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1. Jadotte YT, Sarkissian NA, Kadire H, Lambert WC: CASE REPORT Superficial Spreading Basal Cell Carcinoma of the Face: A Surgical Challenge. Eplasty; 2010;10:e46

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CASE REPORT Superficial Spreading Basal Cell Carcinoma of the Face: A Surgical Challenge.
  • OBJECTIVE: We present the case of a white man with a facial nodule suspicious for basal cell carcinoma.
  • METHODS: Biopsy revealed clusters of basaloid tumor cells with peripheral palisading, consistent with a superficial spreading variant of basal cell carcinoma.
  • RESULTS: The patient was treated with Mohs micrographic surgery, with clear margins achieved after the second stage of excision.
  • However, since it was a superficial spreading basal cell carcinoma, this was followed by topical imiquimod treatment.
  • CONCLUSION: Topical chemotherapy with imiquimod or 5-fluorouracil may be valuable alternatives or adjuncts, given the increased likelihood of recurrence after surgical excision of superficial spreading basal cell carcinoma.
  • Mohs surgery is of limited value in the management of superficial spreading basal cell carcinoma because it characteristically shows areas of uninvolved skin between tumor nests.

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  • (PMID = 20596236.001).
  • [ISSN] 1937-5719
  • [Journal-full-title] Eplasty
  • [ISO-abbreviation] Eplasty
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2890390
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2. Seidl H, Kreimer-Erlacher H, Bäck B, Soyer HP, Höfler G, Kerl H, Wolf P: Ultraviolet exposure as the main initiator of p53 mutations in basal cell carcinomas from psoralen and ultraviolet A-treated patients with psoriasis. J Invest Dermatol; 2001 Aug;117(2):365-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultraviolet exposure as the main initiator of p53 mutations in basal cell carcinomas from psoralen and ultraviolet A-treated patients with psoriasis.
  • Basal cell carcinoma, the most frequent skin cancer in humans, is often linked to chronic sun exposure.
  • In psoralen and ultraviolet A-treated psoriatic patients, basal cell carcinomas may occur even more frequently; however, the exact etiology and mechanisms of tumorigenesis in psoriatic patients are unclear because psoralen and ultraviolet A is not only a carcinogen but also an immunosuppressor and because psoralen and ultraviolet A-treated psoriatic patients often have other (co)carcinogenic risk factors (e.g, therapeutic exposure to ultraviolet B, X-ray radiation, arsenic, tar, and/or chemotherapeutic agents such as methotrexate).
  • In this study, we analyzed the DNA of 13 basal cell carcinomas from five psoralen and ultraviolet A-treated psoriatic patients for mutations of the p53 tumor suppressor gene.
  • DNA sequencing revealed a total of 11 mis-sense, two non-sense, and four silent mutations in seven of the 13 basal cell carcinomas (54%).
  • Of the 13 total mis-sense or non-sense mutations, 12 (92%) occurred at dipyrimidine sites and nine (69%) were of the ultraviolet fingerprint type (eight C-->T transitions and one CC-->TT transition).
  • Thus, whether these mutations were induced by ultraviolet or psoralen and ultraviolet A was not clear.
  • In addition, two other mutations (15%) occurred at 5'-TpG sites, one (8%) occurred at a 5'-TpA site (the most frequent site of psoralen binding and mutagenesis in cell and murine studies), and one (8%) involved a G-->T transversion.
  • These results suggest that (i) the major initiator of p53 mutations in basal cell carcinoma in psoralen and ultraviolet A-treated psoriasis patients is environmental and/or therapeutic ultraviolet(B) exposure, and that (ii) psoralen and ultraviolet A itself causes only a smaller portion of p53 mutations in psoralen and ultraviolet A-associated basal cell carcinomas.
  • [MeSH-major] Carcinoma, Basal Cell / genetics. PUVA Therapy / adverse effects. Psoriasis / drug therapy. Skin Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics. Ultraviolet Rays / adverse effects
  • [MeSH-minor] Adult. Aged. Female. Ficusin / adverse effects. Humans. Incidence. Male. Middle Aged. Photosensitizing Agents / adverse effects. Point Mutation / drug effects. Point Mutation / radiation effects. Polymorphism, Single-Stranded Conformational

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  • [ErratumIn] J Invest Dermatol 2001 Dec;117(6):1688
  • (PMID = 11511317.001).
  • [ISSN] 0022-202X
  • [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 / Photosensitizing Agents; 0 / Tumor Suppressor Protein p53; KTZ7ZCN2EX / Ficusin
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3. Herschkowitz JI, He X, Fan C, Perou CM: The functional loss of the retinoblastoma tumour suppressor is a common event in basal-like and luminal B breast carcinomas. Breast Cancer Res; 2008;10(5):R75
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  • [Title] The functional loss of the retinoblastoma tumour suppressor is a common event in basal-like and luminal B breast carcinomas.
  • One of these groups, the basal-like subtype, is poorly differentiated, highly metastatic, genomically unstable, and contains specific genetic alterations such as the loss of tumour protein 53 (TP53).
  • The loss of the retinoblastoma tumour suppressor encoded by the RB1 locus is a well-characterised occurrence in many tumour types; however, its role in breast cancer is less clear with many reports demonstrating a loss of heterozygosity that does not correlate with a loss of RB1 protein expression.
  • METHODS: We used gene expression analysis for tumour subtyping and polymorphic markers located at the RB1 locus to assess the frequency of loss of heterozygosity in 88 primary human breast carcinomas and their normal tissue genomic DNA samples.
  • RESULTS: RB1 loss of heterozygosity was observed at an overall frequency of 39%, with a high frequency in basal-like (72%) and luminal B (62%) tumours.
  • These tumours also concurrently showed low expression of RB1 mRNA. p16INK4a was highly expressed in basal-like tumours, presumably due to a previously reported feedback loop caused by RB1 loss.
  • An RB1 loss of heterozygosity signature was developed and shown to be highly prognostic, and was potentially a predictive marker of response to neoadjuvant chemotherapy.
  • CONCLUSIONS: These results suggest that the functional loss of RB1 is common in basal-like tumours, which may play a key role in dictating their aggressive biology and unique therapeutic responses.

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  • (PMID = 18782450.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058223; United States / NCI NIH HHS / CA / R01 CA101227
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1
  • [Other-IDs] NLM/ PMC2614508
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4. Wong NA, Brett L, Stewart M, Leitch A, Longley DB, Dunlop MG, Johnston PG, Lessells AM, Jodrell DI: Nuclear thymidylate synthase expression, p53 expression and 5FU response in colorectal carcinoma. Br J Cancer; 2001 Dec 14;85(12):1937-43
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  • [Title] Nuclear thymidylate synthase expression, p53 expression and 5FU response in colorectal carcinoma.
  • Nuclear expression of TS in human tissue in vivo has not been characterised and its clinicopathological correlates in malignancy are unknown.
  • 52 cases of primary colorectal carcinoma (CRC) and 24 cases of matched metastatic carcinoma were studied immunohistochemically using the monoclonal antibody TS106.
  • Strong nuclear immunostaining was seen in normal basal crypt colonocytes and germinal centre cells, and in a varying proportion of adenocarcinoma cells.
  • Higher TS nuclear expression also showed a significant association with poorer response to protracted venous infusional 5FU therapy.
  • There was no clear association between TS nuclear expression and Ki67 or p53 expression assessed immunohistochemically.
  • There was a strong positive correlation between TS nuclear expression in primary and metastatic CRC but the latter generally showed higher expression than matched primary tumour tissue.
  • [MeSH-major] Adenocarcinoma / genetics. Antimetabolites, Antineoplastic / therapeutic use. Cell Nucleus / enzymology. Colorectal Neoplasms / genetics. Enzyme Inhibitors / therapeutic use. Fluorouracil / therapeutic use. Neoplasm Proteins / biosynthesis. Thymidylate Synthase / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Drug Resistance, Neoplasm / genetics. Enzyme Induction. Female. Gene Expression Profiling. Genes, p53. Humans. Ki-67 Antigen / biosynthesis. Ki-67 Antigen / genetics. Male. Middle Aged. Neoplasm Metastasis. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Reproducibility of Results. Survival Analysis. Treatment Outcome

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  • (PMID = 11747337.001).
  • [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] Scotland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Suppressor Protein p53; EC 2.1.1.45 / Thymidylate Synthase; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2364004
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5. Palayoor ST, Burgos MA, Shoaibi A, Tofilon PJ, Coleman CN: Effect of radiation and ibuprofen on normoxic renal carcinoma cells overexpressing hypoxia-inducible factors by loss of von Hippel-Lindau tumor suppressor gene function. Clin Cancer Res; 2004 Jun 15;10(12 Pt 1):4158-64
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  • [Title] Effect of radiation and ibuprofen on normoxic renal carcinoma cells overexpressing hypoxia-inducible factors by loss of von Hippel-Lindau tumor suppressor gene function.
  • PURPOSE: Tumor hypoxia is a major limiting factor for radiation therapy.
  • Hypoxia-inducible factors (HIFs) are overexpressed in several human cancers and are considered prognostic markers and potential targets for cancer therapy.
  • EXPERIMENTAL DESIGN: Renal clear cell carcinoma (RCC) cell lines overexpressing HIFs under normoxic conditions because of inactivation of von Hippel-Lindau tumor suppressor gene function (VHL-ve) and their matched pairs in which overexpression of HIFs was abolished by expression of functional VHL (VHL+ve) were irradiated.
  • The effect of ibuprofen on radiosensitization and HIF and VHL proteins was compared in RCC matched-pair cell lines.
  • RESULTS: The data showed only small differences in the radiosensitivity between the cells overexpressing HIFs and cells with basal HIF levels.
  • Ibuprofen inhibited HIFs in VHL+ve cells expressing basal levels of HIFs.
  • [MeSH-major] Carcinoma / drug therapy. Carcinoma / radiotherapy. Ibuprofen / pharmacology. Kidney Neoplasms / drug therapy. Kidney Neoplasms / radiotherapy. Trans-Activators / physiology. Transcription Factors / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Basic Helix-Loop-Helix Transcription Factors. Blotting, Western. Cell Line. Cell Survival. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Enzyme-Linked Immunosorbent Assay. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Immunoblotting. Mutation. Oxygen / metabolism. Prognosis. Radiation Tolerance. Time Factors. Transfection. Up-Regulation. Vascular Endothelial Growth Factor A / metabolism. Von Hippel-Lindau Tumor Suppressor Protein

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  • (PMID = 15217953.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / endothelial PAS domain-containing protein 1; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein; S88TT14065 / Oxygen; WK2XYI10QM / Ibuprofen
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6. Watson S, Serrate C, Vignot S: [Sonic Hedgehog signaling pathway: from embryology to molecular targeted therapies]. Bull Cancer; 2010 Dec;97(12):1477-83
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  • [Title] [Sonic Hedgehog signaling pathway: from embryology to molecular targeted therapies].
  • During the past few years its implication in carcinogenesis has become clear and today it is acknowledged that this pathway plays a role in the malignant transformation of multiple cell types, either owing to the mutation of some of its components or to its erratic activation.
  • New molecular targeted therapies that inhibit the pathway have shown their unquestionable efficiency in several tumours -among which basal cell carcinoma, medulloblastoma, or pancreatic adenocarcinoma.
  • The assessment of these inhibitors in other types of tumours is currently underway with promising results, suggesting that the Sonic hedgehog signalling pathway may become one of the therapeutic targets of the future.
  • [MeSH-major] Embryonic Development / physiology. Hedgehog Proteins / antagonists & inhibitors. Hedgehog Proteins / physiology. Molecular Targeted Therapy / methods. Neoplasms / drug therapy. Neoplasms / genetics
  • [MeSH-minor] Anilides / therapeutic use. Animals. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / genetics. Cerebellar Neoplasms / genetics. Embryonic Induction / physiology. Humans. Lung Neoplasms / genetics. Medulloblastoma / genetics. Mutation / physiology. Neoplastic Stem Cells / physiology. Pancreatic Neoplasms / genetics. Patient Selection. Pyridines / therapeutic use. Receptors, Cell Surface / physiology. Signal Transduction / drug effects. Signal Transduction / physiology. Skin Neoplasms / drug therapy. Skin Neoplasms / genetics. Small Cell Lung Carcinoma / genetics

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  • (PMID = 21220225.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anilides; 0 / Hedgehog Proteins; 0 / HhAntag691; 0 / Pyridines; 0 / Receptors, Cell Surface; 0 / patched receptors
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7. Prignano F, Lotti T, Spallanzani A, Berti S, de Giorgi V, Moretti S: Sequential effects of photodynamic treatment of basal cell carcinoma. J Cutan Pathol; 2009 Apr;36(4):409-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sequential effects of photodynamic treatment of basal cell carcinoma.
  • BACKGROUND: Photodynamic therapy (PDT) of superficial basal cell carcinoma (SBCC) acts as a biological response modifier or killing target cells, but sequential biological effects have not been reported in depth in humans.
  • At baseline, SBCC cells expressed stem cell factor in all cases, and granulocyte-monocyte colony-stimulating factor, basic fibroblastic growth factor, interleukin (IL)-8 and vascular endothelial growth factor in most cases.
  • CONCLUSIONS: We show a clear time-dependent profile of apoptotic markers and inflammatory infiltrate composition in SBCC after ALA-PDT.
  • [MeSH-major] Aminolevulinic Acid / therapeutic use. Carcinoma, Basal Cell / drug therapy. Photosensitizing Agents / therapeutic use. Skin Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Cytokines / drug effects. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inflammation / chemically induced. Inflammation / immunology. Inflammation / pathology. Microscopy, Electron, Transmission. Photochemotherapy

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  • (PMID = 19278425.001).
  • [ISSN] 1600-0560
  • [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 / Cytokines; 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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8. Thompson MS, Andersson-Engels S, Svanberg S, Johansson T, Palsson S, Bendsoe N, Derjabo A, Kapostins J, Stenram U, Spigulis J, Svanberg K: Photodynamic therapy of nodular basal cell carcinoma with multifiber contact light delivery. J Environ Pathol Toxicol Oncol; 2006;25(1-2):411-24
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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 of nodular basal cell carcinoma with multifiber contact light delivery.
  • To overcome the limited treatment depth of superficial photodynamic therapy we investigate interstitial light delivery.
  • In the present work the treatment light was delivered using a system in which three or six clear-cut fibers were placed in direct contact with the tumor area.
  • Twelve nodular basal cell carcinomas were treated employing delta-aminolevulinic acid and 635 nm laser irradiation.
  • The treatment efficacy, judged at a 28-month follow-up, showed a 100% complete response.
  • The outcome of the treatments was comparable to superficial photodynamic therapy in terms of histological, clinical, and cosmetic results.
  • [MeSH-major] Carcinoma, Basal Cell / drug therapy. Lasers. Photochemotherapy / methods. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aminolevulinic Acid / therapeutic use. Female. Fluorescence. Humans. Male. Middle Aged. Photosensitizing Agents / therapeutic use. Protoporphyrins / metabolism

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  • (PMID = 16566732.001).
  • [ISSN] 0731-8898
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Protoporphyrins; 553-12-8 / protoporphyrin IX; 88755TAZ87 / Aminolevulinic Acid
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9. Huber A, Huber JD, Skinner RB Jr, Kuwahara RT, Haque R, Amonette RA: Topical imiquimod treatment for nodular basal cell carcinomas: an open-label series. Dermatol Surg; 2004 Mar;30(3):429-30
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topical imiquimod treatment for nodular basal cell carcinomas: an open-label series.
  • BACKGROUND: Imiquimod has been used for basal cell carcinomas (BCCs).
  • This is the first open-label series using imiquimod for nodular BCC with Mohs surgery resection for confirmation of treatment.
  • RESULTS: After 12 weeks for three times a week application, treatment sites at week 15 were surgically excised using Mohs micrographic surgery.
  • All 15 treatment subjects were clear of BCC.
  • CONCLUSION: Imiquimod 5% cream may be another treatment modality for nodular BCC.
  • [MeSH-major] Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Carcinoma, Basal Cell / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 15008876.001).
  • [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] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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10. Torres A, Niemeyer A, Berkes B, Marra D, Schanbacher C, González S, Owens M, Morgan B: 5% imiquimod cream and reflectance-mode confocal microscopy as adjunct modalities to Mohs micrographic surgery for treatment of basal cell carcinoma. Dermatol Surg; 2004 Dec;30(12 Pt 1):1462-9
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 5% imiquimod cream and reflectance-mode confocal microscopy as adjunct modalities to Mohs micrographic surgery for treatment of basal cell carcinoma.
  • BACKGROUND: Imiquimod is an immune response modifier that up-regulates cytokines and has been shown in clinical studies to reduce or clear basal cell carcinoma tumors when applied topically.
  • OBJECTIVE: The objectives were to evaluate the efficacy of 5% imiquimod cream in treating basal cell carcinoma preceding excision by Mohs micrographic surgery and to determine if reflectance-mode confocal microscopy is useful to establish the need for surgical intervention after imiquimod treatment.
  • METHODS: Subjects applied study cream to one biopsy-confirmed basal cell carcinoma tumor 5 x/week for 2, 4, or 6 weeks in this vehicle-controlled, double-blind study.
  • Confocal microscopy was used for the 6-week treatment group to examine the target tumor area at each interval visit and immediately before Mohs micrographic surgery.
  • After the Mohs micrographic surgery excision, the tissue was evaluated histologically, and the excision area was measured.
  • CONCLUSION: Imiquimod improved excision results relative to vehicle when used for treating basal cell carcinoma before Mohs micrographic surgery.
  • Confocal microscopy assessments correlated well with tumor response to therapy, suggesting that confocal microscopy may help determine the need for surgery.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / surgery. Skin Neoplasms / drug therapy. Skin Neoplasms / surgery
  • [MeSH-minor] Administration, Cutaneous. Aged. Boston. California. Chemotherapy, Adjuvant. Combined Modality Therapy. Double-Blind Method. Female. Hospitals, University. Humans. Male. Microscopy, Confocal. Middle Aged. Mohs Surgery / instrumentation. Mohs Surgery / methods. Predictive Value of Tests. Treatment Outcome

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  • (PMID = 15606733.001).
  • [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] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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11. Wu JK, Siller G, Whitehead K: Treatment of Bowen's disease and basal cell carcinoma of the nose with imiquimod 5% cream. Australas J Dermatol; 2003 May;44(2):123-5
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  • [Title] Treatment of Bowen's disease and basal cell carcinoma of the nose with imiquimod 5% cream.
  • Treatment was applied on a once-a-day regimen, and a total of 32 applications over 9 weeks were used.
  • A florid local skin reaction occurred early in the treatment, necessitating a rest period and decreasing the frequency of application.
  • The Bowen's disease was coexistent with a multifocal superficial basal cell carcinoma (BCC) that had a partial response.
  • Persistent BCC at 4 weeks post treatment was surgically excised.
  • The Bowen's disease remains clinically clear at 12-months follow up.
  • [MeSH-major] Aminoquinolines / administration & dosage. Bowen's Disease / drug therapy. Carcinoma, Basal Cell / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Biopsy, Needle. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Immunohistochemistry. Middle Aged. Treatment Outcome

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  • (PMID = 12752186.001).
  • [ISSN] 0004-8380
  • [Journal-full-title] The Australasian journal of dermatology
  • [ISO-abbreviation] Australas. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Aminoquinolines; 99011-02-6 / imiquimod
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12. Barnetson RS, Satchell A, Zhuang L, Slade HB, Halliday GM: Imiquimod induced regression of clinically diagnosed superficial basal cell carcinoma is associated with early infiltration by CD4 T cells and dendritic cells. Clin Exp Dermatol; 2004 Nov;29(6):639-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imiquimod induced regression of clinically diagnosed superficial basal cell carcinoma is associated with early infiltration by CD4 T cells and dendritic cells.
  • Imiquimod is presumed to clear basal cell carcinoma (BCC) through apoptosis mediated by cytokines and lymphocytes, with erosion often observed correlating with complete clearance.
  • The objective was to determine the cellular immune response early in the course of treatment in order to examine whether cell mediated immunity could be responsible for imiquimod mediated regression of BCC.
  • Sixteen adults with clinically diagnosed BCC were openly assigned to 5 days per week of drug (1, 2 or 4 weeks) or placebo (2 weeks) in groups of four.
  • Post-treatment excision specimens were examined by routine and immunohistochemical staining.
  • Treatment was associated with the early appearance of CD4 cells, activated dendritic cells and macrophages, with later infiltration by CD8 T cells.
  • Dendritic cells continually increased with time, while macrophages reached a maximum at 1 week and then declined slightly.
  • The results are consistent with a cell mediated immune response being responsible for the clearance of the BCC.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Lymphocytes, Tumor-Infiltrating / drug effects. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. CD4-Positive T-Lymphocytes / drug effects. Dendritic Cells / drug effects. Humans. Treatment Outcome

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  • (PMID = 15550144.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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13. Schiessl C, Wolber C, Tauber M, Offner F, Strohal R: Treatment of all basal cell carcinoma variants including large and high-risk lesions with 5% imiquimod cream: histological and clinical changes, outcome, and follow-up. J Drugs Dermatol; 2007 May;6(5):507-13
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 all basal cell carcinoma variants including large and high-risk lesions with 5% imiquimod cream: histological and clinical changes, outcome, and follow-up.
  • Forty-one patients with 47 basal cell carcinomas (BCCs; 15 superficial, 26 nodular, and 6 sclerodermiform) were treated with 5% imiquimod cream once daily 5 times a week for 6 weeks in an open-label clinical trial.
  • Local side effects occurred in 68% of the patients as mild to moderate reactions with a clear association to the histological BCC subtype.
  • Overall, imiquimod represents a safe and effective treatment option for a selected cohort of BCC patients.
  • Notably, by the second week of treatment 72.7% of BCC biopsies were histologically tumor-free, which correlated with a substantial decrease of the inflammatory infiltrate by up to 58% between weeks 3 to 6.
  • This early imiquimod response might have important implications for the final definition of potentially shorter imiquimod treatment periods.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Neoplasm Recurrence, Local. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 17679185.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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14. Ezughah FI, Affleck AG, Evans A, Ibbotson SH, Fleming CJ: Confirmation of histological clearance of superficial basal cell carcinoma with multiple serial sectioning and Mohs' micrographic surgery following treatment with imiquimod 5% cream. J Dermatolog Treat; 2008;19(3):156-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Confirmation of histological clearance of superficial basal cell carcinoma with multiple serial sectioning and Mohs' micrographic surgery following treatment with imiquimod 5% cream.
  • BACKGROUND: Although the effectiveness of daily dosing regimens of 5% imiquimod cream for the treatment of superficial basal cell carcinomas (sBCC) has been documented by recent studies, concerns about long-term outcome remain.
  • OBJECTIVE: To assess the efficacy of 5% imiquimod cream for sBCC using detailed histological assessment 1 year after completion of treatment.
  • METHODS: Nine individuals with biopsy-proven sBCC treated with 5% imiquimod cream 1 year previously and who remained clinically clear were recruited.
  • RESULTS: Eight of nine individuals, 89% (95% CI 56% to 97%) were histologically clear of sBCC at 52 weeks.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Neoplasm Recurrence, Local / pathology. Skin / pathology. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Aged. Aged, 80 and over. Female. Follow-Up Studies. Histocytological Preparation Techniques. Humans. Male. Middle Aged. Mohs Surgery. Treatment Outcome

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  • (PMID = 18569271.001).
  • [ISSN] 1471-1753
  • [Journal-full-title] The Journal of dermatological treatment
  • [ISO-abbreviation] J Dermatolog Treat
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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15. Quirk C, Gebauer K, Owens M, Stampone P: Two-year interim results from a 5-year study evaluating clinical recurrence of superficial basal cell carcinoma after treatment with imiquimod 5% cream daily for 6 weeks. Australas J Dermatol; 2006 Nov;47(4):258-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two-year interim results from a 5-year study evaluating clinical recurrence of superficial basal cell carcinoma after treatment with imiquimod 5% cream daily for 6 weeks.
  • Imiquimod 5% cream is approved in the USA, Europe and Australia to treat superficial basal cell carcinoma, using a regimen of once daily, 5 times per week for 6 weeks.
  • Vehicle-controlled, phase III clinical trials show that imiquimod is safe and effective for treating superficial basal cell carcinoma with dosing 5 or 7 times per week for 6 weeks.
  • This phase III, open-label study evaluates the long-term (5 years) clinical efficacy and safety of dosing once daily, for which this manuscript reports the 2-year time point in the follow-up period.
  • For the 169 enrolled subjects, the tumour selected for treatment was assessed clinically to determine initial clearance at the 12-week post-treatment visit.
  • If clinically clear of superficial basal cell carcinoma, subjects entered a 5-year, long-term follow-up period.
  • The initial clearance rate at 12 weeks post treatment was 94.1%.
  • The proportion of subjects who were clinically clear at the 2-year follow-up visit was estimated to be 82.0%.
  • The recurrence rate observed suggests that once daily dosing and 5x/week dosing yield similar clearance rates, but daily dosing increases local skin reactions.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Neoplasm Recurrence, Local / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Adult. Aged. Aged, 80 and over. Australia. Drug Administration Schedule. Female. Humans. Male. Middle Aged. New Zealand. Severity of Illness Index. Treatment Outcome


16. Gollnick H, Barona CG, Frank RG, Ruzicka T, Megahed M, Tebbs V, Owens M, Stampone P: Recurrence rate of superficial basal cell carcinoma following successful treatment with imiquimod 5% cream: interim 2-year results from an ongoing 5-year follow-up study in Europe. Eur J Dermatol; 2005 Sep-Oct;15(5):374-81
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrence rate of superficial basal cell carcinoma following successful treatment with imiquimod 5% cream: interim 2-year results from an ongoing 5-year follow-up study in Europe.
  • Imiquimod is an immune response modifier that acts through Toll-like receptor 7 to induce innate and cell-mediated immune responses.
  • This ongoing phase III, open-label study conducted in Europe is evaluating the long-term (5 year) clinical efficacy and safety of imiquimod 5% cream applied once daily 5 times per week (5 x/week) for 6 weeks for the treatment of superficial basal cell carcinoma (sBCC).
  • The initial sBCC clearance rate was 90% (12-week post treatment), whereas the proportion of subjects who were clinically clear at 2 years (current time point) was estimated to be 79.4%.
  • Local skin/application site reactions were the most frequently reported safety findings.
  • Initial efficacy rates of imiquimod applied 5 x/week for 6 weeks demonstrate its clinical utility as an alternative approach to the treatment of sBCC.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Carcinoma, Basal Cell / drug therapy. Neoplasm Recurrence, Local. Skin Neoplasms / drug therapy

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  • (PMID = 16172048.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Ointments; 99011-02-6 / imiquimod
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17. Quirk C, Gebauer K, De'Ambrosis B, Slade HB, Meng TC: Sustained clearance of superficial basal cell carcinomas treated with imiquimod cream 5%: results of a prospective 5-year study. Cutis; 2010 Jun;85(6):318-24
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sustained clearance of superficial basal cell carcinomas treated with imiquimod cream 5%: results of a prospective 5-year study.
  • We conducted a prospective, multicenter, phase 3, open-label study to assess long-term sustained clearance of superficial basal cell carcinomas (sBCCs) treated with imiquimod cream 5%.
  • A biopsy-confirmed tumor (area > or = 0.5 cm2 and diameter < or = 2.0 cm) was treated once daily 7 times per week for 6 weeks.
  • Tumor recurrence, serious adverse events (AEs), local skin reactions (LSRs), and skin quality assessments (SQAs) were measured.
  • Estimated sustained clearance (proportion of participants who achieved initial clearance at the 12-week posttreatment visit and remained clinically clear at each time point during the long-term follow-up period; N=157) was 85.4% at 60 months (life-table method: 95% confidence interval [CI], 79.3%-91.6%).
  • The overall estimate of treatment success was 80.4% at 60 months (N=169; 95% CI, 74.4%-86.4%).
  • Local skin reactions and application site reactions, the AEs reported by the most participants, occurred predominantly during the treatment period and resolved posttreatment.
  • Compared to baseline, investigator-assessed SQA scores for the target tumor site improved for skin surface abnormalities and hyperpigmentation, and worsened for hypopigmentation.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Follow-Up Studies. Humans. Neoplasm Recurrence, Local. Prospective Studies. Treatment Outcome

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  • (PMID = 20666194.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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18. Ljuca D, Fatusić Z, Iljazović E, Ahmetović B: Monitoring of chemotherapy successfulness of platina/taxol chemotherapy protocol by using determination of serum urokinase plasminogen activator (uPA) and soluble urokinase plasminogen activator receptor (suPAR) in patients with ovarian carcinoma FIGO II and III stage. Bosn J Basic Med Sci; 2007 May;7(2):111-6
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  • [Title] Monitoring of chemotherapy successfulness of platina/taxol chemotherapy protocol by using determination of serum urokinase plasminogen activator (uPA) and soluble urokinase plasminogen activator receptor (suPAR) in patients with ovarian carcinoma FIGO II and III stage.
  • In about 70% of cases, ovarian carcinoma has been diagnosed at an advanced stage.
  • Invasion and metastasis of solid tumors request protease activity resulting in basal membrane destruction and surrounding matrix.
  • In that process, urokinase plasminogen activator (uPA) and its receptor, urokinase plasminogen activator receptor (suPAR) play a key role, that via plasmin activation lead to basal membrane and matrix degradation in surrounding of the tumor, enable to its invasion and metastasis.
  • Their serum concentrations in ovarian cancer patients may help in good monitoring of remission or progression during chemotherapy treatment.
  • In late 1950s and ear1y 1960s, when it was found out that malignant ovarian tumors were chemosensitive, their chemotherapy treatment has begun.
  • In the beginning it was used only mono-therapy, and by discovering new cytostatics it was replaced by poly-chemotherapy.
  • Now days, in the therapy of advanced stages of ovarian carcinoma combination of cisplatine or carboplatine with paclitaxel is considering as standard treatment.
  • Aim of this study was to determine serum uPA, suPAR and CEA in FIGO II and III patients with different histological type (serous, mucinous, clear cell tumor) before and after PT chemotherapy protocol during following three cycles.
  • In this prospective study we have analyzed 17 patients with ovarian carcinoma, those have been after surgery treated by chemotherapy.
  • Results of this study have shown that uPA, suPAR and CEA met criteria for prognostic markers for monitoring of successfulness of platina/taxol chemotherapy protocol for serous, mucinous and clear cell tumor FIGO II and III stage of ovarian carcinoma.
  • In case of PT chemotherapy protocol suPAR was better prognostic marker for monitoring of chemotherapy successfulness (Pearson coefficient 0,9 do 1,0; p<0,00l) than uPA (Pearson coefficient between 0,86 and 0,92; p<0,02) and CEA (Pearson coefficient 0,5 do 0,89; p<0,04).

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  • (PMID = 17489744.001).
  • [ISSN] 1512-8601
  • [Journal-full-title] Bosnian journal of basic medical sciences
  • [ISO-abbreviation] Bosn J Basic Med Sci
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
  • [Chemical-registry-number] 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; BG3F62OND5 / Carboplatin; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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19. Gao Y, Lin LP, Zhu CH, Chen Y, Hou YT, Ding J: Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma. Cancer Biol Ther; 2006 Aug;5(8):978-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma.
  • In this study, we reveal that C75 is a cell cycle arrest inducer and explore the potential mechanisms for this effect in hepatocellular carcinoma (HCC) cell lines with abundant FAS expression: HepG2 and SMMC7721 cells with wt-p53, and Hep3B cells with null p53.
  • The results showed FAS protein expression and basal activity levels were higher in HepG2 cells than in the other two HCC cell lines.
  • Treatment with C75 inhibited FAS activity within 30 min of administration and induced G(2) phase arrest accompanied by p53 overexpression in HepG2 and SMMC7721 cells.
  • However, we observed a clear correlation between p38 MAPK activation triggered by C75 and the induction of cell cycle arrest in all three HCC cells.
  • Furthermore, treatment with the p38 MAPK inhibitor SB203580 reduced p38 MAPK activity and cell cycle arrest, and also partially restored cyclin A, cyclin B1, cyclin D1 and p21 protein levels.
  • Collectively, it was p38 MAPK but not p53 involved in C75-mediated tumor cell growth arrest in HCC cells.
  • [MeSH-major] 4-Butyrolactone / analogs & derivatives. Carcinoma, Hepatocellular / metabolism. Fatty Acid Synthases / antagonists & inhibitors. G2 Phase / drug effects. Liver Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Antigens, CD95 / metabolism. Blotting, Western. Cell Proliferation. Cyclin A / metabolism. Cyclin B / metabolism. Cyclin B1. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Flow Cytometry. Humans. Immunoprecipitation. Plasmids / genetics. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured

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  • [CommentIn] Cancer Biol Ther. 2006 Aug;5(8):986-7 [16998303.001]
  • (PMID = 16855382.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methylene-2-octyl-5-oxofuran-3-carboxylic acid; 0 / Antigens, CD95; 0 / CCNB1 protein, human; 0 / Cyclin A; 0 / Cyclin B; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; EC 2.3.1.85 / Fatty Acid Synthases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; OL659KIY4X / 4-Butyrolactone
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20. Shore RE: Radiation-induced skin cancer in humans. Med Pediatr Oncol; 2001 May;36(5):549-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiation-induced skin cancer in humans.
  • The principal epidemiologic studies of ionizing radiation and skin cancer have all shown that radiation causes basal cell carcinoma but have not found dose-related excesses of squamous cell carcinoma or malignant melanoma.
  • The Japanese atomic bomb study indicates that doses of radiation under about 1 Gy confer less risk per unit dose than higher doses do.
  • All available studies show that skin cancer risk is greater from radiation exposure at young ages than at older ages.
  • Finding few excess skin cancers among irradiated African-Americans as compared to Caucasians with a comparable dose indicates that skin susceptibility to ultraviolet exposure modifies the excess risk from ionizing radiation.
  • Available evidence indicates that the excess risk of skin cancer lasts for 45 years or more following irradiation.
  • Several studies indicate a risk of nonmelanoma skin cancer (NMSC) following cancer therapy; however, most of the studies reporting on NMSC have not distinguished between patients who received radiotherapy versus chemotherapy.
  • It is not clear from the studies how much, if any, of the excess melanoma risk is attributable to radiotherapy.
  • [MeSH-major] Neoplasms, Radiation-Induced / epidemiology. Skin Neoplasms / epidemiology
  • [MeSH-minor] Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Humans. Melanoma / epidemiology. Risk Factors

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11340610.001).
  • [ISSN] 0098-1532
  • [Journal-full-title] Medical and pediatric oncology
  • [ISO-abbreviation] Med. Pediatr. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA43175; United States / NIEHS NIH HHS / ES / ES-00260; United States / NCI NIH HHS / CA / P30CA16087
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 48
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21. Attili SK, Lesar A, McNeill A, Camacho-Lopez M, Moseley H, Ibbotson S, Samuel ID, Ferguson J: An open pilot study of ambulatory photodynamic therapy using a wearable low-irradiance organic light-emitting diode light source in the treatment of nonmelanoma skin cancer. Br J Dermatol; 2009 Jul;161(1):170-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An open pilot study of ambulatory photodynamic therapy using a wearable low-irradiance organic light-emitting diode light source in the treatment of nonmelanoma skin cancer.
  • BACKGROUND: Photodynamic therapy (PDT) is a popular treatment for nonmelanoma skin cancer with clearance rates of between 70% and 100%.
  • Although reported to have a superior cosmetic outcome, the inconvenience of hospital visits and discomfort during therapy are considered drawbacks.
  • METHODS: Twelve patients with Bowen's disease (eight) and superficial basal cell carcinoma (four) < 2 cm in diameter were recruited into the study following histological confirmation of the diagnosis.
  • Two treatments (45-60 J cm(-2) red light, 550-750 nm, peak 620 nm, irradiance 5 mW cm(-2)) were administered 1 month apart following application of aminolaevulinic acid for 4 h.
  • RESULTS: At the 12-month follow-up, seven of the 12 patients remained clear, with four of the nonresponders demonstrating peripheral margin failure.
  • Patients were scored for pain during and immediately after treatment using the numerical rating scale (NRS; 1-10).
  • [MeSH-major] Bowen's Disease / drug therapy. Carcinoma, Basal Cell / drug therapy. Lasers, Semiconductor / therapeutic use. Photochemotherapy / methods. Skin Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Ambulatory Care. Aminolevulinic Acid / therapeutic use. Female. Humans. Male. Middle Aged. Pain Measurement. Photosensitizing Agents / therapeutic use. Pilot Projects. Treatment Outcome

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  • (PMID = 19302071.001).
  • [ISSN] 1365-2133
  • [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 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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22. Bhatia N: Imiquimod as a possible treatment for keratoacanthoma. J Drugs Dermatol; 2004 Jan-Feb;3(1):71-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imiquimod as a possible treatment for keratoacanthoma.
  • To date, the approved use is for condyloma acuminata; approval for use in treating basal cell carcinoma (BCC) has been filed with the FDA and is expected to be approved in the coming months.
  • In the interim, the expansion of the horizons for this immunomodulator depends on the application of the science and immunology behind the drug to the appropriate disease states.
  • There are studies currently underway as well as anecdotal data published for its possible use in treating squamous cell carcinoma (SCC), although this is not as widely accepted for off-label use as BCC among many dermatologists.
  • This is a case of an elderly patient who could not undergo surgery that presented with a large keratoacanthoma and was clear of her tumor after five months using imiquimod 5% cream on a daily basis.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Keratoacanthoma / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 14964750.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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23. Moseley H, Allen JW, Ibbotson S, Lesar A, McNeill A, Camacho-Lopez MA, Samuel ID, Sibbett W, Ferguson J: Ambulatory photodynamic therapy: a new concept in delivering photodynamic therapy. Br J Dermatol; 2006 Apr;154(4):747-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ambulatory photodynamic therapy: a new concept in delivering photodynamic therapy.
  • BACKGROUND: Photodynamic therapy (PDT) has been shown to be effective in treating Bowen's disease, superficial basal cell carcinoma and actinic keratosis.
  • In accordance with our usual practice, patients received two treatments at a 4-week interval.
  • RESULTS: Four of five patients were clear at follow-up (range 6-13 months, median 9).
  • Pain was classified as none or mild in 80% of treatments and moderate in the remainder.
  • CONCLUSIONS: There are many potential benefits of ambulatory PDT, including the possibility of a much higher patient throughput, and allowing effective treatment at home.
  • [MeSH-major] Ambulatory Care / methods. Bowen's Disease / drug therapy. Photochemotherapy / methods. Skin Neoplasms / drug therapy
  • [MeSH-minor] Equipment Design. Feasibility Studies. Humans. Lighting / instrumentation. Pain / etiology. Pilot Projects. Treatment Outcome

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  • (PMID = 16536822.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
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24. Fayter D, Corbett M, Heirs M, Fox D, Eastwood A: A systematic review of photodynamic therapy in the treatment of pre-cancerous skin conditions, Barrett's oesophagus and cancers of the biliary tract, brain, head and neck, lung, oesophagus and skin. Health Technol Assess; 2010 Jul;14(37):1-288
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A systematic review of photodynamic therapy in the treatment of pre-cancerous skin conditions, Barrett's oesophagus and cancers of the biliary tract, brain, head and neck, lung, oesophagus and skin.
  • BACKGROUND: Photodynamic therapy (PDT) is the use of a light-sensitive drug, in combination with light of a visible wavelength, to destroy target cells.
  • PDT is used either as a primary treatment or as an adjunctive treatment.
  • It is fairly well accepted in clinical practice for some types of skin cancer but has yet to be fully explored as a treatment for other forms of cancer.
  • OBJECTIVE: To systematically review the clinical effectiveness and safety of PDT in the treatment of Barrett's oesophagus, pre-cancerous skin conditions and the following cancers: biliary tract, brain, head and neck, lung, oesophageal and skin.
  • STUDY DESIGNS: Randomised controlled trials (RCTs) in skin conditions and Barrett's oesophagus, non-randomised trials for all other sites.
  • PARTICIPANTS: People with Barrett's oesophagus, pre-cancerous skin conditions or primary cancer in the following sites: biliary tract, brain, head and neck, lung, oesophageal and skin.
  • INTERVENTION: Any type of PDT for either curative or palliative treatment.
  • COMPARATORS: Any comparator including differing applications of PDT treatments (relevant comparators varied according to the condition).
  • For actinic keratosis (AK), the only clear evidence of effectiveness was that PDT appeared to be superior to placebo.
  • For basal cell carcinoma (BCC), PDT may result in similar lesion response rates to surgery or cryotherapy but with better cosmetic outcomes.
  • CONCLUSIONS: Evidence of effectiveness was found for PDT in the treatment of AK and nodular BCC in relation to placebo, and possibly for treating Barrett's oesophagus.
  • However, the effectiveness of PDT in relation to other treatments is not yet apparent.
  • [MeSH-major] Neoplasms / drug therapy. Photochemotherapy / methods. Precancerous Conditions / drug therapy
  • [MeSH-minor] Barrett Esophagus / drug therapy. Barrett Esophagus / mortality. Biliary Tract Neoplasms / drug therapy. Biliary Tract Neoplasms / mortality. Brain Neoplasms / drug therapy. Brain Neoplasms / mortality. Clinical Trials as Topic. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / mortality. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / mortality. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / mortality. Quality of Life. Skin Neoplasms / drug therapy. Skin Neoplasms / mortality

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  • (PMID = 20663420.001).
  • [ISSN] 2046-4924
  • [Journal-full-title] Health technology assessment (Winchester, England)
  • [ISO-abbreviation] Health Technol Assess
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
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