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1. Bifulco G, Mandato VD, Piccoli R, Giampaolino P, Mignogna C, Mignogna MD, Costagliola L, Nappi C: Early invasive vulvar squamous cell carcinoma arising in a woman with vulvar pemphigus vulgaris and systemic lupus erythematosus. BMC Cancer; 2010;10:324
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  • [Title] Early invasive vulvar squamous cell carcinoma arising in a woman with vulvar pemphigus vulgaris and systemic lupus erythematosus.
  • BACKGROUND: Pemphigus vulgaris (PV) is an autoimmune blistering disease of the skin and mucous membranes.
  • Systemic lupus erythematosus (SLE) is an autoimmune disease that may affect many parts of the body and the skin with occasional bullous lesions.
  • Here, we report the first case of a woman affected with SLE presenting with early invasive squamous cell carcinoma (SCC) arising from Pemphigus Vulgaris of the vulva.
  • One month later a new biopsy revealed progression from VIN 3 to early SCC.
  • Despite chemotherapy, no remission of disease was observed.
  • She died six months after diagnosis CONCLUSION: Our case underlines PV as another chronic inflammatory disease of the lower genital tract predisposing to VIN-SCC.
  • It suggests the need for careful follow-up of patients with chronic inflammatory disease, especially when concomitant autoimmune disorders are present.
  • Moreover, a biopsy should be always performed if there are PV lesions because of the possibility of neoplastic disease.
  • [MeSH-major] Carcinoma in Situ / etiology. Carcinoma, Squamous Cell / etiology. Lupus Erythematosus, Systemic / complications. Pemphigus / complications. Vulvar Diseases / complications. Vulvar Neoplasms / etiology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Disease Progression. Fatal Outcome. Female. Humans. Neoplasm Invasiveness. Neoplasm Staging. Time Factors


2. Li L, Shukla S, Lee A, Garfield SH, Maloney DJ, Ambudkar SV, Yuspa SH: The skin cancer chemotherapeutic agent ingenol-3-angelate (PEP005) is a substrate for the epidermal multidrug transporter (ABCB1) and targets tumor vasculature. Cancer Res; 2010 Jun 1;70(11):4509-19
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  • [Title] The skin cancer chemotherapeutic agent ingenol-3-angelate (PEP005) is a substrate for the epidermal multidrug transporter (ABCB1) and targets tumor vasculature.
  • Ingenol-3-angelate (Ing3A), extracted from Euphorbia peplus, is currently in clinical trials for eradicating basal cell carcinoma, actinic keratosis, and squamous cell carcinoma (SCC) in situ by topical application.
  • Although structurally related to phorbol esters and a protein kinase C activator, topical Ing3A, but not phorbol 12-myristate 13-acetate (PMA), inhibited the growth of subcutaneous tumors derived from PAM212 (mouse SCC) and B16 (mouse melanoma).
  • Ing3A and PMA both induced acute neutrophilic inflammation on mouse skin, but only Ing3A caused subcutaneous hemorrhage and vascular damage.
  • Both Ing3A and PMA activated extracellular signal-regulated kinase 1/2 (ERK1/2) in epidermis, but Ing3A also activated ERK1/2 in skin dermal fibroblasts and endothelial cells.
  • Ing3A, but not PMA, blocked photoaffinity labeling of human P-gp with [(125)I]iodoaryazidoprazosin and inhibited P-gp-mediated drug resistance to HCT-15 cells.
  • The intracellular levels of Ing3A were significantly lower in P-gp-expressing cells, and treatment with XR9576 increased the levels to those of cells that do not express P-gp, showing that Ing3A binds to and is transported by P-gp.
  • [MeSH-major] Antineoplastic Agents / metabolism. Diterpenes / metabolism. P-Glycoprotein / metabolism. Skin Neoplasms / drug therapy. Skin Neoplasms / metabolism
  • [MeSH-minor] Administration, Topical. Animals. Carcinoma, Squamous Cell / blood supply. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / metabolism. Cell Line, Tumor. Drug Eruptions / enzymology. Drug Eruptions / etiology. Enzyme Activation / drug effects. Humans. Keratinocytes / drug effects. Keratinocytes / enzymology. Melanoma, Experimental / blood supply. Melanoma, Experimental / drug therapy. Melanoma, Experimental / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. P-Glycoproteins. Protein Binding. Protein Kinase C / metabolism. Skin / drug effects. Skin / enzymology. Tetradecanoylphorbol Acetate / pharmacology

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20460505.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC005445-24
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-ingenyl angelate; 0 / ABCB1 protein, human; 0 / Antineoplastic Agents; 0 / Diterpenes; 0 / P-Glycoprotein; 0 / P-Glycoproteins; EC 2.7.11.13 / Protein Kinase C; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ NIHMS193846; NLM/ PMC2880198
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3. Buechner SA: Common skin disorders of the penis. BJU Int; 2002 Sep;90(5):498-506
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  • [Title] Common skin disorders of the penis.
  • Diseases of the male genitalia range from infectious lesions to inflammatory and neoplastic conditions, including many genital manifestations of more general skin diseases.
  • This review highlights the clinical features, diagnosis and treatment of the most common dermatoses of the male genitalia.
  • The most common causal agents for condyloma acuminatum are low-risk HPV 6 and 11; high-risk HPV types 16 and 18 are associated with premalignant and malignant lesions.
  • Treatment for genital warts remains unsatisfactory; recurrences are common.
  • Imiquimod, a new topical immunotherapeutic agent, which induces interferon and other cytokines, has the potential to be a first-line therapy for genital warts.
  • Scabies and pediculosis are transmitted by skin-to-skin contact and sexual transmission is common, with the penis and scrotum favourite locations for scabious lesions.
  • Oral ivermectin, a highly active antiparasitic drug, is likely to be the treatment of choice, but until approval is granted it should be reserved for special forms of scabies.
  • Common skin diseases, e.g. psoriasis and lichen planus, may have an atypical appearance in the genital area.
  • Lichen sclerosus is a chronic inflammatory disease that occurs as atrophic white patches on the glans penis and foreskin.
  • Plasma cell balanitis is a benign, idiopathic condition presenting as a solitary, smooth, shiny, red-orange plaque of the glans and prepuce of a middle-aged to older man.
  • Squamous cell carcinoma (SCC) in situ, e.g. erythroplasia of Queyrat and Bowen's disease, cannot be excluded clinically; their apparent clinical benignity may lead to lengthy periods of misdiagnosis and biopsy is required to confirm the diagnosis.
  • SCC is the most common malignancy of the penis and the role of oncogenic HPV-types has been also established in SCC of the penis.
  • Prevention of SCC of the penis presupposes an identification of risk factors, early detection of all pre-cancerous lesions and treatment of phimosis.
  • [MeSH-major] Penile Diseases. Skin Diseases
  • [MeSH-minor] Balanitis / diagnosis. Balanitis / therapy. Humans. Male. Mite Infestations / diagnosis. Mite Infestations / therapy. Penile Neoplasms / diagnosis. Penile Neoplasms / therapy. Skin Diseases, Parasitic / diagnosis. Skin Diseases, Parasitic / therapy. Skin Diseases, Viral / diagnosis. Skin Diseases, Viral / therapy

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  • (PMID = 12175386.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 39
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4. Arlette JP: Treatment of Bowen's disease and erythroplasia of Queyrat. Br J Dermatol; 2003 Nov;149 Suppl 66:43-9
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  • [Title] Treatment of Bowen's disease and erythroplasia of Queyrat.
  • Bowen's disease of the skin may have differing clinical presentations depending on the skin surface on which it presents, but has the same histologic features of squamous cell carcinoma in situ wherever it occurs.
  • The choice of therapy requires a consideration for retention of form, function and cosmosis while offering a high cure rate.
  • The immunodualtory agent imiquimod has been shown to be an effective treatment on a variety of skin surfaces.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Aminoquinolines / therapeutic use. Bowen's Disease / drug therapy. Erythroplasia / drug therapy. Penile Neoplasms / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 14616349.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 99011-02-6 / imiquimod
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5. Stockfleth E, Ulrich C, Meyer T, Christophers E: Epithelial malignancies in organ transplant patients: clinical presentation and new methods of treatment. Recent Results Cancer Res; 2002;160:251-8
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  • [Title] Epithelial malignancies in organ transplant patients: clinical presentation and new methods of treatment.
  • Transplantation of solid organs has been well established as a mode of therapy for the treatment of various end-stage organ diseases for many years.
  • Nowadays immunosuppressive therapies consist mainly in prednisolone, azathioprine, cyclosporine, anti-T-lymphocyte-globulin (ATG), anti-CD 3 antibody (OKT3) and substances of a new generation, such as tacrolimus or mycophenolic acid.
  • Chronically altered immune responsiveness is especially associated with a dramatically increased risk of malignancy, most frequently non-Hodgkin's lymphoma and skin cancer.
  • Within the first 5 years of immunosuppression 40% of transplant recipients experience premalignant skin tumors such as actinic keratoses and Bowen's disease, and also such skin cancers as squamous cell carcinomas and basal cell carcinomas.
  • Cancer is now responsible for a mortality rate of 5-8% in organ transplant patients.
  • Prophylactic strategies therefore include the development of virus-like particles (VLPs) as anticancer vaccines, which might become a very interesting approach to preventing HPV-associated cancer.
  • The prevention of precancerous conditions and mature skin cancers in grafted patients includes protective clothing and adequate protection of UV-exposed skin regions, including lips, from sunlight with appropriate sunscreen.
  • Close dermatological surveillance through a specialized outpatient department should be ensured to detect potentially fatal skin malignancies at an early stage.
  • Early treatment of precancerous lesions includes topical retinoids, such as tretionin, tazarotene or adapalene.
  • The drug has been shown to have both antiviral and antitumor activity.
  • [MeSH-major] Organ Transplantation / adverse effects. Skin Neoplasms / pathology

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  • (PMID = 12079221.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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6. Micali G, Nasca MR, De Pasquale R: Erythroplasia of Queyrat treated with imiquimod 5% cream. J Am Acad Dermatol; 2006 Nov;55(5):901-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Imiquimod is an immune response-modifying agent with potent antiviral and antitumor activity effective in the treatment of various skin disorders, including in situ carcinoma of the skin (Bowen's disease).
  • The case of a 64-year-old man affected by an in situ carcinoma of the glans mucosa, namely erythroplasia of Queyrat, successfully treated with imiquimod 5% cream is described.
  • This compound may represent an alternative treatment in patients with erythroplasia of Queyrat, although the dosing schedule and treatment duration require further evaluation.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Aminoquinolines / therapeutic use. Carcinoma in Situ / drug therapy. Erythroplasia / drug therapy. Penile Neoplasms / drug therapy
  • [MeSH-minor] Drug Administration Schedule. Humans. Male. Middle Aged. Ointments. Treatment Outcome

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  • (PMID = 17052503.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Ointments; 99011-02-6 / imiquimod
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7. Gaitanis G, Mitsou G, Tsiouri G, Alexis I, Bassukas ID: Cryosurgery during imiquimod cream treatment ("immunocryosurgery") for Bowen's disease of the skin: a case series. Acta Derm Venereol; 2010 Sep;90(5):533-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cryosurgery during imiquimod cream treatment ("immunocryosurgery") for Bowen's disease of the skin: a case series.
  • [MeSH-major] Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Bowen's Disease / drug therapy. Bowen's Disease / surgery. Cryosurgery. Skin Neoplasms / drug therapy. Skin Neoplasms / surgery
  • [MeSH-minor] Administration, Topical. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Drug Administration Schedule. Female. Greece. Humans. Male. Middle Aged. Ointments. Time Factors. Treatment Outcome

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  • (PMID = 20814639.001).
  • [ISSN] 1651-2057
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Ointments; 99011-02-6 / imiquimod
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8. Management of Bowen's disease of the skin. Drug Ther Bull; 2004 Feb;42(2):13-6
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  • [Title] Management of Bowen's disease of the skin.
  • Each year around 15 per 100,000 people in the UK develop intra-epidermal squamous cell carcinoma--Bowen's disease.
  • The lesions of Bowen's disease are slow-growing, erythematous scaly skin plaques that cause few, if any, symptoms.
  • However, if left untreated, they progress to invasive squamous cell carcinoma in 3-5% of patients.
  • Here we review the management of Bowen's disease.
  • [MeSH-major] Bowen's Disease / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Aged. Antimetabolites, Antineoplastic / therapeutic use. Costs and Cost Analysis. Cryotherapy / methods. Fluorouracil / therapeutic use. Humans. Middle Aged. Photochemotherapy / methods

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  • (PMID = 15067953.001).
  • [ISSN] 0012-6543
  • [Journal-full-title] Drug and therapeutics bulletin
  • [ISO-abbreviation] Drug Ther Bull
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
  • [Number-of-references] 36
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9. Ferrándiz C: Update on actinic keratosis in clinical trial experience with imiquimod. Br J Dermatol; 2007 Dec;157 Suppl 2:32-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Actinic keratoses (AK) is a sun induced cutaneous lesion, currently considered as a squamous cell carcinoma in situ that has the potential to progress to invasive SCC.
  • To treat them, numerous, ablative and no ablative, therapeutic approaches exist.
  • Among them, imiquimod, a toll like receptor agonist, recently approved to treat them in the US and Europe, has demonstrated to be effective and safe with an acceptable tolerability in the treatment of these lesions.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Keratosis / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Humans. Neoplasms, Radiation-Induced / drug therapy. Randomized Controlled Trials as Topic. Treatment Outcome. Ultraviolet Rays / adverse effects

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  • (PMID = 18067629.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
  • [Number-of-references] 9
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10. Newman MD, Weinberg JM: Topical therapy in the treatment of actinic keratosis and basal cell carcinoma. Cutis; 2007 Apr;79(4 Suppl):18-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topical therapy in the treatment of actinic keratosis and basal cell carcinoma.
  • AK also is known as solar keratosis and squamous cell carcinoma (SCC) in situ, either solar keratotic type or keratinocytic intraepidermal neoplasia.
  • AKs can be treated with destructive or topical therapies.
  • This article reviews current and evolving topical therapeutic options for AKs, several of which have been shown to offer substantial benefit in the alleviation of these lesions.
  • The topical therapies include 5-fluorouracil (5-FU), diclofenac sodium, colchicine, retinoids, and imiquimod.
  • Topical treatment of basal cell carcinoma (BCC) with imiquimod also will be discussed.
  • [MeSH-major] Carcinoma, Basal Cell / drug therapy. Keratosis / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 17508492.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclooxygenase Inhibitors; 0 / Retinoids; 0 / Tubulin Modulators
  • [Number-of-references] 44
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11. Del Rosso JQ: The treatment of viral infections and nonmelanoma skin cancers. Cutis; 2007 Apr;79(4 Suppl):29-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The treatment of viral infections and nonmelanoma skin cancers.
  • Immunomodulatory therapy, which functions to upregulate immune response, may be directed against a variety of disease states, including viral infections and skin malignancies.
  • Topical imiquimod has been studied for a variety of different disorders including human papillomavirus infection, molluscum contagiosum, actinic keratosis (AK), squamous cell carcinoma (SCC) in situ, superficial basal cell carcinoma (sBCC), nodular basal cell carcinoma (nBCC), and lentigo maligna.
  • Case reports also have demonstrated use for select cases of extramammary Paget disease.
  • This article focuses on therapies designed to augment immune response to treat viral infections and nonmelanoma skin cancers and reviews clinical applications, efficacy, recommended treatment regimens, monitoring of response, and avoidance of pitfalls associated with the use of topical imiquimod.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Interferons / therapeutic use. Skin Diseases, Viral / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 17508493.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 9008-11-1 / Interferons; 99011-02-6 / imiquimod
  • [Number-of-references] 53
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12. Love WE, Bernhard JD, Bordeaux JS: Topical imiquimod or fluorouracil therapy for basal and squamous cell carcinoma: a systematic review. Arch Dermatol; 2009 Dec;145(12):1431-8
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  • [Title] Topical imiquimod or fluorouracil therapy for basal and squamous cell carcinoma: a systematic review.
  • OBJECTIVES: To conduct a systematic review to determine clearance rates and adverse effects of topical imiquimod or fluorouracil therapy in the treatment of nonmelanoma skin cancers such as basal (BCC) and squamous cell carcinoma (SCC), and to develop recommendations for the use of topical imiquimod or fluorouracil to treat BCC and SCC.
  • DATA EXTRACTION: We calculated the rate of clearance and adverse effects for BCC subtypes and invasive and in situ SCC treated with topical imiquimod or fluorouracil.
  • DATA SYNTHESIS: Clearance rates varied by drug regimen, and most of the studies lacked long-term follow-up.
  • Imiquimod use produced the following clearance rates: 43% to 100% for superficial BCC, 42% to 100% for nodular BCC, 56% to 63% for infiltrative BCC, 73% to 88% for SCC in situ, and 71% for invasive SCC.
  • Fluorouracil use produced the following clearance rates: 90% for superficial BCC and 27% to 85% for SCC in situ.
  • CONCLUSIONS: Evidence supports the use of topical imiquimod as monotherapy for superficial BCC and topical fluorouracil as monotherapy for superficial BCC and SCC in situ.
  • Based on the available evidence, the strength of any recommendations for the use of these 2 agents in the primary treatment of these tumors is weak.
  • We recommend that their use be limited to patients with small tumors in low-risk locations who will not or cannot undergo treatment with better-established therapies for which long-term clearance rates have been determined.
  • Limitations of therapy include high rates of adverse effects, lower clearance rates than other treatment modalities, dependence on patient adherence to treatment, and higher costs than other therapies.
  • [MeSH-major] Aminoquinolines / pharmacokinetics. Antineoplastic Agents / pharmacokinetics. Carcinoma, Basal Cell / drug therapy. Carcinoma, Squamous Cell / drug therapy. Fluorouracil / pharmacokinetics. Skin Neoplasms / drug therapy

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  • (PMID = 20026854.001).
  • [ISSN] 1538-3652
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod; U3P01618RT / Fluorouracil
  • [Number-of-references] 47
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13. Lober BA, Fenske NA: Optimum treatment strategies for actinic keratosis (intraepidermal squamous cell carcinoma). Am J Clin Dermatol; 2004;5(6):395-401
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  • [Title] Optimum treatment strategies for actinic keratosis (intraepidermal squamous cell carcinoma).
  • Actinic keratoses are superficial squamous cell carcinomas.
  • Treatment of these lesions is indicated to prevent the cells from invading the dermis and possibly metastasizing.
  • Cryosurgical destruction, the most common treatment employed, has been shown to be 98.8% effective in eliminating the lesions.
  • When a patient has a multitude of actinic keratoses, the use of other treatments including fluorouracil, nonsteroidal anti-inflammatory preparations, immune response modifiers, and photodynamic therapy should be considered.
  • However, none of these treatments has proven to be as effective overall as cryosurgical destruction.
  • If a lesion does not respond to treatment, obtaining a biopsy of the lesion should be considered to be certain that the lesion is not an invasive squamous cell carcinoma.
  • [MeSH-major] Carcinoma, Squamous Cell / therapy. Keratosis / therapy. Skin Neoplasms / drug therapy

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  • (PMID = 15663336.001).
  • [ISSN] 1175-0561
  • [Journal-full-title] American journal of clinical dermatology
  • [ISO-abbreviation] Am J Clin Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
  • [Number-of-references] 54
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14. Patel GK, Goodwin R, Chawla M, Laidler P, Price PE, Finlay AY, Motley RJ: Imiquimod 5% cream monotherapy for cutaneous squamous cell carcinoma in situ (Bowen's disease): a randomized, double-blind, placebo-controlled trial. J Am Acad Dermatol; 2006 Jun;54(6):1025-32
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  • [Title] Imiquimod 5% cream monotherapy for cutaneous squamous cell carcinoma in situ (Bowen's disease): a randomized, double-blind, placebo-controlled trial.
  • BACKGROUND: We conducted a double-blind, placebo-controlled, randomized trial to evaluate the preliminary efficacy and safety of imiquimod 5% cream treatment for cutaneous squamous cell carcinoma (SCC) in situ.
  • METHODS: In all, 31 patients with biopsy-proven cutaneous SCC in situ were randomly assigned to placebo (vehicle) (n = 16) or imiquimod 5% cream (n = 15) daily for 16 weeks.
  • Patients were assessed at week 28 for the primary end point, resolution of cutaneous SCC in situ.
  • Intention-to-treat analysis revealed 11 of the 15 patients (73%) in the imiquimod group achieved resolution of cutaneous SCC in situ, with no relapse during the 9-month follow-up period; none in the placebo group achieved resolution (P < .001).
  • LIMITATIONS: Topical imiquimod 5% cream has proven to be an effective treatment for cutaneous SCC in situ.
  • However, studies to define the ideal dosing regimen and cost-effectiveness are required before it can be accepted as a recognized therapy.
  • CONCLUSIONS: In this controlled trial, patients with cutaneous SCC in situ receiving topical imiquimod 5% cream as monotherapy experienced a high degree of clinical benefit compared with placebo.
  • [MeSH-major] Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Bowen's Disease / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 16713457.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Dosage Forms; 99011-02-6 / imiquimod
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15. Chow KC, Lu MP, Wu MT: Expression of dihydrodiol dehydrogenase plays important roles in apoptosis- and drug-resistance of A431 squamous cell carcinoma. J Dermatol Sci; 2006 Mar;41(3):205-12
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  • [Title] Expression of dihydrodiol dehydrogenase plays important roles in apoptosis- and drug-resistance of A431 squamous cell carcinoma.
  • Previous clinical studies have demonstrated the over-expression of DDH in various types of cancers, including cutaneous squamous cell carcinoma (SCC), and its correlation with tumor progression and grave prognosis.
  • METHODS: DDH expression in SCC A431 cell line was examined by quantitative real-time PCR and immunoblotting.
  • RESULTS: DDH was found highly expressed by SCC A431 cells, which was barely detectable in other normal or malignant cutaneous cells, including keratinocytes, fibroblast, and basal cell carcinoma cell line.
  • RNAi Inhibition of DDH expression in A431 cells led to increased sensitivity to UVB-induced apoptosis and cytotoxicity of bleomycin treatment.
  • CONCLUSION: DDH may play important roles in tumor progression of SCC via induction of apoptosis- and drug-resistance.
  • [MeSH-major] Apoptosis. Carcinoma, Squamous Cell / drug therapy. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Oxidoreductases / biosynthesis
  • [MeSH-minor] Bleomycin / pharmacology. Caspase 3. Caspases / metabolism. Cell Line. Cell Line, Tumor. Disease Progression. Fibroblasts / metabolism. Humans. In Situ Nick-End Labeling. Keratinocytes / metabolism. Models, Statistical. Polycyclic Hydrocarbons, Aromatic / metabolism. Prognosis. RNA Interference. Skin Neoplasms / drug therapy. Skin Neoplasms / enzymology. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. Ultraviolet Rays. Up-Regulation

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  • (PMID = 16361083.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Polycyclic Hydrocarbons, Aromatic; 0 / Tetrazolium Salts; 0 / Thiazoles; 11056-06-7 / Bleomycin; 298-93-1 / thiazolyl blue; EC 1.- / Oxidoreductases; EC 1.3.1.20 / trans-1,2-dihydrobenzene-1,2-diol dehydrogenase; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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16. Smith KJ, Germain M, Skelton H: Bowen's disease (squamous cell carcinoma in situ) in immunosuppressed patients treated with imiquimod 5% cream and a cox inhibitor, sulindac: potential applications for this combination of immunotherapy. Dermatol Surg; 2001 Feb;27(2):143-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bowen's disease (squamous cell carcinoma in situ) in immunosuppressed patients treated with imiquimod 5% cream and a cox inhibitor, sulindac: potential applications for this combination of immunotherapy.
  • OBJECTIVE: To determine if combination therapy using topical imiquimod cream 5% and the oral cyclooxygenase (COX) inhibitor are useful in the therapy of squamous cell carcinoma in situ (SCC in situ)/Bowen's disease in patients with long-standing CLL.
  • METHODS: Five CLL patients with head and neck cutaneous SCC in situ, which met criteria for Bowen's disease, were treated with topical 5% topical imiquimod cream and an oral COX inhibitor, sulindac 200 mg twice a day.
  • RESULTS: All patients showed clinical resolution and histologic clearing of the tumors after 16 weeks of therapy.
  • CONCLUSION: The local immune modulator, 5% imiquimod, in combination with a COX inhibitor, with its many potential antitumor effects may stimulate the innate and possibly the adaptive immune responses to clear these malignancies.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Bowen's Disease / drug therapy. Carcinoma in Situ / therapy. Cyclooxygenase Inhibitors / administration & dosage. Immunosuppression. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Neoplasms, Second Primary / drug therapy. Skin Neoplasms / drug therapy. Sulindac / administration & dosage
  • [MeSH-minor] Administration, Topical. Aged. Drug Therapy, Combination. Female. Humans. Immunotherapy. Male. Middle Aged. Ointments


17. Schön M, Bong AB, Drewniok C, Herz J, Geilen CC, Reifenberger J, Benninghoff B, Slade HB, Gollnick H, Schön MP: Tumor-selective induction of apoptosis and the small-molecule immune response modifier imiquimod. J Natl Cancer Inst; 2003 Aug 6;95(15):1138-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The incidence of nonmelanoma skin cancer, basal cell carcinomas (BCCs), and squamous cell carcinomas (SCCs) is increasing, representing a major medical and economic problem.
  • We examined the mechanism by which imiquimod induces apoptosis in cancer cells.
  • METHODS: Apoptosis was assessed by enzyme-linked immunosorbent assay, western blot analysis, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays in five SCC cell lines, HaCaT cells (a spontaneously immortalized human keratinocyte cell line), and normal keratinocytes treated with imiquimod, with its analog resiquimod, or with neither.
  • Differences between treated and untreated cells and tumors were determined using a two-tailed Student's t test.
  • RESULTS: Imiquimod, but not resiquimod, induced apoptosis in all SCC cell lines and HaCaT cells.
  • CONCLUSION: Imiquimod has the potential to induce apoptosis in skin cancer cells, possibly by circumventing mechanisms developed by malignant tumors to resist apoptotic signals.
  • [MeSH-major] Aminoquinolines / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / immunology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / immunology. Imidazoles / pharmacology. Immunologic Factors / pharmacology
  • [MeSH-minor] Blotting, Western. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / immunology. Caspase 3. Caspases / drug effects. Cytochrome c Group / drug effects. DNA Fragmentation / drug effects. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Gene Expression Regulation, Neoplastic / drug effects. Humans. In Situ Nick-End Labeling. Keratinocytes / drug effects. Keratinocytes / immunology. Proto-Oncogene Proteins c-bcl-2 / drug effects. Receptors, Tumor Necrosis Factor / drug effects. Tumor Cells, Cultured. Up-Regulation / drug effects

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  • (PMID = 12902443.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Cytochrome c Group; 0 / Imidazoles; 0 / Immunologic Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Tumor Necrosis Factor; 99011-02-6 / imiquimod; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; V3DMU7PVXF / resiquimod
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18. Ross AH, Kennedy CT, Collins C, Harrad RA: The use of imiquimod in the treatment of periocular tumours. Orbit; 2010 Apr;29(2):83-7
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  • [Title] The use of imiquimod in the treatment of periocular tumours.
  • PURPOSE: To review our experience with 5% topical Imiquimod in the treatment of periocular tumours.
  • Two patients were diagnosed with basal cell carcinoma of the eyelid, one patient with actinic keratosis, one with intraepidermal squamous cell carcinoma (Bowen's disease) and one patient had concomitant squamous cell carcinoma and intraepidermal squamous cell carcinoma.
  • RESULTS: All 5 patients, with various eyelid neoplastic/pre-neoplastic pathology, responded well with clinical resolution, to treatment with topical Imiquimod.
  • CONCLUSIONS: There is limited experience and published literature on the use of topical 5% Imiquimod in the treatment of periocular tumours.
  • In our experience, it is a safe and effective treatment for periocular lesions, including actinic keratosis, intraepidermal squamous cell carcinoma, basal cell carcinoma and squamous cell carcinoma.
  • To our knowledge, this is the first published description of the successful use of 5% Imiquimod in treating moderately differentiated squamous cell carcinoma of the eyelid.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Eyelid Neoplasms / drug therapy. Keratosis, Actinic / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Aged. Bowen's Disease / drug therapy. Bowen's Disease / pathology. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Female. Humans. Male. Middle Aged. Ophthalmic Solutions. Retrospective Studies. Treatment Outcome

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  • (PMID = 20394545.001).
  • [ISSN] 1744-5108
  • [Journal-full-title] Orbit (Amsterdam, Netherlands)
  • [ISO-abbreviation] Orbit
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Ophthalmic Solutions; 99011-02-6 / imiquimod
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19. Bukhari MH, Niazi S, Anwar M, Chaudhry NA, Naeem S: Prognostic significance of new immunohistochemistry scoring of p53 protein expression in cutaneous squamous cell carcinoma of mice. Ann N Y Acad Sci; 2008 Sep;1138:1-9
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  • [Title] Prognostic significance of new immunohistochemistry scoring of p53 protein expression in cutaneous squamous cell carcinoma of mice.
  • This study was conducted to investigate the prognostic value and therapeutic response of treatment modalities on p53 protein expression and AgNOR index in squamous cell carcinoma (SCC).
  • Sixty albino mice were given 7,12-dimethylbenz[a]anthracine (DMBA) and 12-O-tetradecanoly Phorbol-13-acetate (TPA) to produce skin tumors.
  • There was no decrease in the expression of both markers in mice harboring malignant neoplasms. p53 IHC scores were 0, I, and II in epidermal hyperplasia, papilloma, and dysplasia, respectively, while they were II, III, IV, and V in SCC in situ, well-differentiated, moderately differentiated, and poorly differentiated SCCs, respectively.
  • Alteration of p53 and AgNOR index occured during the development of SCC.
  • Both markers might be used as a supportive tool with routinely performed Hematoxylin and Eosin staining and may help in the diagnosis of SCC.
  • It will also help the oncologists to assess the prognosis and effectiveness of their chemotherapy.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Skin Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18837875.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Tumor Suppressor Protein p53; 0 / nucleolar organizer region associated proteins
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20. Reichrath J, Rafi L, Rech M, Mitschele T, Meineke V, Gärtner BC, Tilgen W, Holick MF: Analysis of the vitamin D system in cutaneous squamous cell carcinomas. J Cutan Pathol; 2004 Mar;31(3):224-31
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  • [Title] Analysis of the vitamin D system in cutaneous squamous cell carcinomas.
  • BACKGROUND: Increasing evidence points at an important function of vitamin D metabolites for growth regulation in various tissues, and new vitamin D analogs are interesting candidates for the treatment of malignancies, including squamous cell carcinomas (SCC).
  • METHODS: We have analyzed expression of vitamin D receptor (VDR), vitamin D-25-hydroxylase (25-OHase), 25-hydroxyvitamin D-1 alpha-hydroxylase (1 alpha-OHase), and 1,25-dihydroxyvitamin D-24-hydroxylase (24-OHase) in SCC.
  • RESULTS: Intensity of VDR immunoreactivity was increased in SCCs as compared to normal human skin.
  • VDR staining did not correlate with histological type or grading, nor with markers for proliferation, differentiation, or apoptotic cells.
  • Incubation of SCC cell lines (SCL-1, SCL-2) with calcitriol resulted in a dose-dependent suppression of cell proliferation (approximately up to 30%) in vitro, as measured by a tetrazolium salt (WST-1)-based colorimetric assay.
  • RNA levels for VDR, 25-OHase, 1 alpha-OHase, and 24-OHase were significantly elevated in SCCs as compared to HS, as measured by real-time polymerase chain reaction.
  • Additionally, SCCs represent potential targets for therapy with new vitamin D analogs that exert little calcemic side effects or for pharmacological modulation of calcitriol synthesis/metabolism in these tumors.
  • [MeSH-major] Calcitriol / physiology. Carcinoma, Squamous Cell / physiopathology. Receptors, Calcitriol / biosynthesis. Skin Neoplasms / physiopathology
  • [MeSH-minor] 25-Hydroxyvitamin D3 1-alpha-Hydroxylase / biosynthesis. Apoptosis / physiology. Cell Division / drug effects. Cell Line, Tumor. Cholestanetriol 26-Monooxygenase. Humans. Immunohistochemistry. In Situ Nick-End Labeling. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Steroid Hydroxylases / biosynthesis

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  • (PMID = 14984574.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Calcitriol; EC 1.14.- / 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.15 / CYP27A1 protein, human; EC 1.14.13.15 / Cholestanetriol 26-Monooxygenase; FXC9231JVH / Calcitriol
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21. Uckun FM, Dibirdik I, Qazi S: Prevention of UVB-induced skin inflammation, genotoxicity, and photocarcinogenesis in mice by WHI-P131, a dual-function inhibitor of Janus kinase 3 and EGF receptor kinase. Arzneimittelforschung; 2010;60(4):218-25
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  • [Title] Prevention of UVB-induced skin inflammation, genotoxicity, and photocarcinogenesis in mice by WHI-P131, a dual-function inhibitor of Janus kinase 3 and EGF receptor kinase.
  • The current study examined the chemopreventive potential of the dual-function JAK3/EGFR tyrosine kinase inhibitor WHI-P131 (CAS 202475-60-3) in photocarcinogenesis of non-melanoma skin cancer (NMSC).
  • Prophylactic WHI-P131 exhibited significant anti-inflammatory activity in the SKH-1 mouse model of sunburn and afforded significant protection against the inflammatory skin damage that results from UVB exposure.
  • UVB exposure (400 mJ/cm2) increased the mutation rate of the transgene target in UVB-exposed skin of BigBlue mice by a factor of 3.7 from 8.6 x 10(-5) to 31.7 x 10(-5) but this genotoxicity was almost completely prevented by topically administered prophylactic WHI-Pl31 (1.5 mg/cm2).
  • Chronic and repetitive exposure of vehicle-treated SKH-1 mice to 35 mJ/cm2 UVB, three times per week for 20 weeks resulted in appearance of a spectrum of lesions from actinic keratoses and squamous cell carcinoma (SCC) in situ to invasive SCC.
  • Both the number and size of the skin lesions progressively increased over time.
  • Notably, topical administration of WHI-P131 (1.0 mg/cm2) over the UVB target skin area on the dorsal surface 15 min before each UVB exposure significantly suppressed the photocarcinogenesis as documented by a 4-week delay in the onset of visible skin lesions, decreased total lesion volume per mouse (1.9 +/- 0.5 mm3 vs. 2.5 +/- 0.5 mm3/lesion at 20 weeks), and decreased number (1.6 +/- 0.4/mouse vs. 4.2 +/- 1.6/mouse at 20 weeks, P < 0.05) as well as smaller size of lesions and consequently a smaller total lesion volume ("skin cancer burden") (10.6 +/- 4.3 mm3 vs. 3.2 +/- 0.9 mm3 at 20 weeks, P < 0.05).
  • [MeSH-major] Antimutagenic Agents. Dermatitis / drug therapy. Janus Kinase 3 / antagonists & inhibitors. Neoplasms, Radiation-Induced / prevention & control. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Radiation Injuries, Experimental / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Skin Neoplasms / prevention & control. Ultraviolet Rays

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  • (PMID = 20486473.001).
  • [ISSN] 0004-4172
  • [Journal-full-title] Arzneimittel-Forschung
  • [ISO-abbreviation] Arzneimittelforschung
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimutagenic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / WHI P131; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / Janus Kinase 3
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22. Tschen EH, Wong DS, Pariser DM, Dunlap FE, Houlihan A, Ferdon MB, Phase IV ALA-PDT Actinic Keratosis Study Group: Photodynamic therapy using aminolaevulinic acid for patients with nonhyperkeratotic actinic keratoses of the face and scalp: phase IV multicentre clinical trial with 12-month follow up. Br J Dermatol; 2006 Dec;155(6):1262-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Photodynamic therapy using aminolaevulinic acid for patients with nonhyperkeratotic actinic keratoses of the face and scalp: phase IV multicentre clinical trial with 12-month follow up.
  • AKs are believed to progress to in situ squamous cell carcinoma (SCC) and potentially, to invasive SCC.
  • Given these facts, the treatment and management of AKs are integral components to quality dermatological health care.
  • OBJECTIVES: Topical aminolaevulinic acid-based photodynamic therapy (ALA-PDT) has been extensively studied over the last several years.
  • (iii) to characterize the histopathology of untreated clinically diagnosed AK lesions in the study population at baseline; and (iv) to evaluate ALA-PDT in darker skin types than previously studied.
  • Individual AK lesions designated for treatment were graded as either grade 1 (lesions slightly palpable and more easily felt than seen) or grade 2 (moderately thick AKs, easily seen and felt).
  • The target AK lesions in the per-protocol population clearing completely in the first and second months following a single ALA-PDT treatment (baseline) were 76% and 72%, respectively.
  • Sixty per cent of the patients received a second ALA-PDT treatment, limited to the target AKs still present at month 2.
  • The percentage of treated target lesions that cleared completely peaked at 86% at month 4 then decreased gradually over time to 78% at month 12.
  • With respect to the lesions biopsied, 91% (127/139) were diagnosed histopathologically as AK, with the balance of lesions being SCC (nine of 139: 7%), basal cell carcinoma (one of 139: 0.7%) and other non-AK diagnoses (two of 139: 1%).
  • Despite concentrated efforts to recruit patients with Fitzpatrick skin types IV-VI, the distribution was as follows: I, 11%; II, 36%; III, 41%; IV, 11%; V, 2%.
  • CONCLUSIONS: ALA-PDT was shown to be an effective and safe therapy for the treatment of AKs of the face and scalp in skin types I-V, with an acceptable rate of recurrence over 12 months of histologically confirmed AKs of 19%.
  • Phototoxicity reactions were all expected, nonserious and had essentially resolved after 1 month post-treatment independent of skin type.
  • [MeSH-major] Aminolevulinic Acid / therapeutic use. Facial Dermatoses / drug therapy. Keratosis / drug therapy. Photochemotherapy. Photosensitizing Agents / therapeutic use. Scalp Dermatoses / drug therapy

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  • (PMID = 17107399.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase IV; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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23. Smith KJ, Germain M, Skelton H: Squamous cell carcinoma in situ (Bowen's disease) in renal transplant patients treated with 5% imiquimod and 5% 5-fluorouracil therapy. Dermatol Surg; 2001 Jun;27(6):561-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Squamous cell carcinoma in situ (Bowen's disease) in renal transplant patients treated with 5% imiquimod and 5% 5-fluorouracil therapy.
  • BACKGROUND: Depending upon the patient's age at transplant, skin type, sun exposure, and the need for immunosuppressive therapy to prevent rejection, there is escalation in the development of cutaneous malignancies in organ transplant patients a number of years after transplantation.
  • OBJECTIVE: To determine if combined therapy with 5% 5-fluorouracil and 5% imiquimod may be useful in the treatment of squamous cell carcinoma in situ.
  • METHODS: We present five renal transplant patients, all more than 10 years posttransplantation, three with insulin-dependent diabetes, who developed multiple areas of squamous cell carcinoma (SCC) in situ.
  • All these patients were on chronic immunosuppressive chemotherapy to prevent rejection, but were otherwise doing well.
  • All the patients had biopsy-proven SCC in situ on their lower extremities that even in normal patients may be a challenge to treat.
  • RESULTS: We treated these five patients with a combination of a local immune therapy, imiquimod cream, and a topical chemotherapeutic agent, 5% 5-fluorouracil (5-FU), with clearing of the areas of SCC in situ.
  • In addition, there is evidence that cytokines induced by imiquimod may improve the therapeutic efficacy of topical 5% 5-FU in the treatment of SCC in situ.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Bowen's Disease / drug therapy. Fluorouracil / therapeutic use. Immunosuppressive Agents / therapeutic use. Kidney Transplantation. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Aged. Drug Administration Schedule. Drug Therapy, Combination. Female. Humans. Leg. Male. Middle Aged. Pilot Projects. Survivors. Treatment Outcome


24. Eklind J, Tartler U, Maschke J, Lidbrink P, Hengge UR: Imiquimod to treat different cancers of the epidermis. Dermatol Surg; 2003 Aug;29(8):890-6; discussion 896
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Topical immunomodulatory therapy with imiquimod has been recently used for the treatment of actinic keratoses, intraepithelial carcinoma, and small basal cell carcinoma (BCC) besides the licensed indication of extragenital warts (condyloma).
  • METHODS: We treated several patients with particular epidermal neoplasias such as squamous cell cancer (SCC) and basal cell cancer of sclerodermiform type three times per week for 4 to 12 weeks.
  • RESULTS: We report several novel aspects of the treatment of epidermal cancers with self-applied, nonpainful, immunomodulatory therapy.
  • First, we treated-for the first time-two immunosuppressed renal transplant patients for invasive SCC with imiquimod.
  • Interestingly, systemic immunosuppression did not adversely affect the response to therapy.
  • Second, one patient with the high-risk and aggressive growth pattern of basal cell cancer (sclerodermiform histology) was cured from his disease at a particular location in the face, suggesting sufficient penetration despite scarring.
  • Third, the treatment of actinic keratoses in the face is substantially shorter (in the order of 4 to 6 weeks) as opposed to other skin cancers.
  • Immunomodulatory treatment with imiquimod led to the demarcation of in situ actinic keratosis lesions that could not be identified using the dermatologist's experience, probably because of the existence of exclusive alterations on the molecular level.
  • CONCLUSION: Several novel aspects of immunomodulatory treatment with imiquimod and new indications such as selected cases of sclerodermiform BCC and SCC have been described.
  • The texture of the skin at various different body locations may explain the varying sensitivities to imiquimod when facial skin is compared with skin on the extremities.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Aminoquinolines / therapeutic use. Keratosis / drug therapy. Neoplasms, Basal Cell / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 12859398.001).
  • [ISSN] 1076-0512
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 99011-02-6 / imiquimod
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25. Pini AM, Koch S, Schärer L, French LE, Läuchli S, Hofbauer GF: Eruptive keratoacanthoma following topical imiquimod for in situ squamous cell carcinoma of the skin in a renal transplant recipient. J Am Acad Dermatol; 2008 Nov;59(5 Suppl):S116-7
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eruptive keratoacanthoma following topical imiquimod for in situ squamous cell carcinoma of the skin in a renal transplant recipient.
  • [MeSH-major] Aminoquinolines / adverse effects. Carcinoma, Squamous Cell / drug therapy. Keratoacanthoma / chemically induced. Kidney Transplantation. Skin Neoplasms / drug therapy
  • [MeSH-minor] Aged, 80 and over. Bowen's Disease / drug therapy. Female. Humans. Keratosis, Actinic / drug therapy






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