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1. Pisano M, Pagnan G, Loi M, Mura ME, Tilocca MG, Palmieri G, Fabbri D, Dettori MA, Delogu G, Ponzoni M, Rozzo C: Antiproliferative and pro-apoptotic activity of eugenol-related biphenyls on malignant melanoma cells. Mol Cancer; 2007;6:8
Hazardous Substances Data Bank. EUGENOL .

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  • [Title] Antiproliferative and pro-apoptotic activity of eugenol-related biphenyls on malignant melanoma cells.
  • BACKGROUND: Malignant melanoma is one of the most aggressive skin cancer and chemotherapeutic agents currently in use are still unsatisfactory.
  • Therefore the search for novel therapeutic approaches is warranted.
  • Aim of this work was to identify and test new compounds with antiproliferative and cytotoxic activity on melanoma cells.
  • We tested eugenol together with six natural and synthetic eugenol-related compounds for their capability to inhibit cell growth on primary melanoma cell lines established from patients' tissue samples.
  • RESULTS: Eugenol and isoeugenol monomers and their respective O-methylated forms did not show to inhibit melanoma cells proliferation.
  • Dose and time dependence curves have been obtained for the enantiomeric form S7-(S).
  • Then IC50 and minimal effective doses and times have been established for the melanoma cell lines tested.
  • Cytotoxic activity and apoptosis induced by treating melanoma cells with eugenol-related biphenyls was partially dependent by caspase activation.
  • CONCLUSION: Our findings demonstrate that the eugenol related biphenyl (S)-6,6'-dibromo-dehydrodieugenol elicits specific antiproliferative activity on neuroectodermal tumour cells partially triggering apoptosis and its activity should be further investigated on in vivo melanoma models in order to evaluate the real anticancer effectiveness on such tumour.
  • [MeSH-major] Biphenyl Compounds / chemistry. Cell Proliferation / drug effects. Eugenol / analogs & derivatives. Eugenol / pharmacology. Melanoma / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis. Cell Line, Tumor. Dimerization. Humans. In Situ Nick-End Labeling. Inhibitory Concentration 50. Time Factors

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  • (PMID = 17233906.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 2L9GJK6MGN / diphenyl; 3T8H1794QW / Eugenol
  • [Other-IDs] NLM/ PMC1785384
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2. Shannan B, Seifert M, Leskov K, Boothman D, Pföhler C, Tilgen W, Reichrath J: Clusterin (CLU) and melanoma growth: CLU is expressed in malignant melanoma and 1,25-dihydroxyvitamin D3 modulates expression of CLU in melanoma cell lines in vitro. Anticancer Res; 2006 Jul-Aug;26(4A):2707-16
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  • [Title] Clusterin (CLU) and melanoma growth: CLU is expressed in malignant melanoma and 1,25-dihydroxyvitamin D3 modulates expression of CLU in melanoma cell lines in vitro.
  • MATERIALS AND METHODS: The expression of CLU was studied immunohistochemically in paraffin sections of primary cutaneous malignant melanomas, metastases of malignant melanomas and acquired melanocytic naevi.
  • Using PCR and Western blotting, the expression of CLU was also investigated in various vitamin D-responsive (MeWo, SK-MEL-28) and vitamin D-resistant melanoma cell lines (SK-MEL-5, SK-MEL-25), as well as in normal human melanocytes (NHM), along with 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] treatment.
  • RESULTS: In contrast to acquired melanocytic naevi, CLU immunoreactivity was found in primary cutaneous malignant melanomas and metastases of malignant melanomas in situ.
  • Both CLU protein and RNA were detected in melanoma cell lines and NHM.
  • Treatment with 1,25(OH)2D3 modulated CLU's expression in vitamin D-responsive but not in -resistant melanoma cell lines.
  • CONCLUSION: CLU may be of importance for the progression of malignant melanoma.
  • The growth regulatory effects of 1,25(OH)2D3 in melanoma cell lines may, at least in part, be mediated via modulation of CLU expression.
  • [MeSH-major] Calcitriol / pharmacology. Clusterin / biosynthesis. Melanoma / drug therapy. Melanoma / metabolism. Skin Neoplasms / drug therapy. Skin Neoplasms / metabolism

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  • (PMID = 16886681.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA013148; United States / NCI NIH HHS / CA / P30 CA142543; United States / NCI NIH HHS / CA / R01 CA078530
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CLU protein, human; 0 / Clusterin; FXC9231JVH / Calcitriol
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3. Nihal M, Ahmad N, Mukhtar H, Wood GS: Anti-proliferative and proapoptotic effects of (-)-epigallocatechin-3-gallate on human melanoma: possible implications for the chemoprevention of melanoma. Int J Cancer; 2005 Apr 20;114(4):513-21
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  • [Title] Anti-proliferative and proapoptotic effects of (-)-epigallocatechin-3-gallate on human melanoma: possible implications for the chemoprevention of melanoma.
  • Melanoma accounts for only about 4% of all skin cancer cases but most of skin cancer-related deaths.
  • Standard systemic therapies such as interferon (IFN) have not been adequately effective in the management of melanoma.
  • Therefore, novel approaches are needed for prevention and treatment of this disease.
  • Here, employing 2 human melanoma cell lines (A-375 amelanotic malignant melanoma and Hs-294T metastatic melanoma) and normal human epidermal melanocytes (NHEM), we studied the antiproliferative effects of epigallocatechin-3-gallate (EGCG), the major polyphenolic antioxidant present in green tea.
  • EGCG treatment was found to result in a dose-dependent decrease in the viability and growth of both melanoma cell lines.
  • EGCG treatment of the melanoma cell lines resulted in decreased cell proliferation (as assessed by Ki-67 and PCNA protein levels) and induction of apoptosis (as assessed cleavage of PARP, TUNEL assay and JC-1 assay).
  • EGCG also significantly inhibited the colony formation ability of the melanoma cells studied.
  • EGCG treatment of melanoma cells resulted in a downmodulation of anti-apoptotic protein Bcl2, upregulation of proapoptotic Bax and activation of caspases -3, -7 and -9.
  • Furthermore, our data demonstrated that EGCG treatment resulted in a significant, dose-dependent decrease in cyclin D1 and cdk2 protein levels and induction of cyclin kinase inhibitors (ckis) p16INK4a, p21WAF1/CIP1 and p27KIP1.
  • Our data suggest that EGCG causes significant induction of cell cycle arrest and apoptosis of melanoma cells that is mediated via modulations in the cki-cyclin-cdk network and Bcl2 family proteins.
  • Thus, EGCG, alone or in conjunction with current therapies, could be useful for the management of melanoma.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Apoptosis. Catechin / analogs & derivatives. Catechin / pharmacology. Melanoma / drug therapy. Melanoma / prevention & control
  • [MeSH-minor] Agar / chemistry. Caspase 3. Caspase 7. Caspase 9. Caspases / metabolism. Cell Cycle. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. Cell Separation. Cell Survival. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Dose-Response Relationship, Drug. Down-Regulation. Flow Cytometry. Humans. Immunoblotting. Immunohistochemistry. In Situ Nick-End Labeling. Ki-67 Antigen / biosynthesis. Melanocytes / metabolism. Membrane Potentials. Mitochondria / metabolism. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Time Factors. bcl-2-Associated X Protein

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  • (PMID = 15609335.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR002136-06
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / BAX protein, human; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 8R1V1STN48 / Catechin; 9002-18-0 / Agar; BQM438CTEL / epigallocatechin gallate; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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4. Feleszko W, Młynarczuk I, Olszewska D, Jalili A, Grzela T, Lasek W, Hoser G, Korczak-Kowalska G, Jakóbisiak M: Lovastatin potentiates antitumor activity of doxorubicin in murine melanoma via an apoptosis-dependent mechanism. Int J Cancer; 2002 Jul 1;100(1):111-8
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  • [Title] Lovastatin potentiates antitumor activity of doxorubicin in murine melanoma via an apoptosis-dependent mechanism.
  • Lovastatin, a drug successfully used in the clinic to prevent and to treat coronary heart disease, has recently been reported to decrease the incidence of melanoma in lovastatin-treated patients.
  • Lovastatin has also been proved to potentiate antitumor effects of both cisplatin and TNF-alpha in murine melanoma models.
  • Recently, an augmented therapeutic effect of lovastatin and doxorubicin has been reported in 3 tumor models in mice.
  • In our preliminary study lovastatin caused retardation of melanoma growth in mice treated with doxorubicin (Feleszko et al.
  • In the present report, we supplement our preliminary observations and demonstrate in 2 murine and 2 human melanoma cell lines that lovastatin effectively potentiates the cytostatic/cytotoxic activity of doxorubicin in vitro via an augmentation of apoptosis (estimated with PARP-cleavage assay, annexin V assay and TUNEL).
  • The combined antiproliferative activity of lovastatin and doxorubicin was evaluated using the combination index (CI) method of Chou and Talalay, revealing synergistic interactions in melanoma cells exposed to lovastatin and doxorubicin.
  • In B16F10 murine melanoma model in vivo, we have demonstrated significantly increased sensitivity to the combined treatment with both lovastatin (5 mg/kg for 14 days) and doxorubicin (4 x 1 mg/kg) as compared with either agent acting alone.
  • Lovastatin treatment resulted also in significant reduction of the number of experimental metastasis in doxorubicin-treated mice.
  • The results of our studies suggest that lovastatin may enhance the effectiveness of chemotherapeutic agents in the treatment of malignant melanomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Doxorubicin / therapeutic use. Lovastatin / therapeutic use. Melanoma, Experimental / drug therapy. Melanoma, Experimental / pathology
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Synergism. Female. Humans. In Situ Nick-End Labeling. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Neoplasm Metastasis / prevention & control. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12115596.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin; 9LHU78OQFD / Lovastatin
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5. Ishihara K, Saida T, Yamamoto A, Japanese Skin Cancer Society Prognosis and Statistical Investigation Committee: Updated statistical data for malignant melanoma in Japan. Int J Clin Oncol; 2001 Jun;6(3):109-16
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  • [Title] Updated statistical data for malignant melanoma in Japan.
  • BACKGROUND: A statistical investigation was conducted of Japanese melanoma patients who had been registered by the Prognosis and Statistical Investigation Committee of the Japanese Skin Cancer Society.
  • METHODS: The data analyzed included age, sex, anatomical distribution, clinical features of primary lesions, Clark's subtype, tumor thickness, Clark's level, disease stage, and treatment.
  • In addition, the results of a nationwide survey of various types of skin malignancies, obtained from 101 medical institutions in Japan between 1987 and 1996, were analyzed.
  • RESULTS: The nationwide survey revealed that the number of patients with malignant melanoma showed a steady increase during the period 1987-1996 in Japan.
  • It is noteworthy that the numbers of actinic keratoses, a type of early squamous cell carcinoma in situ, showed a steep increase in recent years.
  • Results revealed in our study of the melanoma registry for the period 1987-1996 were as follows:.
  • (1) the male-to-female ratio was 1 to 1.06, (2) the survival rate of female patients was higher than that of male patients (10-year survival in group B: female, 71.6% vs male, 55.9%), (3) the commonest site of melanoma in both sexes was the sole of the foot, (4) with respect to Clark's subtype, acral lentiginous melanoma was commonest, accounting for about half of all melanomas, (5) nodular melanoma showed the worst prognosis among the subtypes, (6) patients in stage IIIB and stage IV had an unfavorable outcome, with 10-year survivals of less than 50% and less than 10%, respectively, (7) Clark's level of invasion, as well as Breslow's tumor thickness of the primary lesions, were confirmed to be important prognostic factors, and (8) prophylactic lymph node dissection in stage II and IIIA and chemotherapy in stage IV seemed to have limited effect on the prognosis.
  • CONCLUSION: The prognosis of advanced melanoma is poor, as it is highly resistant to chemotherapy.
  • Thus, to improve the prognosis, early detection is mandatory, and this is possible because this neoplasm appears as a distinctive pigmented lesion on the skin.
  • [MeSH-major] Melanoma / epidemiology. Neoplasm Staging. Registries. Skin Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Japan / epidemiology. Lymph Node Excision. Male. Middle Aged. Neoplasm Invasiveness. Prevalence. Prognosis

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  • (PMID = 11706778.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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6. Ray CM, Kluk M, Grin CM, Grant-Kels JM: Successful treatment of malignant melanoma in situ with topical 5% imiquimod cream. Int J Dermatol; 2005 May;44(5):428-34
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  • [Title] Successful treatment of malignant melanoma in situ with topical 5% imiquimod cream.
  • BACKGROUND: Current treatment recommendations for malignant melanoma in situ include surgical excision with at least 0.5 cm margins.
  • On the head or neck, obtaining adequate surgical margins for melanoma can be challenging and often disfiguring.
  • METHODS: We report herein three cases of malignant melanoma in situ on the face treated with topical imiquimod cream.
  • RESULTS: Complete regression of malignant melanoma in situ was observed on treatment with 5% topical imiquimod cream.
  • The varied treatment regimens, rationale for using imiquimod rather than performing surgery, and the possible mechanisms of action are discussed.
  • CONCLUSIONS: Topical imiquimod can be used successfully for the treatment of malignant melanoma in situ on the face.
  • [MeSH-major] Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Facial Neoplasms / drug therapy. Melanoma / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Aged. Aged, 80 and over. Drug Administration Schedule. Female. Humans. Male. Treatment Outcome

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  • (PMID = 15869545.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. 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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7. Sadownik LA, Crawford RI: Post-surgical treatment of melanoma in situ of the vulva with imiquimod. J Obstet Gynaecol Can; 2010 Aug;32(8):771-4
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  • [Title] Post-surgical treatment of melanoma in situ of the vulva with imiquimod.
  • BACKGROUND: Melanoma in situ is a rare malignant lesion of the vulva.
  • The standard treatment is surgical excision.
  • CASE: We describe a case of melanoma in situ of the vulva in a 72-year-old woman that reoccurred after surgical excision and was treated successfully with topical 5% imiquimod.
  • CONCLUSION: There may be a role for imiquimod in treating melanoma in situ of the vulva.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Melanoma / drug therapy. Melanoma / surgery. Vulvar Neoplasms / drug therapy. Vulvar Neoplasms / surgery
  • [MeSH-minor] Aged. Combined Modality Therapy. Female. Humans

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  • (PMID = 21050510.001).
  • [ISSN] 1701-2163
  • [Journal-full-title] Journal of obstetrics and gynaecology Canada : JOGC = Journal d'obstétrique et gynécologie du Canada : JOGC
  • [ISO-abbreviation] J Obstet Gynaecol Can
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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8. Thallinger C, Wolschek MF, Wacheck V, Maierhofer H, Günsberg P, Polterauer P, Pehamberger H, Monia BP, Selzer E, Wolff K, Jansen B: Mcl-1 antisense therapy chemosensitizes human melanoma in a SCID mouse xenotransplantation model. J Invest Dermatol; 2003 Jun;120(6):1081-6
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  • [Title] Mcl-1 antisense therapy chemosensitizes human melanoma in a SCID mouse xenotransplantation model.
  • Much less is known about the role the more recently described Bcl-2 family member Mcl-1 might play in tumor biology and resistance to chemotherapy.
  • Using an antisense strategy, we here address this issue in melanoma, a paradigm of a treatment-resistant malignancy.
  • After in vitro proof of principle supporting an antisense mechanism of action with specific reduction of Mcl-1 protein as a consequence of nuclear uptake of the Mcl-1 antisense oligonucleotides employed, antisense and universal control oligonucleotides were administered systemically in combination with dacarbazine in a human melanoma SCID mouse xenotransplantation model.
  • Dacarbazine, available now for more than three decades, still remains the most active single agent for treatment of advanced melanoma.
  • Mcl-1 antisense oligonucleotides specifically reduced target protein expression as well as the apoptotic threshold of melanoma xenotransplants.
  • Combined Mcl-1 antisense oligonucleotide plus dacarbazine treatment resulted in enhanced tumor cell apoptosis and led to a significantly reduced mean tumor weight (mean 0.16 g, 95% confidence interval 0.08-0.26) compared to the tumor weight in universal control oligonucleotide plus dacarbazine treated animals (mean 0.35 g, 95% confidence interval 0.2-0.44) or saline plus dacarbazine treated animals (mean 0.39 g, 95% confidence interval 0.25-0.53).
  • We thus show that Mcl-1 is an important factor contributing to the chemoresistance of human melanoma in vivo.
  • Antisense therapy against the Mcl-1 gene product, possibly in combination with antisense strategies targeting other antiapoptotic Bcl-2 family members, appears to be a rational and promising approach to help overcome treatment resistance of malignant melanoma.
  • [MeSH-major] Melanoma / drug therapy. Oligonucleotides, Antisense / therapeutic use. Proto-Oncogene Proteins c-bcl-2. Skin Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / therapeutic use. Apoptosis. Dacarbazine / therapeutic use. Drug Synergism. Drug Therapy, Combination. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, SCID. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / antagonists & inhibitors. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm Transplantation. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 12787138.001).
  • [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 / Antineoplastic Agents, Alkylating; 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 7GR28W0FJI / Dacarbazine
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9. Reutter JC, Long EM, Morrell DS, Thomas NE, Groben PA: Eruptive post-chemotherapy in situ melanomas and dysplastic nevi. Pediatr Dermatol; 2007 Mar-Apr;24(2):135-7
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  • [Title] Eruptive post-chemotherapy in situ melanomas and dysplastic nevi.
  • A 22-year-old white man without a personal or family history of atypical nevi had received chemotherapy for pre-B-cell acute lymphocytic leukemia at age 17 that included L-asparaginase, prednisone, methotrexate, mercaptopurine, daunorubicin, and cytoxan.
  • Two to three months after completing maintenance chemotherapy, the patient reports he developed many moles, which remained stable for approximately 2 years.
  • Histology of specimens of both types of lesions revealed three moderately atypical compound dysplastic melanocytic nevi and three in situ melanomas.
  • The lesions with in situ melanomas in addition demonstrated pagetoid spread, extension down adnexal structures, and more severe cytologic atypia.
  • Malignant melanoma has been associated with chronic immunosuppression, and benign nevi have been reported to erupt after chemotherapy.
  • We report an occurrence of multiple eruptive dysplastic nevi and in situ melanomas appearing shortly after completion of chemotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Drug Eruptions / etiology. Dysplastic Nevus Syndrome / chemically induced. Immunosuppressive Agents / adverse effects. Melanoma / chemically induced. Skin Neoplasms / chemically induced

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  • (PMID = 17461808.001).
  • [ISSN] 0736-8046
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents
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10. Jawaid S, Khan TH, Osborn HM, Williams NA: Tyrosinase activated melanoma prodrugs. Anticancer Agents Med Chem; 2009 Sep;9(7):717-27
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  • [Title] Tyrosinase activated melanoma prodrugs.
  • Metastatic malignant melanoma remains a highly aggressive form of skin cancer for which no reliable methods for treatment exist.
  • Within this article, methods for treating melanoma are reviewed and discussed with particular attention focusing on prodrugs that are activated by the tyrosinase enzyme.
  • This enzyme is up-regulated and is of elevated activity within malignant melanomas compared with healthy melanocytes, providing an ideal in-situ tool for the activation of melanoma prodrugs.
  • By way of background to the prodrug strategies discussed within this review, the causes of melanoma, the enzymology of tyrosinase, and the chemistry of the biosynthetic pathways associated with melanogenesis are presented.
  • Aspects of the design, mode of action, and biological profiles of key prodrugs that are activated by tyrosinase, and that show potential for the treatment of melanoma, are then presented and compared.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Melanoma / drug therapy. Monophenol Monooxygenase / metabolism. Prodrugs / therapeutic use

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  • (PMID = 19538169.001).
  • [ISSN] 1875-5992
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Melanins; 0 / Prodrugs; EC 1.14.18.1 / Monophenol Monooxygenase
  • [Number-of-references] 72
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11. Chen RY, Chen HX, Jian P, Xu L, Li J, Fan YM, Tu YT: Intratumoral injection of pEGFC1-IGFBP7 inhibits malignant melanoma growth in C57BL/6J mice by inducing apoptosis and down-regulating VEGF expression. Oncol Rep; 2010 Apr;23(4):981-8
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  • [Title] Intratumoral injection of pEGFC1-IGFBP7 inhibits malignant melanoma growth in C57BL/6J mice by inducing apoptosis and down-regulating VEGF expression.
  • Malignant melanoma (MM) is a type of aggressive skin cancer, and the effective therapy for MM is highly desired.
  • In this study, we constructed pEGFC1-IGFBP7 to try to obtain high expression of IGFPB7 and then we demonstrated that this plasmid inhibited proliferation of B16-F10 melanoma cells efficiently in vitro.
  • These results suggest a potential new clinical strategy for MM treatment.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Genetic Therapy / methods. Insulin-Like Growth Factor Binding Proteins / genetics. Melanoma / therapy. Vascular Endothelial Growth Factor A / drug effects
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Caspase 3 / biosynthesis. Caspase 3 / drug effects. Cell Separation. DNA, Complementary. Down-Regulation. Female. Flow Cytometry. Genetic Vectors. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, Inbred C57BL. Microscopy, Confocal. Plasmids. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 20204282.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / DNA, Complementary; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / insulin-like growth factor binding protein-related protein 1; EC 3.4.22.- / Caspase 3
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12. Prasad ML, Busam KJ, Patel SG, Hoshaw-Woodard S, Shah JP, Huvos AG: Clinicopathologic differences in malignant melanoma arising in oral squamous and sinonasal respiratory mucosa of the upper aerodigestive tract. Arch Pathol Lab Med; 2003 Aug;127(8):997-1002
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  • [Title] Clinicopathologic differences in malignant melanoma arising in oral squamous and sinonasal respiratory mucosa of the upper aerodigestive tract.
  • The oral melanomas were more likely to be detected in the early in situ or microinvasive stage (4 cases vs none, P =.008) and were more frequently amelanotic (14 vs 12, P =.049) than sinonasal melanomas.
  • The sinonasal melanomas were frequently thicker (median thickness, 9 vs 2.6 mm), polypoid (29 vs none), ulcerated (57 vs 20), and necrotic (57 vs 14) than oral melanoma (P <.001).
  • Sinonasal melanoma showed vascular and deep tissue invasion more frequently than oral melanoma; however, no significant difference in disease-specific survival was noted (median survival, 2.8 years vs 3.0 years; 5-year survival, 37% vs 35%, respectively).
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Head and Neck Neoplasms / pathology. Maxillary Sinus Neoplasms / pathology. Melanoma / pathology. Mouth Mucosa / pathology. Mouth Neoplasms / pathology. Nose Neoplasms / pathology. Respiratory Mucosa / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Nasal Mucosa / drug effects. Nasal Mucosa / pathology. Nasal Mucosa / surgery. Neoplasm Invasiveness / pathology. Paranasal Sinus Neoplasms / drug therapy. Paranasal Sinus Neoplasms / mortality. Paranasal Sinus Neoplasms / pathology. Paranasal Sinus Neoplasms / surgery


13. Andreeff M, Studeny M, Dembinski J, Konopleva M, Wang RY, Yang HY, Fueyo J, Champlin RE, Lang F, Marini FC: Mesenchymal stem cells as delivery systems for cancer and leukemia gene therapy. J Clin Oncol; 2004 Jul 15;22(14_suppl):3194

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  • [Title] Mesenchymal stem cells as delivery systems for cancer and leukemia gene therapy.
  • : 3194 Background: We previously demonstrated that intravenously (IV) injected bone marrow-derived mesenchymal stem cells (MSC) integrate into solid tumors as stromal fibroblasts and proliferate selectively in situ.
  • We here propose a novel cancer therapy concept based on the intratumoral drug production by gene-modified MSC.
  • METHODS: MSC were transduced with adeno (AdV)- or adeno-associated (AAV) virus carrying marker- or therapeutic genes.
  • RESULTS: MSC were found only in tumors, where they proliferate not in normal tissues.
  • MSC producing human interferon-beta (IFNβ-MSC) directly inhibited the growth of metastatic A375 melanoma and MDA 231 breast carcinoma following IV injection (p=0.0073), while recombinant IFNβ protein injected subcutaneously (SC) did not (p=0.14).
  • MSC injected into the carotid artery (IA) of mice with gliomas selectively proliferated in gliomas, not in normal brain tissues.
  • The melanoma differentiation-associated gene 7 (MDA7) produced by MSC, preferentially inhibited Gleevec resistant KBM5 CML blast crisis cells.
  • Tumor inhibition required spatial proximity of MSC to the malignant cells.
  • The findings suggest that therapeutic proteins or oncolytic replicating adenovirus have potent anti-tumor effects when produced in situ and suggest the use of MSC as tumor-selective gene therapy delivery systems.

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  • (PMID = 28015893.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Berman B, Poochareon VN, Villa AM: Novel dermatologic uses of the immune response modifier imiquimod 5% cream. Skin Therapy Lett; 2002 Nov;7(9):1-6
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  • Imiquimod is the first of a new class of drugs to emerge in the treatment of various dermatologic disorders.
  • It is currently approved for the treatment of external genital and perianal warts, but has also been found to be an effective treatment for a host of other virus-associated dermatologic lesions, including common and flat warts, molluscum contagiosum and herpes simples 2.
  • Oncological lesions showing improvement with the use of imiquimod include basal cell carcinoma, actinic keratosis, squamous cell carcinoma in situ, malignant melanoma, cutaneous T-cell lymphoma, and cutaneous extramammary Paget's disease.
  • This extensive array of disorders treated successfully with imiquimod warrants further study of this novel and valuable drug.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Aminoquinolines / therapeutic use. Skin Diseases / drug therapy

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  • (PMID = 12548325.001).
  • [ISSN] 1201-5989
  • [Journal-full-title] Skin therapy letter
  • [ISO-abbreviation] Skin Therapy Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 99011-02-6 / imiquimod
  • [Number-of-references] 53
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15. Garraway LA, Widlund HR, Rubin MA, Getz G, Berger AJ, Ramaswamy S, Beroukhim R, Milner DA, Granter SR, Du J, Lee C, Wagner SN, Li C, Golub TR, Rimm DL, Meyerson ML, Fisher DE, Sellers WR: Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma. Nature; 2005 Jul 7;436(7047):117-22
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  • [Title] Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma.
  • Here, by integrating SNP array-based genetic maps with gene expression signatures derived from NCI60 cell lines, we identified the melanocyte master regulator MITF (microphthalmia-associated transcription factor) as the target of a novel melanoma amplification.
  • BRAF mutation and p16 inactivation accompanied MITF amplification in melanoma cell lines.
  • Ectopic MITF expression in conjunction with the BRAF(V600E) mutant transformed primary human melanocytes, and thus MITF can function as a melanoma oncogene.
  • Reduction of MITF activity sensitizes melanoma cells to chemotherapeutic agents.
  • Targeting MITF in combination with BRAF or cyclin-dependent kinase inhibitors may offer a rational therapeutic avenue into melanoma, a highly chemotherapy-resistant neoplasm.
  • Together, these data suggest that MITF represents a distinct class of 'lineage survival' or 'lineage addiction' oncogenes required for both tissue-specific cancer development and tumour progression.
  • [MeSH-major] Cell Lineage. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Genomics. Melanoma / genetics. Melanoma / pathology. Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Chromosomes, Human, Pair 3 / genetics. Disease Progression. Gene Dosage. Gene Expression Regulation, Neoplastic. Humans. In Situ Hybridization, Fluorescence. Microphthalmia-Associated Transcription Factor. Polymerase Chain Reaction. Polymorphism, Single Nucleotide / genetics


16. Mustika R, Budiyanto A, Nishigori C, Ichihashi M, Ueda M: Decreased expression of Apaf-1 with progression of melanoma. Pigment Cell Res; 2005 Feb;18(1):59-62
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  • [Title] Decreased expression of Apaf-1 with progression of melanoma.
  • Defects in apoptotic system may contribute in the pathogenesis and resistance of malignant melanoma cells to chemotherapy.
  • It is not known, however, whether Apaf-1 protein is lost during melanoma progression from localized to metastatic tumor.
  • To this end, we evaluated Apaf-1 protein expression by immunohistochemistry in 10 cases of human nevi, 11 melanomas in situ, 26 primary melanomas and 15 metastases.
  • These data demonstrated that there is an inverse correlation between Apaf-1 expression and pathologic stage of melanoma.
  • This suggests that the decreased expression of Apaf-1 seen in correlation with melanoma progression renders melanoma more resistant to chemotherapy.

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  • (PMID = 15649154.001).
  • [ISSN] 0893-5785
  • [Journal-full-title] Pigment cell research
  • [ISO-abbreviation] Pigment Cell Res.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / APAF1 protein, human; 0 / Apoptotic Protease-Activating Factor 1; 0 / Biomarkers, Tumor; 0 / Proteins
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17. Giudice S, Benassi L, Bertazzoni G, Costi MP, Gelain A, Venturelli A, Bernardi C, Gualdi G, Coppi A, Rossi T, Giannetti A, Magnoni C: New thymidylate synthase inhibitors induce apoptosis in melanoma cell lines. Toxicol In Vitro; 2007 Mar;21(2):240-8
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  • [Title] New thymidylate synthase inhibitors induce apoptosis in melanoma cell lines.
  • Malignant melanoma is particularly resistant to conventional chemotherapy and radiotherapy.
  • For this reason in the past years a huge variety of new compounds has been developed with potential chemotherapeutic activity which needs to be tested in vitro and in vivo.
  • The response of two melanoma cell lines (SK-MEL-2 derived from malignant melanoma metastasis and SK-MEL-28 derived from primary malignant melanoma) was examined after treatment with these substances.
  • These results were supported by the use of the pan-caspases inhibitor Z-VAD-FMK that almost completely decreased the amount of apoptosis in both the melanoma cell lines treated with antifolate.
  • [MeSH-major] Apoptosis / drug effects. Enzyme Inhibitors / pharmacology. Melanoma / drug therapy. Thymidylate Synthase / antagonists & inhibitors
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Caspase 8 / metabolism. Caspase 9 / metabolism. Cell Line, Tumor. DNA Fragmentation / drug effects. Folic Acid Antagonists / pharmacology. Humans. In Situ Nick-End Labeling. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Tumor Suppressor Protein p53 / physiology. bcl-2-Associated X Protein / physiology

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  • (PMID = 17118621.001).
  • [ISSN] 1879-3177
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / BAX protein, human; 0 / Enzyme Inhibitors; 0 / Folic Acid Antagonists; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; EC 2.1.1.45 / Thymidylate Synthase; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9
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18. Stern RS, PUVA Follow up Study: The risk of melanoma in association with long-term exposure to PUVA. J Am Acad Dermatol; 2001 May;44(5):755-61
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  • [Title] The risk of melanoma in association with long-term exposure to PUVA.
  • BACKGROUND: Oral methoxsalen (psoralen) and ultraviolet A radiation (PUVA) is a highly effective therapy for psoriasis and many other skin conditions.
  • Previously we reported an increased risk of melanoma that first emerged 15 years after first treatment.
  • OBJECTIVE: Our purpose is to present additional data concerning the associations of previous exposure to PUVA, the passage of time, and the risk of malignant melanoma.
  • We have documented the occurrence of melanoma and in this report compare the observed and expected incidence of melanoma in this cohort, particularly melanomas developing since our earlier report (ie, after March 1996).
  • RESULTS: Since 1975, 23 patients have developed 26 invasive or in situ cutaneous melanomas.
  • CONCLUSION: Beginning 15 years after first exposure to PUVA, an increased risk of melanoma is observed in our cohort of PUVA-treated patients.
  • This risk is greater in patients exposed to high doses of PUVA, appears to be increasing with the passage of time, and should be considered in determining the risks and benefits of this therapy.
  • [MeSH-major] Melanoma / chemically induced. Melanoma / epidemiology. PUVA Therapy / adverse effects. Psoriasis / drug therapy. Skin Neoplasms / chemically induced. Skin Neoplasms / epidemiology

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  • (PMID = 11312420.001).
  • [ISSN] 0190-9622
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / N01-AR-0-2246; United States / NIAMS NIH HHS / AR / N01-AR-4-2214
  • [Publication-type] Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] U4VJ29L7BQ / Methoxsalen
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19. Chevalier J, Bonastre J, Avril MF: The economic burden of melanoma in France: assessing healthcare use in a hospital setting. Melanoma Res; 2008 Feb;18(1):40-6
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  • [Title] The economic burden of melanoma in France: assessing healthcare use in a hospital setting.
  • The objective of this experiment was to describe healthcare use for the treatment of melanoma in a hospital setting and to assess the related annual cost using French hospital records for the year 2004.
  • Hospital stays related to melanoma care were extracted from this database, which exhaustively records hospital stays in the country.
  • We selected stays that included at least one diagnosis of melanoma: International Classification of Diseases (ICD)-10 codes C43 'malignant melanoma of skin' or D03 'melanoma in situ'.
  • For each diagnosis-related group involved in melanoma care, we calculated an average cost per day from this database.
  • Unit costs were then applied to the duration of each hospital stay related to melanoma from the 2004 national database.
  • A total of 42,911 stays related to melanoma were identified for the year 2004.
  • New patients, estimated by the number of surgical stays with a melanoma ICD code as the main diagnosis, amounted to 6897.
  • Annual hospital costs for melanoma care were estimated at 59 million euros.
  • The main cost drivers were surgery (38% of hospital costs), follow-up evaluations (20%) and chemotherapy (17%).
  • It was concluded that the impact of melanoma on hospital expenditures for cancer was modest.
  • Hospital costs for stays related to melanoma represented less than 1% of total annual hospital costs for cancer for the year 2004.
  • [MeSH-major] Delivery of Health Care / utilization. Hospital Costs. Melanoma / economics. Patient Care / economics. Skin Neoplasms / economics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Child. Child, Preschool. Cost-Benefit Analysis. Female. Follow-Up Studies. France / epidemiology. Humans. Infant. Infant, Newborn. Male. Middle Aged. Radiotherapy, Computer-Assisted

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  • (PMID = 18227707.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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20. Ito A, Saito H, Mitobe K, Minamiya Y, Takahashi N, Maruyama K, Motoyama S, Katayose Y, Ogawa J: Inhibition of heat shock protein 90 sensitizes melanoma cells to thermosensitive ferromagnetic particle-mediated hyperthermia with low Curie temperature. Cancer Sci; 2009 Mar;100(3):558-64
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  • [Title] Inhibition of heat shock protein 90 sensitizes melanoma cells to thermosensitive ferromagnetic particle-mediated hyperthermia with low Curie temperature.
  • Heat shock protein (Hsp) 90 is a key regulator of a variety of oncogene products and cell-signaling molecules, and the therapeutic benefit of its inhibition in combination with radiation or chemotherapy has been investigated.
  • In addition, hyperthermia has been used for many years to treat various malignant tumors.
  • We previously described a system in which hyperthermia was induced using thermosensitive ferromagnetic particles (FMP) with a Curie temperature (Tc = 43 degrees C) low enough to mediate automatic temperature control, and demonstrated its antitumor effect in a mouse melanoma model.
  • In cultured B16 melanoma cells, GA exerted an antitumor effect by increasing the cells' susceptibility to hyperthermia and reducing expression of Akt.
  • In an in vivo study, melanoma cells were subcutaneously injected into the backs of C57BL/6 mice.
  • FMP were then injected into the resultant tumors, and the mice were divided into four groups: group I, no treatment (control); group II, one hyperthermia treatment; group III, GA alone; and group IV, GA with hyperthermia.
  • When exposed to a magnetic field, the temperature of tissues containing FMP increased and stabilized at the Tc.
  • Thus, the combination of FMP-mediated, self-regulating hyperthermia with Hsp90 inhibition has important implications for the treatment of cancer.
  • [MeSH-major] Ferric Compounds / therapeutic use. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Hyperthermia, Induced / methods. Melanoma, Experimental / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / administration & dosage. Benzoquinones / administration & dosage. Blotting, Western. Cell Line, Tumor. Combined Modality Therapy. Female. In Situ Nick-End Labeling. Lactams, Macrocyclic / administration & dosage. Mice. Mice, Inbred C57BL. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 19154416.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Benzoquinones; 0 / Ferric Compounds; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 1317-54-0 / ferrite; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; Z3K3VJ16KU / geldanamycin
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21. Yan H, Thomas J, Liu T, Raj D, London N, Tandeski T, Leachman SA, Lee RM, Grossman D: Induction of melanoma cell apoptosis and inhibition of tumor growth using a cell-permeable Survivin antagonist. Oncogene; 2006 Nov 2;25(52):6968-74
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  • [Title] Induction of melanoma cell apoptosis and inhibition of tumor growth using a cell-permeable Survivin antagonist.
  • The inhibitor of apoptosis gene family member Survivin is highly expressed in most tumors, and appears to be a promising target for cancer therapy.
  • Although a variety of Survivin antagonists have been shown to induce apoptosis in malignant cells, the potential utility of these agents is limited by inefficient delivery and cell impermeability.
  • We generated recombinant fusion proteins containing the TAT protein transduction domain and either wild-type Survivin (TAT-Surv-WT) or a dominant-negative mutant (TAT-Surv-T34A).
  • Whereas TAT-Surv-WT had minimal effect on YUSAC2 or WM793 melanoma cells, TAT-Surv-T34A induced cell detachment, DNA fragmentation, caspase-3 activation and mitochondrial release of apoptosis-inducing factor at low microM concentrations.
  • Intraperitoneal (i.p.) injection of mice bearing subcutaneous YUSAC2 xenografts with TAT-Surv-T34A (10 mg/kg) was associated with rapid tumor accumulation at 1 h, and increased tumor cell apoptosis and aberrant nuclei formation in situ.
  • These studies demonstrate the feasibility of systemic tumor treatment using a cell-permeable Survivin antagonist.

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  • (PMID = 16702945.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / AR050102-03; United States / NIAMS NIH HHS / AR / R01 AR050102; United States / NIAMS NIH HHS / AR / AR050102; United States / NIAMS NIH HHS / AR / R01 AR050102-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Gene Products, tat; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Fusion Proteins
  • [Other-IDs] NLM/ NIHMS44270; NLM/ PMC2292411
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22. Lugini L, Lozupone F, Matarrese P, Funaro C, Luciani F, Malorni W, Rivoltini L, Castelli C, Tinari A, Piris A, Parmiani G, Fais S: Potent phagocytic activity discriminates metastatic and primary human malignant melanomas: a key role of ezrin. Lab Invest; 2003 Nov;83(11):1555-67
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  • [Title] Potent phagocytic activity discriminates metastatic and primary human malignant melanomas: a key role of ezrin.
  • To address the phenomenon of phagocytosis, its underlying mechanism(s), and its possible role in tumor biology, we used human melanoma cells as a prototypic model.
  • Our results showed that a process of phagocytosis of apoptotic cells occurs in vivo in human melanoma.
  • This finding was consistent with evidence that human melanoma cells in vitro express all of the known lysosomal and phagocytic markers on their cytoplasmic vesicles and that a process of phagocytosis occurs in these vesicles.
  • However, exclusively human melanoma cells deriving from metastatic lesions possess an efficient phagocytic machinery responsible for a macrophage-like activity against latex beads, yeast, and apoptotic cells of different origins, which was comparable to that of human primary macrophages.
  • Moreover, the actin-binding protein ezrin was expressed on phagocytic vacuoles of melanoma cells and of cells deriving from a human adenocarcinoma; both treatment with cytochalasin B and specific inhibition of ezrin synthesis strongly affected the phagocytic activity of melanoma cells.
  • Hence our data provide evidence for a potent phagocytic activity exerted by metastatic melanoma cells possibly involved in determining the level of aggressiveness of human melanoma.
  • This suggests that the assessment of phagocytic activity may be exploited as a new tool to evaluate the malignancy of human melanoma.
  • Moreover, our data suggest that gene therapy or drug treatments aimed at inhibiting actin assembly to the phagosomal membranes may be proposed as a new strategy for the control of tumor aggressiveness.
  • [MeSH-major] Melanoma / metabolism. Neurofibromin 2 / metabolism. Phagocytosis / physiology. Skin Neoplasms / metabolism
  • [MeSH-minor] Apoptosis / physiology. Biomarkers / analysis. Cell Line, Tumor. Cytoskeleton / physiology. Flow Cytometry. Humans. Immunoenzyme Techniques. In Situ Nick-End Labeling

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  • (PMID = 14615410.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Neurofibromin 2
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23. Wolf IH, Kodama K, Cerroni L, Kerl H: Nature of inflammatory infiltrate in superficial cutaneous malignancies during topical imiquimod treatment. Am J Dermatopathol; 2007 Jun;29(3):237-41
Hazardous Substances Data Bank. Imiquimod .

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  • [Title] Nature of inflammatory infiltrate in superficial cutaneous malignancies during topical imiquimod treatment.
  • Topical imiquimod (IQ) is an effective treatment for genital warts and various malignant tumors of the skin.
  • We investigated the composition of the inflammatory cell infiltrate before, during, and after the treatment of 10 superficial cutaneous malignancies (melanoma in situ (n = 4), melanoma metastasis (n = 1), squamous cell carcinoma in situ (n = 4), and basal cell carcinoma (n = 1) with 5% IQ cream.
  • Immunophenotyping revealed in all cases during treatment an increased population of T-lymphocytes positive for CD3, CD4 and CD8, as well as a considerable number of cytotoxic cells (TIA-1+, granzyme B+) and plasmacytoid dendritic cells (CD 123+).
  • The population of infiltrative inflammatory cells was similar in all patients irrespective of the type of tumor.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Aminoquinolines / therapeutic use. Inflammation / pathology. Melanoma / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Bowen's Disease / chemistry. Bowen's Disease / drug therapy. Bowen's Disease / pathology. Carcinoma in Situ / chemistry. Carcinoma in Situ / drug therapy. Carcinoma in Situ / pathology. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / pathology. Female. Humans. Hutchinson's Melanotic Freckle / chemistry. Hutchinson's Melanotic Freckle / drug therapy. Hutchinson's Melanotic Freckle / pathology. Keratosis / drug therapy. Keratosis / metabolism. Keratosis / pathology. Male. Middle Aged

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  • (PMID = 17519620.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Biomarkers, Tumor; 99011-02-6 / imiquimod
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24. Dessars B, De Raeve LE, Morandini R, Lefort A, El Housni H, Ghanem GE, Van den Eynde BJ, Ma W, Roseeuw D, Vassart G, Libert F, Heimann P: Genotypic and gene expression studies in congenital melanocytic nevi: insight into initial steps of melanotumorigenesis. J Invest Dermatol; 2009 Jan;129(1):139-47
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  • Large congenital melanocytic nevi (CMNs) are said to have a higher propensity to malignant transformation compared with acquired nevi.
  • We have performed genotypic (karyotype, fluorescence in situ hybridization, and mutational analyses) and differential expression studies on a large cohort of medium (n=3) and large (n=24) CMN.
  • Furthermore, the observed alterations linked to chemoresistance might partially account for the well-known inefficacy of chemotherapy in malignant melanoma.
  • [MeSH-minor] Cell Movement. Cell Proliferation. Chromosome Aberrations. Cohort Studies. DNA Mutational Analysis. Genotype. Humans. In Situ Hybridization. In Situ Hybridization, Fluorescence. Karyotyping. Neoplasm Invasiveness. Neovascularization, Pathologic


25. Antonescu CR, Busam KJ, Francone TD, Wong GC, Guo T, Agaram NP, Besmer P, Jungbluth A, Gimbel M, Chen CT, Veach D, Clarkson BD, Paty PB, Weiser MR: L576P KIT mutation in anal melanomas correlates with KIT protein expression and is sensitive to specific kinase inhibition. Int J Cancer; 2007 Jul 15;121(2):257-64
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  • Activating mutations in either BRAF or NRAS are seen in a significant number of malignant melanomas, but their incidence appears to be dependent to ultraviolet light exposure.
  • More recently, activating KIT mutations have been described in rare cases of metastatic melanoma, without further reference to their clinical phenotypes.
  • In vitro drug testing of stable transformant Ba/F3 KIT(L576P) mutant cells showed sensitivity for dasatinib (previously known as BMS-354825), a dual SRC/ABL kinase inhibitor, and imatinib.
  • These results suggest that a subset of anal melanomas show activating KIT mutations, which are susceptible for therapy with specific kinase inhibitors.

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17372901.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA047179; United States / NCI NIH HHS / CA / P01 CA064593; United States / NCI NIH HHS / CA / P30 CA008748; United States / NIDDK NIH HHS / DK / HL/DK55748
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; RBZ1571X5H / Dasatinib
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26. Khong JJ, Muecke J: Complications of mitomycin C therapy in 100 eyes with ocular surface neoplasia. Br J Ophthalmol; 2006 Jul;90(7):819-22
Hazardous Substances Data Bank. MITOMYCIN C .

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  • [Title] Complications of mitomycin C therapy in 100 eyes with ocular surface neoplasia.
  • AIM: To determine the complications associated with mitomycin C (MMC) in the treatment of ocular surface neoplasia.
  • Outcome measures included complications of MMC and the treatment required for these complications.
  • RESULTS: One to three 7 day cycles of topical MMC 0.04% four times a day were given to 59 eyes with localised corneal-conjunctival intraepithelial neoplasia (CIN), 19 eyes with diffuse CIN, six eyes with recurrent CIN, one eye with ocular surface squamous cell carcinoma, three eyes with primary acquired melanosis (PAM) with atypia, nine eyes with conjunctival malignant melanoma (MM), two eyes with sebaceous carcinoma with pagetoid spread, and one eye with recurrent atypical fibroxanthoma.
  • 31 (34%) cases developed an allergic reaction to MMC and 14 (14%) eyes had epiphora secondary to punctal stenosis at a mean follow up period of 26.5 months.
  • CONCLUSION: In the largest study looking at complications of topical MMC in the treatment of ocular surface neoplasia, allergic reaction and punctal stenosis are relatively common.
  • [MeSH-major] Antibiotics, Antineoplastic / adverse effects. Drug Hypersensitivity / etiology. Eye Neoplasms / drug therapy. Mitomycin / adverse effects
  • [MeSH-minor] Adenocarcinoma, Sebaceous / drug therapy. Carcinoma in Situ / drug therapy. Carcinoma, Squamous Cell / drug therapy. Conjunctival Neoplasms / drug therapy. Corneal Diseases / drug therapy. Female. Follow-Up Studies. Histiocytoma, Benign Fibrous / drug therapy. Humans. Lacrimal Apparatus Diseases / chemically induced. Lacrimal Duct Obstruction / chemically induced. Male. Melanoma / drug therapy. Melanosis / drug therapy. Retrospective Studies

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  • (PMID = 16672325.001).
  • [ISSN] 0007-1161
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin
  • [Other-IDs] NLM/ PMC1857172
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27. Cartsburg O, Kallen C, Hillenkamp J, Sundmacher R, Pomjanski N, Böcking A: Topical mitomycin C and radiation induce conjunctival DNA-polyploidy. Anal Cell Pathol; 2001;23(2):65-74
Hazardous Substances Data Bank. MITOMYCIN C .

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  • INTRODUCTION: Atypical cell changes often occur following treatment of premalignant or malignant conjunctival neoplasias with topical mitomycin C (MMC) and/or radiation.
  • Our aim was to investigate changes in the nuclear DNA-distribution of conjunctival epithelial cells after MMC- and radiation therapy by DNA-image-cytometry.
  • METHODS: Conjunctival brush smears were obtained from 13 patients (13 eyes) with squamous cell carcinomas and six patients (6 eyes) with conjunctival malignant melanomas in situ before, during and after treatment.
  • The patients were treated with MMC-drops (0.02% or 0.04%) alone (n=12), with radiation therapy (n=3) or both (n=4).
  • We considered these alterations as reactive to treatment.
  • CONCLUSION: Measurements of DNA-content revealed euploid polyploidisation of morphological suspicious but benign squamous cells which is the biologic correlate of well known secondary morphologic changes following topical chemotherapy and/or radiation.
  • DNA-image-cytometry is a useful tool in the differention of euploid polyploidization as a sign of reactive cell changes following treatment and tumor recurrences.
  • [MeSH-major] Antibiotics, Antineoplastic / adverse effects. Conjunctival Neoplasms / drug therapy. Conjunctival Neoplasms / pathology. Melanoma / drug therapy. Melanoma / pathology. Mitomycin / adverse effects
  • [MeSH-minor] Adult. Aged. Biopsy. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / radiotherapy. Combined Modality Therapy. Conjunctiva / pathology. Humans. Middle Aged. Neoplasm Recurrence, Local. Polyploidy

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  • (PMID = 11904462.001).
  • [ISSN] 0921-8912
  • [Journal-full-title] Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology
  • [ISO-abbreviation] Anal Cell Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin
  • [Other-IDs] NLM/ PMC4617513
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28. Stefanidou M, Tosca A, Themelis G, Vazgiouraki E, Balas C: In vivo fluorescence kinetics and photodynamic therapy efficacy of delta-aminolevulinic acid-induced porphyrins in basal cell carcinomas and actinic keratoses; implications for optimization of photodynamic therapy. Eur J Dermatol; 2000 Jul-Aug;10(5):351-6
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  • [Title] In vivo fluorescence kinetics and photodynamic therapy efficacy of delta-aminolevulinic acid-induced porphyrins in basal cell carcinomas and actinic keratoses; implications for optimization of photodynamic therapy.
  • Photodynamic therapy (PDT) with topical d-aminolevulinic acid (ALA) has become a therapeutic option of growing interest for superficial non-melanoma precancerous and malignant lesions.
  • After application of ALA, in situ conversion to endogenous porphyrins is accomplished in a gradual manner.
  • Therefore, the determination of fluorescence kinetics and spatial distribution in vivo versus time is a crucial point for the success of ALA-PDT.
  • In vivo spatial and quantitative detection of the fluorescence intensity versus time showed considerable variations among tumors of the same type, so light irradiation was performed according to patient individualities.
  • The results of fluorescence studies suggest that optimum irradiation time for BCC is approximately 3.5-5 hrs and for AK 5 hrs after ALA application, when relative maximal fluorescence intensity in correlation with fluorescence selectivity on the lesion, is obtained.
  • [MeSH-major] Aminolevulinic Acid / therapeutic use. Carcinoma, Basal Cell / drug therapy. Keratosis / drug therapy. Photochemotherapy. Photosensitizing Agents / therapeutic use. Porphyrins / metabolism. Precancerous Conditions / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Aged. Female. Fluorescence. Head and Neck Neoplasms / drug therapy. Humans. Kinetics. Male. Time Factors. Treatment Outcome

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  • (PMID = 10882942.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] FRANCE
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Porphyrins; 88755TAZ87 / Aminolevulinic Acid
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29. Senés AT, Badet L, Lyonnet D, Rouvière O: Granulomatous renal masses following intravesical bacillus Calmette Guérin therapy: the central unaffected calyx sign. Br J Radiol; 2007 Oct;80(958):e230-3
MedlinePlus Health Information. consumer health - Kidney Diseases.

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  • [Title] Granulomatous renal masses following intravesical bacillus Calmette Guérin therapy: the central unaffected calyx sign.
  • A 67-year-old man with a history of melanoma, treated surgically 7 years before, was referred for vomiting and right flank pain after three intravesical instillations of bacillus Calmette-Guérin (BCG) for superficial bladder cancer.
  • Percutaneous biopsy, obtained because of melanoma history, showed granulomatous reaction caused by BCG infection.
  • The renal mass disappeared after 9 months of anti-tuberculous treatment.
  • The presence of an unaffected calyx in the centre of the renal mass is an interesting finding for both teaching purposes--it clearly illustrates the pathogeny of the disease, with the bacillus invading the renal parenchyma through the papilla--and diagnostic purposes--a malignant tumour is likely to displace or destroy neighbouring calyces rather than leaving them unaffected.
  • [MeSH-minor] Administration, Intravesical. Aged. Carcinoma in Situ / drug therapy. Carcinoma, Transitional Cell / drug therapy. Humans. Male. Tomography, X-Ray Computed. Urinary Bladder Neoplasms / drug therapy

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  • (PMID = 17959911.001).
  • [ISSN] 1748-880X
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / BCG Vaccine
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30. Shin SJ, DeLellis RA, Ying L, Rosen PP: Small cell carcinoma of the breast: a clinicopathologic and immunohistochemical study of nine patients. Am J Surg Pathol; 2000 Sep;24(9):1231-8
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  • Two patients had a previous history of cutaneous malignant melanoma and one had prior lobular carcinoma in situ and atypical duct hyperplasia in the same breast as the small cell carcinoma.
  • An in situ component was seen in seven tumors; five were of the small cell type in ducts and two were of the ductal type with high nuclear grade.
  • Seven patients received adjuvant chemotherapy and four patients received radiation.
  • Two patients also received tamoxifen treatment.
  • Metastases developed in two patients (22%) with a follow-up period of 11 and 32 months.
  • All patients were alive at last follow up 3 to 35 months after treatment.
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Immunohistochemistry. Keratins / metabolism. Middle Aged. Receptors, Estrogen / metabolism

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  • [CommentIn] Am J Surg Pathol. 2001 Jun;25(6):831-2 [11395567.001]
  • (PMID = 10976697.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 68238-35-7 / Keratins
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31. Singh N, Jani PD, Suthar T, Amin S, Ambati BK: Flt-1 intraceptor induces the unfolded protein response, apoptotic factors, and regression of murine injury-induced corneal neovascularization. Invest Ophthalmol Vis Sci; 2006 Nov;47(11):4787-93
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  • Human malignant melanoma cells (which express VEGFR-2 but not Flt), were transfected with pCMV.Flt24K, and lysates underwent immunoprecipitation with anti-FLT antibody, and Western blot analysis for VEGF and VEGFR-2.
  • [MeSH-major] Apoptosis. Burns, Chemical / drug therapy. Corneal Neovascularization / drug therapy. DNA-Binding Proteins / metabolism. Endothelium, Vascular / pathology. Eye Burns / chemically induced. Nuclear Proteins / metabolism. Vascular Endothelial Growth Factor Receptor-1 / physiology
  • [MeSH-minor] Animals. Blotting, Western. Caspase 12 / metabolism. Caspase 3 / metabolism. Cornea / drug effects. Cornea / metabolism. Genetic Vectors. Humans. In Situ Nick-End Labeling. Mice. Mice, Inbred BALB C. Receptors, Peptide / physiology. Recombinant Fusion Proteins / physiology. Reverse Transcriptase Polymerase Chain Reaction. Sodium Hydroxide / toxicity. Transcription Factors. Transfection. Vascular Endothelial Growth Factor Receptor-2 / metabolism

  • Hazardous Substances Data Bank. SODIUM HYDROXIDE .
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  • [ErratumIn] Invest Ophthalmol Vis Sci. 2007 Nov;48(11):4900
  • (PMID = 17065489.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / KDEL receptor; 0 / Nuclear Proteins; 0 / Receptors, Peptide; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / regulatory factor X transcription factors; 55X04QC32I / Sodium Hydroxide; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.4.22.- / Caspase 12; EC 3.4.22.- / Caspase 3
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32. Albert A, Cruz O, Montaner A, Vela A, Badosa J, Castañón M, Morales L: [Congenital solid tumors. A thirteen-year review]. Cir Pediatr; 2004 Jul;17(3):133-6
MedlinePlus Health Information. consumer health - Wilms Tumor.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This is an interesting group of tumors because their type, relative incidence, natural history and response to treatment differ from those seen in older children.
  • Treatment was surgical resection alone in 17 cases (68%) and surgery + chemotherapy in 8 (32%) (5 neuroblastomas, one CNS tumor, one Wilms tumor and one presacral teratoma who developed a yolk sac tumor); 3 patients died (11%): one at surgery, one of tumoural airway obstruction at birth and one with craniopharyngioma.
  • Among the 14 tumors that were initially not malignant, two can be locally agressive, one was an immature teratoma, the giant nevus with hamartoma developed in situ melanoma, the other nevus had meningeal melanosis with hydrocephalus, and one mature presacral teratoma developed a yolk sac tumor.
  • Complete surgical excision is the treatment of choice, most cases not need adjuvant chemotherapy.
  • [MeSH-major] Central Nervous System Neoplasms / congenital. Kidney Neoplasms / congenital. Liver Neoplasms / congenital. Neuroblastoma / congenital. Skin Neoplasms / congenital. Soft Tissue Neoplasms / congenital. Teratoma / congenital. Wilms Tumor / congenital
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Infant, Newborn. Male. Neoplasm Recurrence, Local. Postoperative Complications. Pregnancy. Prenatal Diagnosis. Time Factors

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  • (PMID = 15503950.001).
  • [ISSN] 0214-1221
  • [Journal-full-title] Cirugía pediátrica : organo oficial de la Sociedad Española de Cirugía Pediátrica
  • [ISO-abbreviation] Cir Pediatr
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
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33. Michalopoulos P, Yawalkar N, Brönnimann M, Kappeler A, Braathen LR: Characterization of the cellular infiltrate during successful topical treatment of lentigo maligna with imiquimod. Br J Dermatol; 2004 Oct;151(4):903-6
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of the cellular infiltrate during successful topical treatment of lentigo maligna with imiquimod.
  • Lentigo maligna (LM) is an in situ melanoma which usually occurs in sun-damaged skin on the head and neck of elderly patients.
  • Depending on the anatomical site and its size treatment of LM can be problematic and usually includes surgical excision or radiotherapy.
  • Recent reports indicate that topical imiquimod may be an effective treatment.
  • However, no data on the underlying immune response in the skin during treatment of LM with topical imiquimod are available so far.
  • Skin biopsy specimens were obtained before, during (at week 10) and 4 weeks after cessation of topical treatment with imiquimod 5% cream.
  • A complete clinical and histological clearance of the skin lesion was achieved, with no recurrence up to 9 months after the end of treatment.
  • In conclusion, our data indicate that imiquimod 5% cream induces a cytotoxic T-cell-mediated immune response in situ which may account for the complete destruction of the malignant melanocytes in LM.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Facial Neoplasms / drug therapy. Hutchinson's Melanotic Freckle / drug therapy. Skin Neoplasms / drug therapy. T-Lymphocyte Subsets / drug effects

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  • (PMID = 15491436.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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34. DeBoyes T, Kouba D, Ozog D, Fincher E, Moy L, Iwata K, Moy R: Reduced number of actinic keratoses with topical application of DNA repair enzyme creams. J Drugs Dermatol; 2010 Dec;9(12):1519-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Actinic keratosis is regarded as a carcinoma in situ by some dermatologists and its incidence continues to rise.
  • Exposure to ultraviolet (UV) radiation is considered to be an important risk factor for developing these pre-malignant lesions.
  • DNA repair enzymes have been shown to reverse sun-damage, resulting in reduced rates of actinic keratoses and non-melanoma skin cancers in specific patient populations.
  • RESULTS: Compared to baseline, a statistically significant reduction in the number of actinic keratoses was seen following the treatment period.
  • [MeSH-major] DNA Repair Enzymes / therapeutic use. Deoxyribonuclease (Pyrimidine Dimer) / therapeutic use. Keratosis, Actinic / drug therapy. Viral Proteins / therapeutic use

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  • (PMID = 21120260.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Liposomes; 0 / Viral Proteins; 0 / endonuclease V, phage T4; EC 3.1.25.1 / Deoxyribonuclease (Pyrimidine Dimer); EC 6.5.1.- / DNA Repair Enzymes
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35. Fleming CJ, Bryden AM, Evans A, Dawe RS, Ibbotson SH: A pilot study of treatment of lentigo maligna with 5% imiquimod cream. Br J Dermatol; 2004 Aug;151(2):485-8
Hazardous Substances Data Bank. Imiquimod .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A pilot study of treatment of lentigo maligna with 5% imiquimod cream.
  • BACKGROUND: Lentigo maligna (LM) is an in situ form of malignant melanoma, and surgical excision is often unsatisfactory.
  • Imiquimod cream is an immune response modifier and induces a predominantly T-helper 1 type response.
  • OBJECTIVES: Assessment of histological and clinical response of surgically resectable LM after treatment with 5% imiquimod cream.
  • RESULTS: Complete or almost complete clearance of pigmentation with minimal residual histological evidence of LM was observed in four patients, one patient showed no clinical or histological improvement, and the remaining patient had almost no residual pigmentation clinically after treatment yet histopathological changes remained as severe as before treatment.
  • CONCLUSIONS: Topical imiquimod cream merits further investigation as a new therapy for LM.
  • [MeSH-major] Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Hutchinson's Melanotic Freckle / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Adult. Aged. Humans. Middle Aged. Pilot Projects. Treatment Outcome

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  • (PMID = 15327559.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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36. Díaz JM, Guirado L, Facundo C, García-Maset R, Solà R: [Assessment of the living renal donor. Analysis of extra-renal pathology as a limitation for donation]. Nefrologia; 2005;25 Suppl 2:51-6
HIV InSite. treatment guidelines - Cardiac Cardiac Manifestations of HIV .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The donation is only reasonable when hypertension is well controlled with less than two drugs.
  • Diabetes mellitus is an absolute contraindication to living donation such as an impaired glucose tolerance or impaired fasting glucose with a family history of type 2 diabetes mellitus.
  • Another contraindication to living donation is malignant disease, and the same standards should be adopted for cadaveric donors.
  • The exceptions are low-grade non-melanoma skin cancer and carcinoma in situ of the uterine cervix.
  • CMV donor and recipient status should be taken into account before transplantation, and the recipients at risk for CMV disease should recieve prophylactic treatment according to the transplant unit policy.
  • [MeSH-minor] Age Factors. Aged. Blood Glucose / analysis. Body Mass Index. Cadaver. Diabetes Mellitus, Type 2 / complications. Female. Humans. Hypertension / complications. Hypertension / drug therapy. Infection / complications. Male. Middle Aged. Neoplasms / complications. Nephrectomy. Postoperative Complications. Virus Diseases / complications. Weight Loss

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  • (PMID = 16050403.001).
  • [ISSN] 0211-6995
  • [Journal-full-title] Nefrología : publicación oficial de la Sociedad Española Nefrologia
  • [ISO-abbreviation] Nefrologia
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Blood Glucose
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