Oct;213(2):180-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic search for the best gene expression markers for melanoma micrometastasis detection.
  • Melanoma is notorious for its high tendency to metastasize and its refractoriness to treatment thereafter.
  • We performed genome-wide gene expression analyses of melanoma lymph node micrometastases and macrometastases, and of primary melanomas and benign naevi, to characterize the early metastatic cells molecularly and to disclose the best diagnostic markers and rational targets for therapy.
  • Furthermore, SPP1 and PRAME proved valuable as melanoma-specific markers capable of differentiating melanoma cells from benign naevi in the sentinel lymph nodes.
  • Importantly, these two genes may also prove to be ideal targets for drug development and therapy.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Melanoma / diagnosis. Melanoma / secondary
  • [MeSH-minor] Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Diagnosis, Differential. Humans. Lymphatic Metastasis. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Nevus / diagnosis. Oligonucleotide Array Sequence Analysis / methods. Osteopontin / genetics. Osteopontin / metabolism. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction / methods. Sentinel Lymph Node Biopsy. Skin Neoplasms / metabolism

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  • (PMID = 17891747.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / PRAME protein, human; 0 / SPP1 protein, human; 106441-73-0 / Osteopontin
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20. Lin SM, Ferrucci S: Primary acquired melanosis of the conjunctiva. Optometry; 2006 May;77(5):223-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The presence or absence of atypia is helpful in determining the potential for malignancy, because PAM without atypia is usually benign, whereas PAM with atypia may convert into a conjunctival melanoma.
  • His ocular history was remarkable for early cataracts and for a choroidal nevus.
  • The lesion was surgically excised, and the conjunctiva was reconstructed with an amniotic membrane graft.
  • The patient was subsequently treated with topical 5-fluorouracil chemotherapy.
  • There have been no signs of recurrence to date after his treatment.
  • If atypia is present, treatment options include local excision, cryotherapy, and topical chemotherapy.

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  • (PMID = 16651212.001).
  • [ISSN] 1529-1839
  • [Journal-full-title] Optometry (St. Louis, Mo.)
  • [ISO-abbreviation] Optometry
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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21. Belloni Fortina A, Piaserico S, Zattra E, Alaibac M: Dermoscopic features of eruptive melanocytic naevi in an adult patient receiving immunosuppressive therapy for Crohn's disease. Melanoma Res; 2005 Jun;15(3):223-4
Hazardous Substances Data Bank. AZATHIOPRINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dermoscopic features of eruptive melanocytic naevi in an adult patient receiving immunosuppressive therapy for Crohn's disease.
  • The induction of multiple eruptive melanocytic naevi has frequently been reported to occur in association with chemotherapy or immunosuppressive regimens, particularly in children and adolescents.
  • We describe the dermoscopic features of eruptive melanocytic naevi in an adult non-transplanted patient receiving immunosuppressive therapy for Crohn's disease.
  • These patients were children, adolescents and young adults with renal allografts receiving immunosuppressive therapy.
  • The findings of our case strongly suggest that this dermoscopic feature may be associated with eruptive naevi developed in association with immunosuppression from any cause.
  • [MeSH-major] Azathioprine / adverse effects. Immunosuppressive Agents / adverse effects. Nevus, Pigmented / etiology. Skin Neoplasms / etiology
  • [MeSH-minor] Adult. Crohn Disease / therapy. Dermoscopy. Female. Humans. Immunosuppression / adverse effects

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  • (PMID = 15917707.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; MRK240IY2L / Azathioprine
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22. Albert A, Cruz O, Montaner A, Vela A, Badosa J, Castañón M, Morales L: [Congenital solid tumors. A thirteen-year review]. Cir Pediatr; 2004 Jul;17(3):133-6
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  • [Transliterated title] Tumores sólidos congénitos. Revisión de 13 años.
  • This is an interesting group of tumors because their type, relative incidence, natural history and response to treatment differ from those seen in older children.
  • There were 8 teratomas (3 sacrocoxigeal, 1 retroperitoneal, 1 in the CNS, 1 orbitary and two oronasal), two hepatic tumors (1 hepatoblastoma, 1 hemangioendothelioma, two CNS tumors, two giant nevus (one on a hamartoma), and one each Wilms tumor, infantile fibrosarcoma and myofibroblastic tumor.
  • Treatment was surgical resection alone in 17 cases (68%) and surgery + chemotherapy in 8 (32%) (5 neuroblastomas, one CNS tumor, one Wilms tumor and one presacral teratoma who developed a yolk sac tumor); 3 patients died (11%): one at surgery, one of tumoural airway obstruction at birth and one with craniopharyngioma.
  • Among the 14 tumors that were initially not malignant, two can be locally agressive, one was an immature teratoma, the giant nevus with hamartoma developed in situ melanoma, the other nevus had meningeal melanosis with hydrocephalus, and one mature presacral teratoma developed a yolk sac tumor.
  • Complete surgical excision is the treatment of choice, most cases not need adjuvant chemotherapy.
  • [MeSH-major] Central Nervous System Neoplasms / congenital. Kidney Neoplasms / congenital. Liver Neoplasms / congenital. Neuroblastoma / congenital. Skin Neoplasms / congenital. Soft Tissue Neoplasms / congenital. Teratoma / congenital. Wilms Tumor / congenital
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Infant, Newborn. Male. Neoplasm Recurrence, Local. Postoperative Complications. Pregnancy. Prenatal Diagnosis. Time Factors

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  • (PMID = 15503950.001).
  • [ISSN] 0214-1221
  • [Journal-full-title] Cirugía pediátrica : organo oficial de la Sociedad Española de Cirugía Pediátrica
  • [ISO-abbreviation] Cir Pediatr
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
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23. Holbach LM, Pogorelov P, Kruse FE: [Differential diagnosis and treatment options for conjunctival tumors]. Ophthalmologe; 2007 Jun;104(6):521-38; quiz 538

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Differential diagnosis and treatment options for conjunctival tumors].
  • Pigmented and nonpigmented melanocytic nevi are the most frequent conjunctival tumors.
  • An important practical biomicroscopic cardinal symptom of the most frequent nevi is the presence of epithelial pseudocysts.
  • Essential in practice is the histopathological confirmation of the clinical diagnosis, e.g., distinguishing between nonpigmented melanomas and sebaceous gland carcinomas with a pagetoid growth pattern or squamous cell carcinomas.
  • Depending on the course and findings, the following therapeutic measures can be indicated: cryotherapy, chemotherapy, radiotherapy, modified enucleation, orbital exenteration, or a combination of different methods.
  • [MeSH-minor] Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / therapy. Combined Modality Therapy. Conjunctiva / pathology. Diagnosis, Differential. Humans. Lymphatic Metastasis / pathology. Melanoma / diagnosis. Melanoma / pathology. Melanoma / therapy. Neoplasm Staging. Nevus, Pigmented / diagnosis. Nevus, Pigmented / pathology. Nevus, Pigmented / therapy. Ophthalmoscopy

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  • (PMID = 17530261.001).
  • [ISSN] 0941-293X
  • [Journal-full-title] Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft
  • [ISO-abbreviation] Ophthalmologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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24. Smith AP, Kirkwood JM, Edington HD, Jukic DM, Farkas DL, Becker D: Fluorescence imaging analysis of upstream regulators and downstream targets of STAT3 in melanoma precursor lesions obtained from patients before and after systemic low-dose interferon-alpha treatment. Mol Imaging; 2003 Jan;2(1):65-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fluorescence imaging analysis of upstream regulators and downstream targets of STAT3 in melanoma precursor lesions obtained from patients before and after systemic low-dose interferon-alpha treatment.
  • Atypical nevi are the precursors and risk markers of melanoma.
  • Apart from persistently monitoring these nevocytic lesions and resecting them at the earliest signs of clinical changes, there is as yet no systemic clinical treatment available to interfere with their progression to melanoma.
  • To explore clinical treatments that might interfere with and possibly prevent atypical nevus progression, a previous study documented that 3 months systemic low-dose interferon-alpha (IFN-alpha) treatment of patients with a clinical history of melanoma and numerous atypical nevi, led to inactivation of the STAT1 and STAT3 transcription factors in atypical nevi.
  • Based upon this finding, we initiated a second study to determine whether systemic low-dose IFN-alpha treatment also impairs the expression of upstream regulators and downstream targets of STAT1 and STAT3 in atypical nevi.
  • Using cyanine dye-conjugated antibodies, fluorescence imaging analysis revealed expression of JAK2, JNK1, AKT1, NF-kappa B, and IFN-alpha/beta receptor in benign and atypical nevi, and early- and advanced-stage melanomas.
  • To determine possible changes in the level of expression of these molecules in atypical nevi, excised before and after 3 months of systemic low-dose IFN-alpha treatment, newly designed optical imaging software was used to quantitate the captured fluorescent hybridization signals on a cell-by-cell basis and across an entire nevus section.
  • The results of this analysis did not provide evidence that systemic low-dose IFN-alpha treatment alters the level of expression of upstream regulators or downstream targets of STAT1 and STAT3.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Interferon-alpha / therapeutic use. Melanoma / drug therapy. Melanoma / metabolism. Microscopy, Fluorescence / methods. Precancerous Conditions / drug therapy. Precancerous Conditions / metabolism. Proto-Oncogene Proteins. Skin Neoplasms / drug therapy. Skin Neoplasms / metabolism. Trans-Activators / metabolism

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  • (PMID = 12926238.001).
  • [ISSN] 1535-3508
  • [Journal-full-title] Molecular imaging
  • [ISO-abbreviation] Mol Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Interferon-alpha; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0 / Receptors, Interferon; 0 / Recombinant Proteins; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Trans-Activators; 156986-95-7 / Receptor, Interferon alpha-beta; 76543-88-9 / interferon alfa-2a; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 8; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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25. Salti GI, Kichina JV, Das Gupta TK, Uddin S, Bratescu L, Pezzuto JM, Mehta RG, Constantinou AI: Betulinic acid reduces ultraviolet-C-induced DNA breakage in congenital melanocytic naeval cells: evidence for a potential role as a chemopreventive agent. Melanoma Res; 2001 Apr;11(2):99-104
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Betulinic acid reduces ultraviolet-C-induced DNA breakage in congenital melanocytic naeval cells: evidence for a potential role as a chemopreventive agent.
  • Melanoma transformation progresses in a multistep fashion from precursor lesions such as congenital naevi.
  • Betulinic acid (BA) was identified by our group as a selective inhibitor of melanoma that functions by inducing apoptosis.
  • The present study was designed to investigate the effect of BA and UV-C (254 nm) on cultured congenital melanocytic naevi (CMN) cells, using the single-cell gel electrophoresis (comet) assay to detect DNA damage.
  • This suggests that p53 can protect against UV-induced DNA damage and subsequent melanoma transformation.
  • These data indicate that BA may have an application as a chemopreventive agent in patients with congenital naevi.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Melanocytes / pathology. Neoplasms, Radiation-Induced / drug therapy. Nevus / metabolism. Triterpenes / pharmacology. Ultraviolet Rays

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  • (PMID = 11333133.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62184; United States / NCI NIH HHS / CA / T32-CA09432
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Triterpenes; 4G6A18707N / betulinic acid; 9007-49-2 / DNA; EC 3.6.5.2 / rho GTP-Binding Proteins
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26. Thomas L, Dalle S: Dermoscopy provides useful information for the management of melanonychia striata. Dermatol Ther; 2007 Jan-Feb;20(1):3-10
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  • In the case of brown longitudinal pigmentation with parallel regular lines, the diagnosis of nail apparatus melanocytic nevus could be made.
  • On the other hand, the presence of a brown pigmentation overlaid by longitudinal lines irregular in their thickness, spacing, color, or parallelism is highly in favor of a melanoma.
  • Gray homogeneous lines are observed in case of lentigo, lentiginoses, ethnic or drug-induced pigmentations, and in post-traumatic pigmentations.
  • Blood spots are characterized by their round-shaped proximal edge and their filamentous distal edge and are highly suggestive of subungual hemorrhages.
  • Dermoscopic examination of the free edge of the nail plate gives information on the lesion location; pigmentation of the dorsum of the nail plate is in favor of a proximal nail matrix lesion, whereas pigmentation the lower part of the nail edge is in favor of a lesion of the distal matrix.
  • [MeSH-minor] Dermoscopy. Diagnosis, Differential. Humans. Melanoma / diagnosis. Melanoma / pathology. Skin Neoplasms / diagnosis. Skin Neoplasms / pathology

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  • (PMID = 17403255.001).
  • [ISSN] 1396-0296
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Number-of-references] 14
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27. Dusza SW, Delgado R, Busam KJ, Marghoob AA, Halpern AC: Treatment of dysplastic nevi with 5% imiquimod cream, a pilot study. J Drugs Dermatol; 2006 Jan;5(1):56-62
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of dysplastic nevi with 5% imiquimod cream, a pilot study.
  • OBJECTIVE: To assess the clinical and histologic effects of topical imiquimod therapy on dysplastic nevi, and to determine the feasibility of using in vivo confocal microscopy (CSLM) to non-invasively monitor histological response of dysplastic nevi to imiquimod therapy.
  • DESIGN: Single-blinded pilot study with patients not blinded as to treatment status.
  • PATIENTS: The study population comprised of 10 patients with clinically dysplastic (atypical) nevi and at least 8 large nevi, (> or =5 mm) on their trunk.
  • INTERVENTION: Sixteen weeks of imiquimod 5% cream applied to treatment lesions 3 times per week.
  • MAIN OUTCOME MEASURE: Clinical response as gauged by comparison of baseline and week 20 1:1 standardized photographs for all study nevi and histological assessment of each patient's 4 largest study nevi at completion of therapy.
  • RESULTS: There were no obvious clinical changes in the size and morphology of the study nevi.
  • Subtle changes in nevus color could not be assessed due to imperfect spectral registration of images over the course of the study.
  • Histologically, 4 of 14 treated nevi and 0 of 14 untreated nevi p=0.03 showed a significant relative reduction of junctional and intraepidermal nevocytes accompanied by papillary dermal fibroses and variable inflammation suggestive of partial regression.
  • Non-invasive CSLM imaging of study nevi demonstrated previously reported in vivo features of dysplastic nevi. but the imaging equipment and protocol utilized proved inconsistent across lesions and time.
  • CONCLUSIONS: The histological changes seen in a subset of treated nevi suggest a possible role for the use of topical immune response modifiers for the treatment of dysplastic nevi with the intent of melanoma chemoprevention.
  • Targeting of dysplastic nevi and intermediate endpoints for melanoma chemoprevention with more intense and/or prolonged treatment regimens with imiquimod or the use of other immune response modifiers seems promising.
  • Technical improvements are required for the use of non-invasive CSLM imaging in lieu of invasive histology for the study of topical nevus therapies.
  • [MeSH-major] Aminoquinolines / administration & dosage. Dysplastic Nevus Syndrome / drug therapy

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  • (PMID = 16468293.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Ointments; 99011-02-6 / imiquimod
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28. Somani N, Martinka M, Crawford RI, Dutz JP, Rivers JK: Treatment of atypical nevi with imiquimod 5% cream. Arch Dermatol; 2007 Mar;143(3):379-85
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of atypical nevi with imiquimod 5% cream.
  • BACKGROUND: 5% Imiquimod cream is a topical immune response modifier that has been used off-label to treat malignant melanocytic proliferations such as lentigo maligna.
  • To our knowledge, imiquimod has not been previously used to treat atypical nevi (AN).
  • Two were consistent with atypical compound nevus on excisional biopsy and demonstrated inflammation, while the third showed congenital features and demonstrated minimal inflammation.
  • Immunohistochemical studies revealed that the AN but not the congenital-like nevus exhibited increased staining for CD4(+) and CD8(+) cells and for a surrogate marker of interferon alpha expression.
  • CONCLUSIONS: Twelve weeks of imiquimod treatment failed to cause lesional resolution.
  • A differential inflammatory response was observed between the AN and the congenital-like nevus.
  • The character of the inflammatory infiltrate was similar to that observed with halo nevi.
  • Uncertainties remain concerning imiquimod use for chemoprevention of AN, and the posttreatment histologic features may be misinterpreted as severe melanocytic atypia or melanoma.
  • [MeSH-major] Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Nevus / drug therapy

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  • (PMID = 17372103.001).
  • [ISSN] 0003-987X
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Dosage Forms; 99011-02-6 / imiquimod
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