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1. Stinco G, Frattasio A, Forcione M, Quinkenstein E, Finato N, Patrone P: The appearance of inflammatory papules in the skin surrounding areas treated with imiquimod cream for basal cell carcinoma. Br J Dermatol; 2008 Feb;158(2):408-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The appearance of inflammatory papules in the skin surrounding areas treated with imiquimod cream for basal cell carcinoma.
  • [MeSH-major] Aminoquinolines / adverse effects. Antineoplastic Agents / adverse effects. Skin Diseases, Papulosquamous / chemically induced
  • [MeSH-minor] Aged. Back. Carcinoma, Basal Cell / drug therapy. Humans. Male. Skin Neoplasms / drug therapy

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  • (PMID = 18028501.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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2. Chen Y, Vujcic S, Liang P, Diegelman P, Kramer DL, Porter CW: Genomic identification and biochemical characterization of a second spermidine/spermine N1-acetyltransferase. Biochem J; 2003 Aug 1;373(Pt 3):661-7
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  • In the polyamine back-conversion pathway, spermine and spermidine are first acetylated by spermidine/spermine N(1) -acetyl-transferase (SSAT-1) and then oxidized by polyamine oxidase to produce spermidine and putrescine respectively.
  • Human SSAT-2 cDNA derived from small-cell lung carcinoma was deduced to encode a 170-amino-acid protein having 46% sequence identity and 64% sequence similarity with SSAT-1.
  • Analysis of mRNA levels in cell lines and ESTs (expressed sequence tags) from various tissues by digiNorthern (a web-based tool for virtually displaying expression profiles of query genes based on EST sequences) indicated that SSAT-1 tends to be more widely and highly expressed than SSAT-2.
  • While SSAT-1 mRNA was inducible by polyamine analogues in a variety of cell lines, SSAT-2 was not.
  • The existence of an active, but possibly sequestered, SSAT-2 enzyme suggests that, under certain conditions, it may be recruited into basal or perturbed polyamine metabolism.


3. Tang XH, Su D, Albert M, Scognamiglio T, Gudas LJ: Overexpression of lecithin:retinol acyltransferase in the epithelial basal layer makes mice more sensitive to oral cavity carcinogenesis induced by a carcinogen. Cancer Biol Ther; 2009 Jul;8(13):1212-3
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  • [Title] Overexpression of lecithin:retinol acyltransferase in the epithelial basal layer makes mice more sensitive to oral cavity carcinogenesis induced by a carcinogen.
  • We targeted human LRAT expression specifically to the basal layer of mouse skin and oral cavity epithelia by using a portion of the human cytokeratin 14 (K14) promoter.
  • The retinyl ester levels in skin of LRAT TG+ mice were 32% +/- 5.4% greater than those in TG- mice, and topical treatment of the back skin with retinol resulted in greater increases in retinyl esters (from 6.9- to 14.3-fold in different TG+ mice) in TG+ mouse skin than in TG- mouse skin (1.3 fold).
  • While carcinogen (4-NQO) treatment induced multifocal precancerous and cancer lesions in the tongues of both TG positive (n=16) and negative mice (n=22), higher percentages of transgenic positive mice (62.5%) developed more severe tongue lesions (grades 3 and 4) than transgenic negative mice (24.8%) after 4-NQO treatment (p < 0.05).
  • Carcinogen treatment also resulted in greater percentages of transgenic positive mouse tongues with hyperplasia (71.4%), dysplasia (85.7%, p < 0.05), and carcinoma (28.6%) than transgenic negative mouse tongues (53.3%, 46.7%, and 20%, respectively).
  • Taken together, these data show that overexpression of human LRAT specifically in oral basal epithelial cells makes these cells more sensitive to carcinogen induced tumorigenesis.

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  • (PMID = 19471114.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / DE010389-15; United States / NCI NIH HHS / CA / T32 CA062948; United States / NIDCR NIH HHS / DE / R01DE10389; United States / NIDCR NIH HHS / DE / R01 DE010389-15; United States / NIDCR NIH HHS / DE / R01 DE010389
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Proliferating Cell Nuclear Antigen; 0 / Receptors, Retinoic Acid; 0 / Retinoids; 136601-57-5 / Cyclin D1; 56-57-5 / 4-Nitroquinoline-1-oxide; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.3.- / Acyltransferases; EC 2.3.1.- / lecithin-retinol acyltransferase
  • [Other-IDs] NLM/ NIHMS209419; NLM/ PMC2882701
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4. Hassan HT: Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy. Leuk Res; 2004 Jul;28(7):667-71
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  • [Title] Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy.
  • The reputation of garlic (Allium sativum) as an effective remedy for tumours extends back to the Egyptian Codex Ebers of 1550 b.c.
  • Several garlic compounds including allicin and its corresponding sulfide inhibit the proliferation and induce apoptosis of several human non-leukaemia malignant cells including breast, bladder, colorectal, hepatic, prostate cancer, lymphoma and skin tumour cell lines.
  • Recently, topic application of ajoene has produced significant clinical response in patients with skin basal cell carcinoma.
  • More significantly, ajoene profoundly enhanced the apoptotic effect of the two chemotherapeutic drugs: cytarabine and fludarabine in human CD34-positive resistant myeloid leukaemia cells through enhancing their bcl-2 inhibitory and caspase-3 activation activities.
  • The two key anti-leukaemia biological actions of ajoene were the inhibition of proliferation and the induction of apoptosis.
  • Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
  • Since acute myeloid leukaemia (AML) is a heterogeneous malignant disease in which disease progression at the level of CD34-positive cells has a major impact on resistance to chemotherapy and relapse and the inability to undergo apoptosis is a crucial mechanism of multi-drug resistance in AML patients.
  • [MeSH-major] Disulfides / therapeutic use. Garlic. Leukemia, Myeloid / drug therapy. Plant Extracts / therapeutic use
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Drug Synergism. Humans

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  • (PMID = 15158086.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Disulfides; 0 / Plant Extracts; 99A0041VG8 / ajoene
  • [Number-of-references] 66
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5. Alessi SS, Sanches JA, Oliveira WR, Messina MC, Pimentel ER, Festa Neto C: Treatment of cutaneous tumors with topical 5% imiquimod cream. Clinics (Sao Paulo); 2009;64(10):961-6
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  • MATERIALS AND METHODS: Here, we present our experience in the treatment of 123 cutaneous tumors of various types, including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), Bowen's disease, erythroplasia of Queyrat, Paget's disease, and trichoepithelioma, with 5% imiquimod cream from 2003 to 2008 in the Cutaneous Oncology Group of the Dermatology Department of Hospital das Clinicas.
  • Patients were divided into two separate groups according to their diagnosis and comorbidities; these comorbidities included epidermodysplasia verruciformis, xeroderma pigmentosum, albinism, basal cell nevus syndrome, Brooke-Spiegler syndrome, HIV, chronic lymphocytic leukemia, B-cell lymphoma, and kidney transplantation.
  • Treatment duration, response to imiquimod, follow-up, recurrence, and local and systemic reactions associated with use of the drug were analyzed.
  • Tumors were located mainly on the face, back, trunk, and legs.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Skin Neoplasms / drug therapy

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  • (PMID = 19841702.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
  • [Other-IDs] NLM/ PMC2763070
  • [Keywords] NOTNLM ; Basal cell carcinoma / Imiquimod / Immunomodulator / Immunotherapy / Non-melanoma skin cancer
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6. Rieger UM, Schlecker C, Pierer G, Haug M: Spontaneous regression of two giant basal cell carcinomas in a single patient after incomplete excision. Tumori; 2009 Mar-Apr;95(2):258-63
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  • [Title] Spontaneous regression of two giant basal cell carcinomas in a single patient after incomplete excision.
  • BACKGROUND: Spontaneous regression of small basal cell carcinoma has been reported.
  • For giant basal cell carcinoma, however, no spontaneous regression has been described to date.
  • CASE REPORT: We present a patient with two independent giant basal cell carcinomas over the left clavicle and the lower back, measuring 7 x 12 cm and 18 x 20 cm, respectively.
  • CONCLUSION; Incompletely excised giant basal cell carcinomas can regress spontaneously.
  • [MeSH-major] Bone Neoplasms / secondary. Carcinoma, Basal Cell / pathology. Carcinoma, Basal Cell / surgery. Materia Medica / therapeutic use. Neoplasm Regression, Spontaneous. Skin Neoplasms / pathology. Skin Neoplasms / surgery
  • [MeSH-minor] Aged. Back. Clavicle / pathology. Humans. Lumbar Vertebrae / pathology. Male. Neoplasm Invasiveness. Spinal Neoplasms / secondary. Wound Healing / drug effects

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  • (PMID = 19579878.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Materia Medica
  • [Number-of-references] 51
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7. Fresini A, Rossiello L, Severino BU, Del Prete M, Satriano RA: Giant basal cell carcinoma. Skinmed; 2007 Jul-Aug;6(4):204-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Giant basal cell carcinoma.
  • A 72-year-old white man presented with a large cutaneous tumor on his back.
  • The patient's history revealed mild hypertension, ischemic cardiopathy treated with percutaneous transluminal coronary angioplasty and anticoagulant drugs, and moderate chronic renal insufficiency.
  • Therefore, a diagnosis of basal cell carcinoma, adenoid subtype, was made.
  • Because the patient was taking anticoagulant drugs and had unstable renal and cardiac function, surgical treatment was at least temporarily excluded, and the patient was referred for radiation therapy.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Skin Neoplasms / pathology

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  • (PMID = 17618177.001).
  • [ISSN] 1540-9740
  • [Journal-full-title] Skinmed
  • [ISO-abbreviation] Skinmed
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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8. Vogt T, McClelland M, Jung B, Popova S, Bogenrieder T, Becker B, Rumpler G, Landthaler M, Stolz W: Progression and NSAID-induced apoptosis in malignant melanomas are independent of cyclooxygenase II. Melanoma Res; 2001 Dec;11(6):587-99
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  • Cyclooxygenase-II (Cox-II) overexpression is involved in the progression of various subtypes of cancer.
  • Basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) were also analysed as controls: the BCCs were consistently Cox-II negative (n = 11), whereas the SCCs showed moderate to strong Cox-II expression in 53% (n = 17).
  • Reverse transcription-polymerase chain reaction and Western blotting of MM cell lines and MM tissues confirmed the lack of Cox-II expression in MM.
  • However, in vitro the Cox-inhibiting non-steroidal anti-inflammatory drug (NSAID) sulindac sulphide (SIS) was significantly more effective in inducing apoptosis than sulindac sulphone (SOS), a derivative with a negligible effect on Cox (P < 0.01).
  • The SIS doses needed for the induction of apoptosis were not significantly different in MM cell lines versus a Cox-II-positive colon carcinoma cell line (HT29).
  • Furthermore, add-back experiments with high doses of the prostaglandins PGE2 and PGF2beta, major Cox-II products, did not abrogate this effect.
  • We conclude that Cox-II expression is not involved in the progression of MM, and NSAID-induced apoptosis in MM cell lines seems to follow pathways independent of Cox-II.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Apoptosis / drug effects. Isoenzymes / metabolism. Melanoma / pathology. Prostaglandin-Endoperoxide Synthases / metabolism. Skin Neoplasms / pathology. Sulindac / analogs & derivatives. Sulindac / pharmacology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Blotting, Western. Carcinoma, Basal Cell / enzymology. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / pathology. Cell Differentiation. Child. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / pharmacology. DNA Primers / chemistry. Disease Progression. Enzyme-Linked Immunosorbent Assay. Humans. Immunoenzyme Techniques. Membrane Proteins. Middle Aged. RNA / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 11725205.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / DNA Primers; 0 / Isoenzymes; 0 / Membrane Proteins; 184SNS8VUH / Sulindac; 63231-63-0 / RNA; 6UVA8S2DEY / sulindac sulfide; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K619IIG2R9 / sulindac sulfone
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