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1. Wilkins K, Turner R, Dolev JC, LeBoit PE, Berger TG, Maurer TA: Cutaneous malignancy and human immunodeficiency virus disease. J Am Acad Dermatol; 2006 Feb;54(2):189-206; quiz 207-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Certain skin cancers occur with increased frequency or altered course in patients infected with HIV.
  • Malignant melanoma and squamous cell carcinoma are examples of cutaneous malignancies that have a more aggressive course in patients with HIV.
  • Others, such as basal cell carcinoma, appear more frequently in this population but do not appear to be more aggressive.
  • Cutaneous T-cell lymphoma (CTCL) is rare in this population.
  • [MeSH-major] HIV Infections / epidemiology. Skin Neoplasms / epidemiology
  • [MeSH-minor] Algorithms. Animals. Anti-Retroviral Agents / administration & dosage. Anus Neoplasms / epidemiology. Anus Neoplasms / pathology. Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / therapy. Herpesviridae Infections / epidemiology. Herpesvirus 8, Human / isolation & purification. Humans. Immunity, Cellular. Immunohistochemistry. Lymphoma, Large-Cell, Anaplastic / epidemiology. Lymphoma, T-Cell, Cutaneous / epidemiology. Lymphoma, T-Cell, Cutaneous / immunology. Lymphoma, T-Cell, Cutaneous / pathology. Melanoma / epidemiology. Melanoma / therapy. Papillomaviridae. Papillomavirus Infections / epidemiology. Risk Factors. Sarcoma, Kaposi / drug therapy. Sarcoma, Kaposi / epidemiology. Seroepidemiologic Studies

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  • (PMID = 16443048.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Retroviral Agents
  • [Number-of-references] 274
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2. Genther Williams SM, Disbrow GL, Schlegel R, Lee D, Threadgill DW, Lambert PF: Requirement of epidermal growth factor receptor for hyperplasia induced by E5, a high-risk human papillomavirus oncogene. Cancer Res; 2005 Aug 1;65(15):6534-42
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  • Alterations in the expression or function of any one of these factors can contribute to disease, including cancer.
  • Many viruses have been implicated in cancer, and some of these modulate cellular signal transduction cascades to carry out their life cycles.
  • High-risk human papillomaviruses (HPVs), the causative agents of most cervical and anogenital cancers, encode three oncogenes.
  • In this study, we generate and characterize transgenic mice in which the E5 gene of the most common high-risk HPV, HPV16, is targeted to the basal layer of the stratified squamous epithelium.
  • [MeSH-major] Cell Transformation, Viral / genetics. Oncogene Proteins, Viral / genetics. Papillomaviridae / genetics. Receptor, Epidermal Growth Factor / physiology. Skin / pathology. Skin Neoplasms / virology
  • [MeSH-minor] Alleles. Animals. Cell Differentiation / genetics. DNA / biosynthesis. Epidermis / pathology. Epidermis / virology. Epithelial Cells / pathology. Epithelial Cells / virology. Humans. Hyperplasia / virology. Mice. Mice, Transgenic. Promoter Regions, Genetic. Signal Transduction

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  • (PMID = 16061632.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA07175; United States / NCI NIH HHS / CA / CA09135; United States / NCI NIH HHS / CA / CA22443
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Viral; 0 / oncogene protein E5, Human papillomavirus type 16; 9007-49-2 / DNA; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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3. Chen MH, Yip GW, Tse GM, Moriya T, Lui PC, Zin ML, Bay BH, Tan PH: Expression of basal keratins and vimentin in breast cancers of young women correlates with adverse pathologic parameters. Mod Pathol; 2008 Oct;21(10):1183-91
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  • [Title] Expression of basal keratins and vimentin in breast cancers of young women correlates with adverse pathologic parameters.
  • Previous studies have suggested that breast cancer in young women has more aggressive biological features and poorer prognosis.
  • We aimed to learn more about this disease in a cohort of 125 young women from Singapore, Japan and Hong Kong, aged 35 years or less, with invasive breast cancer by evaluating the expression of vimentin and the basal cytokeratins CK14, CK5/6 and 34 beta E12.
  • Basal cytokeratins and vimentin showed significant inverse relationship with estrogen and progesterone receptor status while CK14 expression was found to be directly associated with c-erbB2 status.
  • Basal cytokeratins and vimentin immunoreactivities were directly associated with CD117 and EGFR expression.
  • Our findings are in concert with reports that expression of basal cytokeratins and vimentin is correlated with adverse pathological parameters.
  • [MeSH-minor] Adult. Cell Line, Tumor. Cohort Studies. Female. Humans. Lymph Nodes / pathology. Lymphatic Metastasis. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism. Tissue Array Analysis

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  • (PMID = 18536655.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Vimentin; 68238-35-7 / Keratins
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4. Jaspers JE, Rottenberg S, Jonkers J: Therapeutic options for triple-negative breast cancers with defective homologous recombination. Biochim Biophys Acta; 2009 Dec;1796(2):266-80
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  • [Title] Therapeutic options for triple-negative breast cancers with defective homologous recombination.
  • Breast cancer is the most common malignancy among women in developed countries, affecting more than a million women per year worldwide.
  • Over the last decades, our increasing understanding of breast cancer biology has led to the development of endocrine agents against hormone receptor-positive tumors and targeted therapeutics against HER2-expressing tumors.
  • However, no targeted therapy is available for patients with triple-negative breast cancer, lacking expression of hormone receptors and HER2.
  • Overlap between BRCA1-mutated breast cancers and triple-negative tumors suggests that an important part of the triple-negative tumors may respond to therapeutics targeting BRCA1-deficient cells.
  • Here, we review the features shared between triple-negative, basal-like and BRCA1-related breast cancers.
  • Finally, we highlight the utility of mouse models for BRCA1-mutated breast cancer to optimize (combination) therapy and to understand drug resistance.
  • [MeSH-minor] Animals. Cell Cycle. DNA Repair. Disease Models, Animal. Drug Resistance, Neoplasm. Female. Genes, BRCA1. Humans. Mice. Mutation. Poly(ADP-ribose) Polymerase Inhibitors. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 19616605.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
  • [Number-of-references] 241
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5. Li TW, Ting JH, Yokoyama NN, Bernstein A, van de Wetering M, Waterman ML: Wnt activation and alternative promoter repression of LEF1 in colon cancer. Mol Cell Biol; 2006 Jul;26(14):5284-99
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  • [Title] Wnt activation and alternative promoter repression of LEF1 in colon cancer.
  • Here we show that promoter 1 is aberrantly activated in colon cancers because it is a direct target of the Wnt pathway.
  • T-cell factor (TCF)-beta-catenin complexes bind to Wnt response elements in exon 1 and dynamically regulate chromatin acetylation and promoter 1 activity.
  • Promoter 2 is nevertheless silent in colon cancer because an upstream repressor selectively targets the basal promoter leading to destabilized TCF-beta-catenin binding.
  • We conclude that the biological outcome of aberrant LEF1 activation in colon cancer is directed by differential promoter activation and repression.

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  • (PMID = 16809766.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096878; United States / NCI NIH HHS / CA / R01 CA108697; United States / NCI NIH HHS / CA / CA096878; United States / NCI NIH HHS / CA / CA108697
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Chromatin; 0 / DNA, Neoplasm; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC1592719
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6. Campbell RM, Barrall D, Wilkel C, Robinson-Bostom L, Dufresne RG Jr: Post-Mohs micrographic surgical margin tissue evaluation with permanent histopathologic sections. Dermatol Surg; 2005 Jun;31(6):655-8; discussion 658
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  • BACKGROUND: Incomplete resection of nonmelanoma skin cancer is associated with a relatively high rate of recurrent tumors.
  • Mohs micrographic surgery provides microscopic evaluation of tumor margins to ensure complete excision of nonmelanoma skin cancers at high risk of recurrence.
  • OBJECTIVE: This purpose of this study is to confirm the histologic accuracy of Mohs excision of facial skin cancers by evaluating an additional layer of tissue with permanent histopathologic sections after Mohs excision.
  • RESULTS: Two excisions of nodular basal cell cancer were determined by the pathologist to have positive tumor involvement on post-Mohs permanent tissue.
  • On additional review, one specimen was interpreted to be more consistent with follicular epithelium, and the second was verified as a focus of nodular basal cell cancer.
  • [MeSH-major] Carcinoma, Basal Cell / surgery. Carcinoma, Squamous Cell / surgery. Facial Neoplasms / surgery. Mohs Surgery. Skin Neoplasms / surgery
  • [MeSH-minor] Female. Humans. Male. Middle Aged. Neoplasms, Adnexal and Skin Appendage / surgery. Postoperative Period. Retrospective Studies

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  • [CommentIn] Dermatol Surg. 2006 Mar;32(3):463 [16640701.001]
  • (PMID = 15996415.001).
  • [ISSN] 1076-0512
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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7. Moulder SL: Does the PI3K pathway play a role in basal breast cancer? Clin Breast Cancer; 2010 Nov;10 Suppl 3:S66-71
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  • [Title] Does the PI3K pathway play a role in basal breast cancer?
  • Many cell kinases exert their proliferative and pro-survival effects through activation of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway.
  • Basal-like breast cancer is a subtype that can be identified by molecular analysis and often includes tumors lacking expression of estrogen receptor/progesterone receptor or human epidermal growth factor receptor, also known as triple-negative breast cancers.
  • Triple-negative cancers comprise < 20% of all breast cancers and have no obvious mechanism driving proliferation, yet these tumors demonstrate higher levels of Akt activation compared with non-triple-negative breast cancers.
  • This suggests a possible role for targeting the PI3K pathway for the treatment of this subset of aggressive cancers.
  • Most clinical trials which have attempted targeting the PI3K/Akt pathway in triple-negative breast cancer have involved the use of EGFR inhibitors with limited success.
  • Novel agents targeting PI3K are under development in early-phase clinical trials and may demonstrate benefit in combination with chemotherapy or other targeted agents such as mitogen-activated protein kinase inhibitors for the treatment of triple-negative or basal-like breast cancer.
  • [MeSH-major] Breast Neoplasms / enzymology. Neoplasm Proteins / physiology. Neoplasms, Basal Cell / enzymology. Phosphatidylinositol 3-Kinase / physiology


8. Shibata H, Yamakoshi H, Sato A, Ohori H, Kakudo Y, Kudo C, Takahashi Y, Watanabe M, Takano H, Ishioka C, Noda T, Iwabuchi Y: Newly synthesized curcumin analog has improved potential to prevent colorectal carcinogenesis in vivo. Cancer Sci; 2009 May;100(5):956-60
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  • Curcumin (diferuloylmethane) has chemopreventive and chemotherapeutic potentials against various types of cancers.
  • The average tumor number in mice fed GO-Y030 was reduced to 61.2% of those that were fed the basal diet (P < 0.05).
  • Compared with Apc(580D/+) mice fed the basal diet (median survival time = 166.5 days), a significantly prolonged lifespan (213 days) was observed in Apc(580D/+) mice fed GO-Y030.
  • [MeSH-major] Benzene Derivatives / chemical synthesis. Benzene Derivatives / pharmacology. Cell Transformation, Neoplastic / pathology. Colorectal Neoplasms / pathology. Colorectal Neoplasms / prevention & control. Curcumin / chemical synthesis. Curcumin / pharmacology. Ketones / chemical synthesis. Ketones / pharmacology

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  • (PMID = 19445025.001).
  • [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 / 1,5-bis(3,5-bis(methoxymethoxy)phenyl)penta-1,4-dien-3-one; 0 / Benzene Derivatives; 0 / Ketones; 0 / beta Catenin; IT942ZTH98 / Curcumin
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9. Stemke-Hale K, Gonzalez-Angulo AM, Lluch A, Neve RM, Kuo WL, Davies M, Carey M, Hu Z, Guan Y, Sahin A, Symmans WF, Pusztai L, Nolden LK, Horlings H, Berns K, Hung MC, van de Vijver MJ, Valero V, Gray JW, Bernards R, Mills GB, Hennessy BT: An integrative genomic and proteomic analysis of PIK3CA, PTEN, and AKT mutations in breast cancer. Cancer Res; 2008 Aug 1;68(15):6084-91
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  • [Title] An integrative genomic and proteomic analysis of PIK3CA, PTEN, and AKT mutations in breast cancer.
  • Phosphatidylinositol 3-kinase (PI3K)/AKT pathway aberrations are common in cancer.
  • By applying mass spectroscopy-based sequencing and reverse-phase protein arrays to 547 human breast cancers and 41 cell lines, we determined the subtype specificity and signaling effects of PIK3CA, AKT, and PTEN mutations and the effects of PIK3CA mutations on responsiveness to PI3K inhibition in vitro and on outcome after adjuvant tamoxifen.
  • PIK3CA mutations were more common in hormone receptor-positive (34.5%) and HER2-positive (22.7%) than in basal-like tumors (8.3%).
  • AKT1 (1.4%) and PTEN (2.3%) mutations were restricted to hormone receptor-positive cancers.
  • Unlike AKT1 mutations that were absent from cell lines, PIK3CA (39%) and PTEN (20%) mutations were more common in cell lines than tumors, suggesting a selection for these but not AKT1 mutations during adaptation to culture.
  • PIK3CA mutations did not have a significant effect on outcome after adjuvant tamoxifen therapy in 157 hormone receptor-positive breast cancer patients.
  • PIK3CA mutations, in comparison with PTEN loss and AKT1 mutations, were associated with significantly less and inconsistent activation of AKT and of downstream PI3K/AKT signaling in tumors and cell lines.
  • Thus, PI3K pathway aberrations likely play a distinct role in the pathogenesis of different breast cancer subtypes.
  • The specific aberration present may have implications for the selection of PI3K-targeted therapies in hormone receptor-positive breast cancer.

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  • (PMID = 18676830.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30CA16672; United States / NCI NIH HHS / CA / R01 CA109311; United States / NCI NIH HHS / CA / R21 CA120248-01; United States / NCI NIH HHS / CA / K23 CA121994-01; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / K23 CA121994; United States / NCI NIH HHS / CA / CA083639-010004; United States / NCI NIH HHS / CA / P30 CA016672-32; United States / NCI NIH HHS / CA / CA016672-32; United States / NCI NIH HHS / CA / P01CA099031; United States / NCI NIH HHS / CA / CA112970-04; United States / NCI NIH HHS / CA / P50 CA098258; United States / NCI NIH HHS / CA / 1R21CA120248-01; United States / NCI NIH HHS / CA / U54 CA 112970; United States / NCI NIH HHS / CA / CA099031-05; United States / NCI NIH HHS / CA / 1K23CA121994-01; United States / NCI NIH HHS / CA / P50 CA 58207; United States / NCI NIH HHS / CA / P01 CA099031-05; United States / NCI NIH HHS / CA / R21 CA120248; United States / NCI NIH HHS / CA / P50 CA058207; United States / NCI NIH HHS / CA / P50 CA083639-010004; United States / NCI NIH HHS / CA / U54 CA112970; United States / NCI NIH HHS / CA / CA058207-13; United States / NCI NIH HHS / CA / P50 CA083639; United States / NCI NIH HHS / CA / U54 CA112970-04; United States / NCI NIH HHS / CA / P01 CA099031; United States / NCI NIH HHS / CA / P50 CA058207-13; United States / NCI NIH HHS / CA / P50CA083639
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ NIHMS67275; NLM/ PMC2680495
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10. Han Y, Huang C, Sun X, Xiang B, Wang M, Yeh ET, Chen Y, Li H, Shi G, Cang H, Sun Y, Wang J, Wang W, Gao F, Yi J: SENP3-mediated de-conjugation of SUMO2/3 from promyelocytic leukemia is correlated with accelerated cell proliferation under mild oxidative stress. J Biol Chem; 2010 Apr 23;285(17):12906-15
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  • [Title] SENP3-mediated de-conjugation of SUMO2/3 from promyelocytic leukemia is correlated with accelerated cell proliferation under mild oxidative stress.
  • However, whether and how SUMO2/3-specific proteases are involved in de-conjugation under cell stress is unclear.
  • Furthermore, de-conjugation of SUMO2/3 from PML is responsible for the accelerated cell proliferation caused by low dose H(2)O(2).
  • Knocking down PML promotes basal cell proliferation as expected.
  • This can be reversed by reconstitution with wild-type PML but not its mutant lacking SUMOylation, indicating that only the SUMOylated PML can play an inhibitory role for cell proliferation.
  • Thus, SENP3 appears to be a key mediator in mild oxidative stress-induced cell proliferation via regulation of the SUMOylation status of PML.
  • Furthermore, SENP3 is over-accumulated in a variety of primary human cancers including colon adenocarcinoma in which PML is hypo-SUMOylated.
  • These results reveal an important role of SENP3 and the SUMOylation status of PML in the regulation of cell proliferation under oxidative stress.
  • [MeSH-major] Cell Proliferation. Cysteine Endopeptidases / metabolism. Nuclear Proteins / metabolism. Oxidative Stress. Small Ubiquitin-Related Modifier Proteins / metabolism. Transcription Factors / metabolism. Tumor Suppressor Proteins / metabolism. Ubiquitins / metabolism

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  • (PMID = 20181954.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oxidants; 0 / SUMO2 protein, human; 0 / SUMO3 protein, human; 0 / Small Ubiquitin-Related Modifier Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Ubiquitins; 143220-95-5 / PML protein, human; BBX060AN9V / Hydrogen Peroxide; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.- / SENP3 protein, human
  • [Other-IDs] NLM/ PMC2857110
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11. Zaravinos A, Kanellou P, Spandidos DA: Viral DNA detection and RAS mutations in actinic keratosis and nonmelanoma skin cancers. Br J Dermatol; 2010 Feb 1;162(2):325-31
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  • [Title] Viral DNA detection and RAS mutations in actinic keratosis and nonmelanoma skin cancers.
  • BACKGROUND: Actinic keratosis (AK) is a well-established precancerous skin lesion that has the potential to progress to squamous cell carcinoma (SCC).
  • Basal cell carcinoma (BCC) is a locally aggressive slowly growing tumour that rarely metastasizes.
  • A number of viruses have been proposed to play a role in the development of nonmelanoma skin cancers (NMSC), but the most plausible evidence to date suggests that cutaneous human papillomavirus (HPV) is the key instigating factor.
  • METHODS: HPV, CMV, HSV and EBV detection was performed using polymerase chain reaction (PCR) in skin biopsies (26 AK, 12 SCC and 15 BCC samples) that were collected from immunocompetent patients.
  • RESULTS: Seventeen out of 53 (32%) skin lesions were found to be positive for HPV DNA.
  • The HPV incidence was eight of 26 (31%) in AK and eight of 53 (15%) in normal skin tissue.
  • Twelve out of 53 (23%) skin lesions were CMV-positive.
  • No normal skin biopsy was found to be positive for CMV.
  • CONCLUSIONS: HPV DNA is detected in NMSC, AK and normal skin biopsies.
  • Our results also indicate that CMV is involved in NMSC at higher levels than in premalignant lesions, whereas the virus was not detected in normal skin biopsies.
  • [MeSH-major] Carcinoma, Basal Cell / virology. Carcinoma, Squamous Cell / virology. DNA, Viral / isolation & purification. Genes, ras / genetics. Keratosis, Actinic / virology. Skin Neoplasms / virology

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  • (PMID = 19849697.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral
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12. Yang L, Xie G, Fan Q, Xie J: Activation of the hedgehog-signaling pathway in human cancer and the clinical implications. Oncogene; 2010 Jan 28;29(4):469-81
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  • [Title] Activation of the hedgehog-signaling pathway in human cancer and the clinical implications.
  • The hedgehog pathway, initially discovered by two Nobel laureates Drs E Wieschaus and C Nusslein-Volhard in Drosophila, is a major regulator for cell differentiation, tissue polarity and cell proliferation.
  • Studies from many laboratories reveal activation of this pathway in a variety of human cancer, including basal cell carcinomas (BCCs), medulloblastomas, leukemia, gastrointestinal, lung, ovarian, breast and prostate cancers.
  • It is thus believed that targeted inhibition of hedgehog signaling may be effective in treatment and prevention of human cancer.
  • Even more exciting is the discovery and synthesis of specific signaling antagonists for the hedgehog pathway, which have significant clinical implications in novel cancer therapeutics.
  • In this review, we will summarize major advances in the last 2 years in our understanding of hedgehog signaling activation in human cancer, interactions between hedgehog signaling and other pathways in carcinogenesis, potential antagonists for hedgehog signaling inhibition and their clinical implications for human cancer treatment.

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  • (PMID = 19935712.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA94160
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hedgehog Proteins
  • [Number-of-references] 194
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13. Xia HH, He H, De Wang J, Gu Q, Lin MC, Zou B, Yu LF, Sun YW, Chan AO, Kung HF, Wong BC: Induction of apoptosis and cell cycle arrest by a specific c-Jun NH2-terminal kinase (JNK) inhibitor, SP-600125, in gastrointestinal cancers. Cancer Lett; 2006 Sep 28;241(2):268-74
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  • [Title] Induction of apoptosis and cell cycle arrest by a specific c-Jun NH2-terminal kinase (JNK) inhibitor, SP-600125, in gastrointestinal cancers.
  • The c-Jun NH(2)-terminal kinase (JNK) is activated in several tumor cell lines.
  • The aim of this study was to determine the effects of SP-600125, a specific JNK inhibitor, on the viability, apoptosis, cell cycle distribution of gastrointestinal cancer cells, and the potential anti-tumor mechanisms.
  • Three gastric cancer cell lines, AGS, BCG-823 and MKN-45, and three colorectal cancer cell lines, SW1116, COLO205 and HT-29, were used.
  • Cells were treated with SP-600125, and cell viability, apoptosis and cell cycle distribution, caspase-3 activity, expression of JNK and apoptosis related proteins were detected.
  • SP-600125 inhibited cell proliferation by 10-80% for the different cell lines, and increased apoptosis by 1.5-4.5 folds for COLO205, BCG-823, MKN-45, AGS cells.
  • SP-600125 caused G2/M cell cycle arrest and elevation of cyclin B1 and p27(kip).
  • The differential response in cells to SP-600125 was associated with the basal level of phosphorylated JNK2.
  • It is concluded that SP-600125 inhibits proliferation, induces apoptosis and causes cell cycle arrest in gastrointestinal cancer cells, indicating that JNK inhibitors have an anti-tumor effect and are potential therapeutic agents for cancers.
  • [MeSH-major] Anthracenes / pharmacology. Apoptosis / drug effects. Cell Division / drug effects. Enzyme Inhibitors / pharmacology. G2 Phase / drug effects. Gastrointestinal Neoplasms / drug therapy. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • [MeSH-minor] Caspases / metabolism. Cell Proliferation / drug effects. Humans. RNA, Messenger / metabolism. Tumor Cells, Cultured

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  • (PMID = 16337741.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Anthracenes; 0 / Enzyme Inhibitors; 0 / RNA, Messenger; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases
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14. Lin Z, Liu M, Li Z, Kim C, Lee E, Kim I: DeltaNp63 protein expression in uterine cervical and endometrial cancers. J Cancer Res Clin Oncol; 2006 Dec;132(12):811-6
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  • [Title] DeltaNp63 protein expression in uterine cervical and endometrial cancers.
  • PURPOSE: To investigate the significance of p63 expression in uterine cervical and endometrial cancers.
  • MATERIALS AND METHODS: DeltaNp63 protein expression was studied in a variety of 127 cases of uterine cervical lesions (20 non-neoplastic cervices, 43 cervical intraepithelial neoplasia [CIN], 54 squamous cell carcinomas (SCCs), 40 adenocarcinomas, and 13 other histologic types) and 30 endometrioid type of endometrial adenocarcinomas by using immunohistochemistry.
  • One SCC cell line (ME-180) and one adenocarcinoma cell line (HeLa) were also included.
  • RESULTS: In uterine cervix, the expression of DeltaNp63 was increased with progression of CIN, and positive in all SCCs, transitional cell carcinomas, and adenoid basal carcinoma, but negative in all adenocarcinomas.
  • Adenosquamous cell carcinoma and mixed neuroendocrine and squamous cell carcinoma were positive in squamous component, but not in adenocarcinoma and neuroendocrine carcinoma components.
  • ME-180 cell line was positive, whereas HeLa cell line was negative.
  • CONCLUSIONS: Immunohistochemical staining for DeltaNp63 is a powerful marker for squamous differentiation and useful in exclusion of glandular and neuroendocrine differentiation in uterine cervical cancers, but not always in endometrial cancers.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. DNA-Binding Proteins / biosynthesis. Endometrial Neoplasms / metabolism. Trans-Activators / biosynthesis. Tumor Suppressor Proteins / biosynthesis. Uterine Cervical Neoplasms / metabolism
  • [MeSH-minor] Antigens, Differentiation / biosynthesis. Cell Line, Tumor. Cervix Uteri / cytology. Cervix Uteri / metabolism. Female. HeLa Cells. Humans. Immunohistochemistry. Transcription Factors

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  • (PMID = 16804722.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / DNA-Binding Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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15. Liu B, Fan Z, Edgerton SM, Deng XS, Alimova IN, Lind SE, Thor AD: Metformin induces unique biological and molecular responses in triple negative breast cancer cells. Cell Cycle; 2009 Jul 1;8(13):2031-40
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  • [Title] Metformin induces unique biological and molecular responses in triple negative breast cancer cells.
  • Triple negative (TN) breast cancer is more frequent in women who are obese or have type II diabetes, as well as young women of color.
  • These cancers do not express receptors for the steroid hormones estrogen or progesterone, or the type II receptor tyrosine kinase (RTK) Her-2 but do have upregulation of basal cytokeratins and the epidermal growth factor receptor (EGFR).
  • These data suggest that aberrations of glucose and fatty acid metabolism, signaling through EGFR and genetic factors may promote the development of TN cancers.
  • The anti-type II diabetes drug metformin has been associated with a decreased incidence of breast cancer, although the specific molecular subtypes that may be reduced by metformin have not been reported.
  • Our data indicates that metformin has unique anti-TN breast cancer effects both in vitro and in vivo.
  • It inhibits cell proliferation (with partial S phase arrest), colony formation and induces apoptosis via activation of the intrinsic and extrinsic signaling pathways only in TN breast cancer cell lines.
  • These data are in stark contrast to our previously published biological and molecular effects of metformin on luminal A and B, or Her-2 type breast cancer cells.
  • Nude mice bearing tumor xenografts of the TN line MDA-MB-231, treated with metformin, show significant reductions in tumor growth (p = 0.0066) and cell proliferation (p = 0.0021) as compared to untreated controls.
  • Given the unique anti-cancer activity of metformin against TN disease, both in vitro and in vivo, it should be explored as a therapeutic agent against this aggressive form of breast cancer.
  • [MeSH-minor] AMP-Activated Protein Kinases / metabolism. Animals. Apoptosis. Caspases / metabolism. Cell Cycle. Cell Proliferation. Female. Humans. Mice. Mice, Nude. Poly(ADP-ribose) Polymerases / metabolism. Signal Transduction. Tumor Cells, Cultured. Xenograft Model Antitumor Assays


16. Nagao K, Togawa N, Fujii K, Uchikawa H, Kohno Y, Yamada M, Miyashita T: Detecting tissue-specific alternative splicing and disease-associated aberrant splicing of the PTCH gene with exon junction microarrays. Hum Mol Genet; 2005 Nov 15;14(22):3379-88
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  • Mutations in the human ortholog of Drosophila patched (PTCH) have been identified in patients with autosomal dominant nevoid basal cell carcinoma syndrome (NBCCS), characterized by minor developmental anomalies and an increased incidence of cancers such as medulloblastoma and basal cell carcinoma.
  • [MeSH-major] Alternative Splicing. Basal Cell Nevus Syndrome / genetics. Exons / genetics. Oligonucleotide Array Sequence Analysis. Receptors, Cell Surface / genetics

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  • (PMID = 16203740.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB214500/ AB214501/ AB233422/ AB233423/ AB233424
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Cell Surface; 0 / patched receptors
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17. Scope A, Benvenuto-Andrade C, Agero AL, Marghoob AA: Nonmelanocytic lesions defying the two-step dermoscopy algorithm. Dermatol Surg; 2006 Nov;32(11):1398-406
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  • Seborrheic keratosis, dermatofibroma, subcorneal hemorrhage, basal cell carcinoma (BCC), and cutaneous metastases of breast and other cancers may contain pigmented globules.
  • [MeSH-major] Algorithms. Dermoscopy / methods. Melanoma, Amelanotic / diagnosis. Nevus / diagnosis. Skin Neoplasms / diagnosis

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  • (PMID = 17083595.001).
  • [ISSN] 1076-0512
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 32
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18. Molinié V, Hervé JM, Lugagne PM, Lebret T, Botto H: Diagnostic utility of a p63/alpha-methyl coenzyme A racemase (p504s) cocktail in ambiguous lesions of the prostate upon needle biopsy. BJU Int; 2006 May;97(5):1109-15
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  • [Title] Diagnostic utility of a p63/alpha-methyl coenzyme A racemase (p504s) cocktail in ambiguous lesions of the prostate upon needle biopsy.
  • OBJECTIVE: To investigate the potential utility of a new combined immunostaining technique for diagnosing prostate cancer from histological analysis of needle biopsy specimens.
  • MATERIALS AND METHODS: Tissue was immunostained with a combination of antibodies against a basal cell marker (p63), and an enzyme commonly overexpressed in prostate cancer (p504s), on 63 small prostate cancer foci (<1 mm) and 109 cases of ambiguous lesions observed in needle biopsies.
  • The final diagnoses retained were: 92 prostate cancers, seven atypical small acinar proliferations suspected of being malignant but undiagnosed, 21 prostatic intraepithelial neoplasia, five atypical adenomatous hyperplasia, and 36 atrophic benign mimickers of cancer.
  • CONCLUSIONS: Combining p504s as a positive marker for prostate cancer and p63 as a negative marker might improve diagnostic performance, sensitivity and specificity, and lead to fewer false-negative results.
  • [MeSH-minor] Antibodies / metabolism. Biopsy, Needle / methods. Cell Transformation, Neoplastic. Humans. Immunohistochemistry / methods. Male. Membrane Proteins / metabolism. Sensitivity and Specificity

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  • (PMID = 16643500.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / CKAP4 protein, human; 0 / Membrane Proteins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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19. Hamid T, Malik MT, Millar RP, Kakar SS: Protein kinase A serves as a primary pathway in activation of Nur77 expression by gonadotropin-releasing hormone in the LbetaT2 mouse pituitary gonadotroph tumor cell line. Int J Oncol; 2008 Nov;33(5):1055-64
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  • [Title] Protein kinase A serves as a primary pathway in activation of Nur77 expression by gonadotropin-releasing hormone in the LbetaT2 mouse pituitary gonadotroph tumor cell line.
  • It plays an important role in a number of biological processes, including regulation of signaling functions in the hypothalamo-pituitary-adrenal axis, regulation of thymocyte apoptosis, regulation of steroidogenesis and regulation of tumor cell proliferation and apoptosis.
  • In previous studies, using DNA microarray analysis of the effects of the gonadotropin-releasing hormone (GnRH) on the mouse pituitary gonadotroph cell line LbetaT2, we identified Nur77 as one of the highly regulated immediate early genes involved in this response, with >40-fold upregulation after 1 h of treatment of the cells with the GnRH agonist [D-Ala6GnRH (GnRHA)].
  • GnRH is a hypothalamic decapeptide that stimulates the secretion and expression of gonadotropins (follicle stimulating hormone, FSH and luteinizing hormone releasing hormone, LH) from anterior pituitary through activation of high affinity receptors present on cell membrane of pituitary gonadotropes.
  • In addition to pituitary, the presence of GnRH high affinity receptors has been reported in various cancers and cancer cell lines.
  • In addition, GnRH and its analogs are clinically used in the treatment of prostate cancer.
  • Nur77 mRNA was upregulated within 30 min of GnRHA treatment and returned to nearly basal level after 24 h of treatment.
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Line, Tumor. Chelating Agents / pharmacology. Cyclic AMP / metabolism. Dose-Response Relationship, Drug. Enzyme Activators / pharmacology. Mice. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / metabolism. Nuclear Receptor Subfamily 4, Group A, Member 1. Protein Kinase Inhibitors / pharmacology. RNA, Messenger / metabolism. Time Factors. Up-Regulation

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  • (PMID = 18949369.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U127681325; United States / NCI NIH HHS / CA / CA60871
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chelating Agents; 0 / DNA-Binding Proteins; 0 / Enzyme Activators; 0 / Nr4a1 protein, mouse; 0 / Nuclear Receptor Subfamily 4, Group A, Member 1; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 0 / Receptors, Steroid; 33515-09-2 / Gonadotropin-Releasing Hormone; 79561-22-1 / LHRH, Ala(6)-Gly(10)-ethylamide-; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; SY7Q814VUP / Calcium
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20. Guler G, Huebner K, Himmetoglu C, Jimenez RE, Costinean S, Volinia S, Pilarski RT, Hayran M, Shapiro CL: Fragile histidine triad protein, WW domain-containing oxidoreductase protein Wwox, and activator protein 2gamma expression levels correlate with basal phenotype in breast cancer. Cancer; 2009 Feb 15;115(4):899-908
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  • [Title] Fragile histidine triad protein, WW domain-containing oxidoreductase protein Wwox, and activator protein 2gamma expression levels correlate with basal phenotype in breast cancer.
  • BACKGROUND: The expression of fragile histidine triad protein (Fhit) and WW domain-containing oxidoreductase protein (Wwox), tumor suppressors that are encoded by fragile (FRA) loci FRA3B and FRA16D, are lost concordantly in breast cancers.
  • In the current study, the authors examined correlations among Fhit, Wwox, the activator protein 2 transcription factors AP2alpha and AP2gamma, cytokeratins 5 and 6 (CK5/6), epidermal growth factor receptor (EGFR), estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2) and their associations with breast cancer phenotypes.
  • METHODS: Tissue microarrays constructed from 837 breast cancer blocks were immunostained.
  • CONCLUSIONS: The results from this investigation suggested that reduced expression levels of Fhit, Wwox, and nuclear AP2gamma have roles in the pathogenesis of basal-like differentiation in breast cancer.
  • Alteration in the expression of fragile site genes occurs in most of these cancers and may contribute to defects in DNA repair, as observed in breast cancer 1 (BRCA1)-deficient cancers.

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  • [Copyright] (c) 2009 American Cancer Society.
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  • (PMID = 19130459.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120516-03; United States / NCI NIH HHS / CA / CA120516; United States / NCI NIH HHS / CA / R01 CA120516; United States / NCI NIH HHS / CA / CA120516-03; United States / NCI NIH HHS / CA / R01 CA132453
  • [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 / Biomarkers, Tumor; 0 / Keratin-5; 0 / Keratin-6; 0 / Neoplasm Proteins; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Transcription Factor AP-2; 0 / Tumor Suppressor Proteins; 0 / fragile histidine triad protein; EC 1.- / Oxidoreductases; EC 1.1.1.- / WWOX protein, human; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.6.- / Acid Anhydride Hydrolases
  • [Other-IDs] NLM/ NIHMS89229; NLM/ PMC2640223
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21. Sakiz D, Turkmenoglu TT, Kabukcuoglu F: The expression of p63 and p53 in keratoacanthoma and intraepidermal and invasive neoplasms of the skin. Pathol Res Pract; 2009;205(9):589-94
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  • [Title] The expression of p63 and p53 in keratoacanthoma and intraepidermal and invasive neoplasms of the skin.
  • p53 is a well-known tumor suppressor gene, and its mutation is a common event in intraepidermal and invasive neoplasms of the skin. p63 is a homologue of the tumor suppressor gene p53, which is expressed in human basal squamous epithelium, and despite its homology to p53, it is considered to act as an oncogene.
  • We evaluated p63 and p53 expression in usual skin cancers, including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), keratoacanthoma (KA), and intraepidermal neoplasms, including Bowen's disease (BD), actinic keratosis (AK), malignant melanoma in situ (MM in situ), and Paget's disease (PD) to clarify the putative role of p63 and p53 in the development and differential diagnosis of these lesions.
  • The mean p53 staining was highest in BD, followed by AK, SCC, PD, KA, BCC, and normal skin.
  • [MeSH-major] Keratoacanthoma / pathology. Skin Diseases / pathology. Skin Neoplasms / pathology. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Carcinoma, Basal Cell / metabolism. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. Keratosis, Actinic / metabolism. Keratosis, Actinic / pathology. Melanoma / metabolism. Melanoma / pathology. Membrane Proteins. Paget Disease, Extramammary / metabolism. Paget Disease, Extramammary / pathology. Precancerous Conditions / metabolism. Precancerous Conditions / pathology


22. Lerma E, Barnadas A, Prat J: Triple negative breast carcinomas: similarities and differences with basal like carcinomas. Appl Immunohistochem Mol Morphol; 2009 Dec;17(6):483-94
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  • [Title] Triple negative breast carcinomas: similarities and differences with basal like carcinomas.
  • The cDNA microarrays allows the classification of breast cancers into 6 groups: luminal A, luminal B, luminal C, normal breast-like, human epidermal growth factor receptor 2-positive, and basal-like.
  • This latter is characterized by the expression of basal cytokeratins (CKs), and frequent negativity for hormone receptors and human epidermal growth factor receptor 2.
  • There is a marked parallelism between triple negative breast carcinomas and basal-like carcinoma, but these are not equivalent terms.
  • Recent studies suggest that basal like carcinomas are originated from mammary stem cells.

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  • (PMID = 19620842.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Receptors, Cell Surface; 68238-35-7 / Keratins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 146
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23. Bashir M, Kirmani D, Bhat HF, Baba RA, Hamza R, Naqash S, Wani NA, Andrabi KI, Zargar MA, Khanday FA: P66shc and its downstream Eps8 and Rac1 proteins are upregulated in esophageal cancers. Cell Commun Signal; 2010;8:13
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  • [Title] P66shc and its downstream Eps8 and Rac1 proteins are upregulated in esophageal cancers.
  • Members of Shc (src homology and collagen homology) family, p46shc, p52shc, p66shc have known to be related to cell proliferation and carcinogenesis.
  • Whereas p46shc and p52shc drive the reaction forward, the role of p66shc in cancers remains to be understood clearly.
  • Hence, their expression in cancers needs to be evaluated carefully so that Shc analysis may provide prognostic information in the development of carcinogenesis.
  • In the present study, the expression of p66shc and its associate targets namely Eps8 (epidermal pathway substrate 8), Rac1 (ras-related C3 botulinum toxin substrate1) and Grb2 (growth factor receptor bound protein 2) were examined in fresh tissue specimens from patients with esophageal squamous cell carcinoma and esophageal adenocarcinoma using western blot analysis.
  • A thorough analysis of both esophageal squamous cell carcinoma and adenocarcinoma showed p66shc expression to be significantly higher in both types of carcinomas as compared to the controls.
  • The controls of adenocarcinoma show a higher basal expression level of p66shc as compared to the controls of squamous cell carcinoma.
  • However the expression of grb2 was found to be equal in both esophageal squamous cell carcinoma and adenocarcinoma.
  • The above results suggest that the pathway operated by p66shc in cancers does not involve the participation of Ras and Grb2 as downstream targets instead it operates the pathway involving Eps8 and Rac1 proteins.
  • From the results it is also suggestive that p66shc may have a role in the regulation of esophageal carcinomas and represents a possible mechanism of signaling for the development of squamous cell carcinoma and adenocarcinoma of esophagus.


24. Smith-Zagone MJ, Schwartz MR: Frozen section of skin specimens. Arch Pathol Lab Med; 2005 Dec;129(12):1536-43
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  • [Title] Frozen section of skin specimens.
  • CONTEXT: Skin cancers are the most common malignancies in this country.
  • CONCLUSIONS: Frozen sections play a vital role in the evaluation of margins of basal cell carcinomas and squamous cell carcinomas.
  • [MeSH-major] Carcinoma, Basal Cell / diagnosis. Carcinoma, Squamous Cell / diagnosis. Frozen Sections / methods. Melanoma / diagnosis. Pathology, Surgical / methods. Skin Neoplasms / diagnosis

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  • (PMID = 16329726.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 34
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25. Thomas GS, Zhang L, Blackwell K, Habelhah H: Phosphorylation of TRAF2 within its RING domain inhibits stress-induced cell death by promoting IKK and suppressing JNK activation. Cancer Res; 2009 Apr 15;69(8):3665-72
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  • [Title] Phosphorylation of TRAF2 within its RING domain inhibits stress-induced cell death by promoting IKK and suppressing JNK activation.
  • Importantly, constitutive TRAF2 phosphorylation increased both basal and inducible NF-kappaB activation and rendered Ha-Ras-V12-transformed cells resistant to stress-induced apoptosis.
  • Moreover, TRAF2 was found to be constitutively phosphorylated in some malignant cancer cell lines and Hodgkin's lymphoma.
  • These results reveal a new level of complexity in TNFalpha-induced IKK activation modulated by TRAF2 phosphorylation and suggest that TRAF2 phosphorylation is one of the events that are responsible for elevated basal NF-kappaB activity in certain human cancers.

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  • (PMID = 19336568.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA107185; United States / NCI NIH HHS / CA / CA78419; United States / NCI NIH HHS / CA / R01 CA107185-02; United States / NCI NIH HHS / CA / R01 CA078419; United States / NCI NIH HHS / CA / CA107185-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TNF Receptor-Associated Factor 2; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.12.2 / MAP Kinase Kinase 4
  • [Other-IDs] NLM/ NIHMS96941; NLM/ PMC2669835
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26. Beaugerie L, Sokol H, Seksik P: Noncolorectal malignancies in inflammatory bowel disease: more than meets the eye. Dig Dis; 2009;27(3):375-81
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  • In the subset of patients with longstanding small bowel lesions, the absolute risk of small bowel adenocarcinoma exceeds 1 per 100 patient-years after 25 years of follow-up and becomes equivalent to the risk of colorectal cancer.
  • Growing evidence suggests that the pathogenesis of small bowel adenocarcinoma arising in inflammatory lesions of Crohn's disease is similar to that of colorectal cancer complicating chronic colonic inflammation (inflammation-dysplasia-cancer sequence).
  • Finally, patients receiving thiopurines and/or TNF-inhibitors are at risk for developing fatal hepatosplenic T cell lymphomas, but this risk is low (no case in the CESAME study).
  • But it is not established whether the risk of uterine cervix cancer and basal and squamous cell skin cancers (that may be associated with chronic human papillomavirus infection) is increased in patients receiving immunomodulators.

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19786768.001).
  • [ISSN] 1421-9875
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 46
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27. Le Brun Keris Y, Jouk PS, Saada-Sebag G, Roux JJ, Mattei B, Bagait L, Paoloni-Giacobino A, Grandchamp B, Soufir N, Lespinasse J: Prenatal manifestation in a family affected by nevoid basal cell carcinoma syndrome. Eur J Med Genet; 2008 Sep-Oct;51(5):472-8
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  • [Title] Prenatal manifestation in a family affected by nevoid basal cell carcinoma syndrome.
  • We report here a three generations family with nevoid basal cell carcinoma syndrome (NBCCS) in which the diagnosis was made only after a second trimester of pregnancy ultrasonography revealing fetal cranio-cerebral malformations.
  • MC1R gene sequencing identified in two NBCCS patients affected by multiple basal cell carcinomas a functional MC1R variant, D294H, previously shown to be associated with skin cancer risk.
  • This variant was absent in the NBCCS patient that did not develop basal cell carcinomas, suggesting that this variant could have favored the development of skin cancers, in patients carrying the PTCH1 mutation.
  • [MeSH-major] Basal Cell Nevus Syndrome / genetics
  • [MeSH-minor] Corpus Callosum / pathology. Craniofacial Abnormalities / diagnosis. Craniofacial Abnormalities / genetics. Exons. Family Health. Female. Gene Deletion. Humans. Mutation. Patched Receptors. Patched-1 Receptor. Pedigree. Pregnancy. Prenatal Diagnosis. Receptor, Melanocortin, Type 1 / genetics. Receptors, Cell Surface / genetics

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  • (PMID = 18539553.001).
  • [ISSN] 1769-7212
  • [Journal-full-title] European journal of medical genetics
  • [ISO-abbreviation] Eur J Med Genet
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / PTCH protein, human; 0 / Patched Receptors; 0 / Patched-1 Receptor; 0 / Receptor, Melanocortin, Type 1; 0 / Receptors, Cell Surface
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28. Ali S, Heathcote DA, Kroll SH, Jogalekar AS, Scheiper B, Patel H, Brackow J, Siwicka A, Fuchter MJ, Periyasamy M, Tolhurst RS, Kanneganti SK, Snyder JP, Liotta DC, Aboagye EO, Barrett AG, Coombes RC: The development of a selective cyclin-dependent kinase inhibitor that shows antitumor activity. Cancer Res; 2009 Aug 01;69(15):6208-15
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  • [Title] The development of a selective cyclin-dependent kinase inhibitor that shows antitumor activity.
  • Normal progression through the cell cycle requires the sequential action of cyclin-dependent kinases CDK1, CDK2, CDK4, and CDK6.
  • Direct or indirect deregulation of CDK activity is a feature of almost all cancers and has led to the development of CDK inhibitors as anticancer agents.
  • The CDK-activating kinase (CAK) plays a critical role in regulating cell cycle by mediating the activating phosphorylation of CDK1, CDK2, CDK4, and CDK6.
  • As such, CDK7, which also regulates transcription as part of the TFIIH basal transcription factor, is an attractive target for the development of anticancer drugs.
  • In MCF-7 cells, BS-181 inhibited the phosphorylation of CDK7 substrates, promoted cell cycle arrest and apoptosis to inhibit the growth of cancer cell lines, and showed antitumor effects in vivo.
  • BS-181 therefore provides the first example of a potent and selective CDK7 inhibitor with potential as an anticancer agent.
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Computer-Aided Design. Drug Design. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Models, Molecular. Xenograft Model Antitumor Assays


29. Hightower KD, Messina JL: Cutaneous protothecosis: a case report and review of the literature. Cutis; 2007 Aug;80(2):129-31
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  • We present a case of an 81-year-old white woman with a history of multiple nonmelanoma skin cancers, including squamous and basal cell carcinomas and actinic keratoses, throughout her legs and thighs bilaterally.
  • Biopsies of skin specimens from the right lower leg revealed a dermal abscess that contained spherical funguslike organisms, with periodic acid-Schiff staining revealing 6- to 10-microm organisms with internal septations, which are characteristic of P wickerhamii.
  • [MeSH-major] Prototheca / pathogenicity. Skin Diseases, Infectious / etiology. Skin Diseases, Infectious / pathology

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  • (PMID = 17944171.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 17
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30. Chistiakov DA: Endogenous and exogenous stem cells: a role in lung repair and use in airway tissue engineering and transplantation. J Biomed Sci; 2010;17:92
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  • The respiratory tract contains several sources of endogenous adult stem cells residing within the basal layer of the upper airways, within or near pulmonary neuroendocrine cell rests, at the bronchoalveolar junction, and within the alveolar epithelial surface, which contribute to the repair of the airway wall.
  • However, an organism is frequently incapable of repairing serious damage and defects of the respiratory tract resulting from acute trauma, lung cancers, and chronic pulmonary and airway diseases.
  • However, implementation of tissue engineering and stem cell therapy-based approaches helps to successfully solve this problem.
  • Most tracheal tissue engineering approaches use biodegradable three-dimensional scaffolds, which are important for neotracheal formation by promoting cell attachment, cell redifferentiation, and production of the extracellular matrix.
  • Current trends in tracheal transplantation include the use of autologous cells, development of bioactive cell-free scaffolds capable of supporting activation and differentiation of host stem cells on the site of injury, with a future perspective of using human native sites as micro-niche for potentiation of the human body's site-specific response by sequential adding, boosting, permissive, and recruitment impulses.
  • [MeSH-minor] Animals. Bioengineering. Extracellular Matrix / physiology. Extracellular Matrix / transplantation. Humans. Regenerative Medicine / methods. Stem Cell Transplantation / trends. Wound Healing

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  • (PMID = 21138559.001).
  • [ISSN] 1423-0127
  • [Journal-full-title] Journal of biomedical science
  • [ISO-abbreviation] J. Biomed. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3004872
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31. Donia AF, Mostafa A, Refaie H, El-Baz M, Kamal MM, Ghoneim MA: Postkidney transplant malignancy in Egypt has a unique pattern: a three-decade experience. Transplantation; 2008 Oct 27;86(8):1139-42
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  • Skin cancers were the fourth among posttransplant malignancies (9.2%) and 85.7% of cases were basal cell carcinoma.

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  • (PMID = 18946354.001).
  • [ISSN] 1534-6080
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Eugene DW, Joshi KD: Xeroderma pigmentosa--a disfiguring disease. Kathmandu Univ Med J (KUMJ); 2006 Jan-Mar;4(1):78-81
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  • Kunwar et al. Those affected are extremely sensitive to the UV portion of the light and have a 2000-fold increased risk of skin cancer in the sun exposed skin.
  • Basal cell carcinoma is the most commonly associated carcinoma followed by Squamous cell carcinoma and Melanoma.
  • The recurring cancer occurring on the face and repeated surgical treatment for the ulcerations have important social and psychological implications not encountered with other cancers.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Melanoma / pathology. Skin Neoplasms / pathology. Xeroderma Pigmentosum / pathology

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  • (PMID = 18603874.001).
  • [ISSN] 1812-2027
  • [Journal-full-title] Kathmandu University medical journal (KUMJ)
  • [ISO-abbreviation] Kathmandu Univ Med J (KUMJ)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Nepal
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33. Johansen P, Berg K, Selbo PK, Hofbauer GF: [Photochemical internalisation (PCI): a further development of photodynamic therapy for the treatment of skin cancer]. Praxis (Bern 1994); 2010 Nov 17;99(23):1423-8
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  • [Title] [Photochemical internalisation (PCI): a further development of photodynamic therapy for the treatment of skin cancer].
  • Recently, several new and non-invasive methods have been introduced for the treatment of skin cancers.
  • Topical creams using the immune modulator imiquimod or the COX inhibitor diclofenac (with hyaluronic acid) are now registered for use against neoplasms such as basal or squamous cell carcinoma.
  • A refined version of PDT, namely photochemical internalisation, is currently subject to a first clinical trial in patients with osteosarcoma, squamous cell carcinoma, head and neck cancer as well as adenocarcinoma of the breast.
  • [MeSH-major] Carcinoma, Basal Cell / drug therapy. Carcinoma, Squamous Cell / drug therapy. Melanoma / drug therapy. Photochemotherapy / methods. Skin Neoplasms / drug therapy


34. Hanson H, Hodgson S: Cancer genetics and reproduction. Best Pract Res Clin Obstet Gynaecol; 2010 Feb;24(1):3-18
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  • [Title] Cancer genetics and reproduction.
  • Cancers of the reproductive organs (i.e., ovaries, uterus and testes), like other cancers, occur as a result of a multi-stage interaction of genetic and environmental factors.
  • A small proportion of cancers of the reproductive organs occur as part of a recognised cancer syndrome, as a result of inheritance of mutations in highly penetrant cancer susceptibility genes (e.g., BRCA1, BRCA2, MLH1 or MSH2).
  • Recognition of individuals and families with inherited cancer predisposition syndromes and individuals at high risk due to familial cancer clustering is fundamentally important for the management and treatment of the current cancer and for future prevention of further cancers for the individual and their extended family.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Basal Cell Nevus Syndrome / genetics. Breast Neoplasms / genetics. Cluster Analysis. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Endometrial Neoplasms / genetics. Evidence-Based Medicine. Female. Founder Effect. Genetic Markers / genetics. Genetic Predisposition to Disease. Genetic Testing. Humans. Jews / genetics. Mass Screening. MutS Homolog 2 Protein / genetics. Neoplastic Syndromes, Hereditary / genetics. Nuclear Proteins / genetics. Ovarian Neoplasms / genetics. Pedigree. Peutz-Jeghers Syndrome / genetics. Population Surveillance. Practice Guidelines as Topic. Prognosis. Risk Factors

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  • (PMID = 19864186.001).
  • [ISSN] 1532-1932
  • [Journal-full-title] Best practice & research. Clinical obstetrics & gynaecology
  • [ISO-abbreviation] Best Pract Res Clin Obstet Gynaecol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Genetic Markers; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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35. Geyer FC, Lambros MB, Natrajan R, Mehta R, Mackay A, Savage K, Parry S, Ashworth A, Badve S, Reis-Filho JS: Genomic and immunohistochemical analysis of adenosquamous carcinoma of the breast. Mod Pathol; 2010 Jul;23(7):951-60
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  • Breast adenosquamous carcinomas are rare tumours characterized by well-developed gland formation intimately admixed with solid nests of squamous cells immersed in a highly cellular spindle cell stroma.
  • Here we studied five cases of adenosquamous carcinomas to determine their genetic profiles and to investigate whether the spindle cell component of these cancers could at least in part stem from the glandular/epithelial components.
  • All cases displayed a triple-negative immunophenotype, consistently expressed 'basal' keratins and showed variable levels of epidermal growth factor receptor expression.
  • In conclusion, breast adenosquamous carcinomas are triple-negative cancers that express 'basal' keratins.
  • Some of the spindle cells in adenosquamous carcinomas are derived from the epithelial component, suggesting that adenosquamous carcinomas may also be part of the group of metaplastic breast carcinomas with spindle cell metaplastic elements.

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  • (PMID = 20453835.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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36. Rebsch CM, Penna FJ 3rd, Copeland PR: Selenoprotein expression is regulated at multiple levels in prostate cells. Cell Res; 2006 Dec;16(12):940-8
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  • Selenium supplementation in a population with low basal blood selenium levels has been reported to decrease the incidence of several cancers including prostate cancer.
  • To address the effects of selenium supplementation on selenoprotein expression in prostate cells, we have undertaken an analysis of antioxidant selenoprotein expression as well as selenium toxicity in non-tumorigenic prostate epithelial cells (RWPE-1) and prostate cancer cells (LNCaP and PC-3).
  • Our results show that two of the glutathione peroxidase family members (GPX1 and GPX4) are highly induced by supplemental selenium in prostate cancer cells but only slightly induced in RWPE-1 cells.
  • Notably and in contrast to previous studies, RWPE-1 cells were significantly more sensitive to selenite than either of the prostate cancer cell lines.
  • [MeSH-minor] Cell Line, Tumor. Glutathione Peroxidase / biosynthesis. Glutathione Peroxidase / genetics. Humans. Male. Selenium / metabolism. Selenium Compounds / pharmacology

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  • [ErratumIn] Cell Res. 2007 Mar;17(3):272
  • (PMID = 17160069.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM077073
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Selenium Compounds; 0 / Selenoproteins; EC 1.11.1.- / GPX2 protein, human; EC 1.11.1.- / glutathione peroxidase GPX1; EC 1.11.1.9 / Glutathione Peroxidase; H6241UJ22B / Selenium
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37. Jiang X, Chen S, Asara JM, Balk SP: Phosphoinositide 3-kinase pathway activation in phosphate and tensin homolog (PTEN)-deficient prostate cancer cells is independent of receptor tyrosine kinases and mediated by the p110beta and p110delta catalytic subunits. J Biol Chem; 2010 May 14;285(20):14980-9
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  • [Title] Phosphoinositide 3-kinase pathway activation in phosphate and tensin homolog (PTEN)-deficient prostate cancer cells is independent of receptor tyrosine kinases and mediated by the p110beta and p110delta catalytic subunits.
  • The PI3K pathway is activated by phosphate and tensin homolog (PTEN) loss in most prostate cancers (PCa), but the contribution of upstream RTKs that may be targeted therapeutically has not been assessed.
  • An interaction with ErbB3 was also detected but was independent of ErbB3 tyrosine phosphorylation and was not required for basal PI3K activity.
  • Basal tyrosine phosphorylation of p110beta and p110delta could be blocked by c-Src inhibitors, but this did not suppress PI3K activity, which was similarly independent of Ras.
  • Basal PI3K activity was mediated by p110beta in PC3 cells and by both p110beta and p110delta in LNCaP cells, whereas p110alpha was required for PI3K activation in response to RTK stimulation by heregulin-beta1.
  • These findings show that basal PI3K activity in PTEN-deficient PCa cells is RTK-independent and can be mediated by p110beta and p110delta.

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  • (PMID = 20231295.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01CA89021; United States / NCI NIH HHS / CA / P50 CA090381; United States / NCI NIH HHS / CA / 1P01CA120964-01A1; United States / NCI NIH HHS / CA / P01 CA089021; United States / NCI NIH HHS / CA / 5P30CA006516-43; United States / NCI NIH HHS / CA / P30 CA006516; United States / NCI NIH HHS / CA / P50 CA90381
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2865293
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38. Fischgräbe J, Götte M, Michels K, Kiesel L, Wülfing P: Targeting endothelin A receptor enhances anti-proliferative and anti-invasive effects of the HER2 antibody trastuzumab in HER2-overexpressing breast cancer cells. Int J Cancer; 2010 Aug 1;127(3):696-706
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  • [Title] Targeting endothelin A receptor enhances anti-proliferative and anti-invasive effects of the HER2 antibody trastuzumab in HER2-overexpressing breast cancer cells.
  • Human epidermal growth factor receptor 2 (HER2) is frequently overexpressed in human breast cancers.
  • It is known to drive tumor growth and progression and represents a prominent target in breast cancer therapy.
  • The endothelin (ET) system, in particular ET-1 and its receptor ET(A)R, is of major relevance for breast cancer growth and invasion.
  • Having previously demonstrated coexpression of ET(A)R and HER2 in breast tumors, this study was designed to investigate molecular interactions of HER2 (including the epidermal growth factor receptor EGFR as its major coreceptor) and ET signaling, and the potential benefit of a combined anti-HER2/ET(A)R treatment in human breast cancer cells.
  • Dual HER2-ET(A)R targeting utilizing trastuzumab (monoclonal anti-HER2 antibody) and the ET(A)R antagonist atrasentan was superior to each agent alone in inhibiting basal and EGF-induced proliferation and invasion of HER2-overexpressing BT-474 and SK-BR-3 cells.
  • EGF-induced invasion was partially inhibited by atrasentan alone, suggesting the involvement of ET(A)R in EGF receptor mediated invasion of breast cancer cells.
  • This study suggests complex interactions between HER2/EGFR and ET pathways in breast cancer and supports the hypothesis that dual HER2-ET(A)R targeting may represent a highly effective approach in breast cancer treatment.
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Blotting, Western. Cell Line, Tumor. Down-Regulation. Drug Synergism. Endothelin-1 / metabolism. Endothelin-1 / secretion. Enzyme-Linked Immunosorbent Assay. Female. Humans. Phosphorylation. Pyrrolidines / pharmacology. Trastuzumab


39. Fazaa B, Cribier B, Zaraa I, Zermani R, Zeglaoui F, Zouari B, Ben Jilani S, Maalej M, Kamoun MR: Low-dose X-ray depilatory treatment induces trichoblastic tumors of the scalp. Dermatology; 2007;215(4):301-7
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  • Patients who underwent this treatment are at high risk of developing scalp tumors or other cancers.
  • Tumors were basal cell carcinomas in 47 cases, trichoblastomas in 10 cases and trichoblastic carcinomas in 4 cases.
  • Mean delay of onset of tumors after radiotherapy was 39.4 years in basal cell carcinoma cases, 38.3 years in trichoblastoma cases and 35.6 years in trichoblastic carcinoma cases.
  • CONCLUSIONS: This series shows that although basal cell carcinoma is the most frequent tumor in this situation, trichoblastomas are common.
  • [MeSH-major] Carcinoma, Basal Cell / etiology. Hair Removal / methods. Neoplasms, Radiation-Induced / etiology. Radiodermatitis / etiology. Skin Neoplasms / etiology. X-Rays / adverse effects

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17911987.001).
  • [ISSN] 1421-9832
  • [Journal-full-title] Dermatology (Basel, Switzerland)
  • [ISO-abbreviation] Dermatology (Basel)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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40. Sharp JA, Mailer SL, Thomson PC, Lefèvre C, Nicholas KR: Identification and transcript analysis of a novel wallaby (Macropus eugenii) basal-like breast cancer cell line. Mol Cancer; 2008;7:1
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  • [Title] Identification and transcript analysis of a novel wallaby (Macropus eugenii) basal-like breast cancer cell line.
  • BACKGROUND: A wide variety of animal models have been used to study human breast cancer.
  • Murine, feline and canine mammary tumor cell lines have been studied for several decades and have been shown to have numerous aspects in common with human breast cancer.
  • It is clear that new comparative approaches to study cancer etiology are likely to be productive.
  • RESULTS: A continuous line of breast carcinoma cells (WalBC) was established from a primary breast cancer that spontaneously arose in a female tammar wallaby (Macropus eugenii).
  • The WalBC cell line was cultured from the primary tumor and passaged for 22 months.
  • Gene expression profiling of WalBC cells was performed using a cDNA microarray of nearly 10,000 mammary gland cDNA clones and compared to normal primary mammary cells and profiles of human breast cancer.
  • WalBC cells exhibited expression of known markers of basal invasive human breast cancers as well as increased KRT17, KRT 14 and KRT 19, DSP, s100A4, NDRG-1, ANXA1, TK1 and AQP3 gene expression and decreased gene expression of TIMP3, VIM and TAGLN.
  • New targets for breast cancer treatment were identified such as ZONAB, PACSIN3, MRP8 and SUMO1 which have human homologues.
  • CONCLUSION: This study demonstrates how novel models of breast cancer can provide new fundamental clues regarding cancer etiology which may lead to new human treatments and therapies.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Down-Regulation. Epithelial Cells / cytology. Female. Gene Expression Profiling. Genes, Neoplasm. Humans. Neoplasm Invasiveness. RNA, Messenger / genetics. RNA, Messenger / metabolism. Up-Regulation


41. Pratt MA, Tibbo E, Robertson SJ, Jansson D, Hurst K, Perez-Iratxeta C, Lau R, Niu MY: The canonical NF-kappaB pathway is required for formation of luminal mammary neoplasias and is activated in the mammary progenitor population. Oncogene; 2009 Jul 30;28(30):2710-22
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  • Analysis of NF-kappaB family proteins and target genes using microarray data from a cohort of human mammary tumors revealed the expression of a canonical NF-kappaB pathway, but not non-canonical pathway proteins in HER2+ luminal cancers.
  • HER2+ tumors also showed differential regulation of specific NF-kappaB target genes relative to basal and ER+ luminal cancers.
  • Isolation of mammary cell populations enriched for stem and progenitor cell characteristics from an NF-kappaB-EGFP reporter mouse by fluorescence-activated cell sorting demonstrated that luminal progenitors contain activated NF-kappaB whereas the mammary stem cell-enriched population, does not.


42. Kapucuoglu N, Basak PY, Bircan S, Sert S, Akkaya VB: Immunohistochemical galectin-3 expression in non-melanoma skin cancers. Pathol Res Pract; 2009;205(2):97-103
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  • [Title] Immunohistochemical galectin-3 expression in non-melanoma skin cancers.
  • It participates in a variety of normal and pathologic processes, including cancer progression.
  • In this study, we evaluated the pattern of expression of galectin-3 in cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), and its correlation with the grade of differentiation in SCC and tumor size.
  • Galectin-3 expression was evaluated by immunohistochemistry in 31 SCCs, 30 BCCs, and 29 non-tumoral skin samples.
  • Galectin-3 expression was higher in normal epidermis than in non-melanoma skin cancers, except for cytoplasmic immunoreactivity in SCC.
  • Cytoplasmic galectin-3 immunoreactivity was significantly higher than nuclear immunoreactivity in non-melanoma skin cancers.
  • Decreased nuclear galectin-3 expression and cytoplasmic immunoreactivity in tumors are important factors in the progression from the normal to the cancerous state in non-melanoma skin cancers.
  • [MeSH-major] Carcinoma, Basal Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Galectin 3 / biosynthesis. Skin Neoplasms / metabolism

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  • (PMID = 18951731.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Galectin 3
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43. Zhao X, Malhotra GK, Lele SM, Lele MS, West WW, Eudy JD, Band H, Band V: Telomerase-immortalized human mammary stem/progenitor cells with ability to self-renew and differentiate. Proc Natl Acad Sci U S A; 2010 Aug 10;107(32):14146-51
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  • There is increasing evidence that breast and other cancers originate from and are maintained by a small fraction of stem/progenitor cells with self-renewal properties.
  • Whether such cancer stem/progenitor cells originate from normal stem cells based on initiation of a de novo stem cell program, by reprogramming of a more differentiated cell type by oncogenic insults, or both remains unresolved.
  • We present evidence that normal and human telomerase reverse transcriptase (hTERT)-immortalized human mammary epithelial cells (hMECs) isolated and maintained in Dana-Farber Cancer Institute 1 (DFCI-1) medium retain a fraction with progenitor cell properties.
  • These cells coexpress basal (K5, K14, and vimentin), luminal (E-cadherin, K8, K18, or K19), and stem/progenitor (CD49f, CD29, CD44, and p63) cell markers.
  • Given the emerging evidence that stem/progenitor cells serve as precursors for cancers, these cellular reagents represent a timely and invaluable resource to explore unresolved questions related to stem/progenitor origin of breast cancer.

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  • (PMID = 20660721.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE22580
  • [Grant] United States / NCI NIH HHS / CA / R01 CA087986; United States / NCI NIH HHS / CA / CA105489; United States / NCI NIH HHS / CA / CA099163-11; United States / NCI NIH HHS / CA / R01 CA099163-09; United States / NCI NIH HHS / CA / R01 CA096844; United States / NCI NIH HHS / CA / CA96844; United States / NCI NIH HHS / CA / CA099163-10; United States / NCI NIH HHS / CA / R01 CA094143; United States / NCI NIH HHS / CA / CA116552; United States / NCI NIH HHS / CA / R01 CA116552; United States / NCI NIH HHS / CA / CA099163-09; United States / NCI NIH HHS / CA / R01 CA105489; United States / NCI NIH HHS / CA / CA94143; United States / NCRR NIH HHS / RR / P20 RR016469; United States / NCI NIH HHS / CA / R01 CA099163-11; United States / NCI NIH HHS / CA / CA99163; United States / NCI NIH HHS / CA / R01 CA099163-10; United States / NCI NIH HHS / CA / R01 CA099163; United States / NCI NIH HHS / CA / CA87986
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2922525
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44. Tran KT, Lamb P, Deng JS: Matrikines and matricryptins: Implications for cutaneous cancers and skin repair. J Dermatol Sci; 2005 Oct;40(1):11-20
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  • [Title] Matrikines and matricryptins: Implications for cutaneous cancers and skin repair.
  • Dermatologists are faced daily with the need to optimize skin repair and excise cutaneous cancers.
  • The extracellular matrix plays a pivotal role in cellular migration, proliferation, and gene regulation during wound healing and progression of melanoma, basal cell carcinoma, and squamous cell carcinoma.
  • Within the last few years, a new class of ligand, the matrikine or matricryptin, has been characterized as subdomains of various ECM proteins capable of signaling to the cell through receptors, such as growth factor receptors.
  • The EGF-like repeats of tenascin-C and laminin-5 signal to EGFR preferentially to upregulate migration during skin repair and tumor progression.
  • Other matrikines in collagen, elastin, decorin, and laminin-1 can promote chemotaxis, mitogenesis, and metastasis in cancers, such as melanoma.
  • Finally, the unique properties of matrikines have been utilized in cancer therapeutics and tissue engineering.
  • Within the next few years, the nature and function of this emerging class of matrikine ligands will have an impact on dermatology, as these proteins are altered in wound repair and skin diseases.
  • [MeSH-major] Extracellular Matrix Proteins / physiology. Skin Neoplasms / etiology
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Adhesion Molecules / physiology. Collagen / physiology. Humans. Ligands. Molecular Sequence Data. Signal Transduction. Tenascin / physiology. Tissue Engineering. Wound Healing

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  • (PMID = 15993569.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Extracellular Matrix Proteins; 0 / Ligands; 0 / Tenascin; 0 / kalinin; 9007-34-5 / Collagen
  • [Number-of-references] 50
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45. Forslund O, Iftner T, Andersson K, Lindelof B, Hradil E, Nordin P, Stenquist B, Kirnbauer R, Dillner J, de Villiers EM, Viraskin Study Group: Cutaneous human papillomaviruses found in sun-exposed skin: Beta-papillomavirus species 2 predominates in squamous cell carcinoma. J Infect Dis; 2007 Sep 15;196(6):876-83
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  • [Title] Cutaneous human papillomaviruses found in sun-exposed skin: Beta-papillomavirus species 2 predominates in squamous cell carcinoma.
  • BACKGROUND: A spectrum of cutaneous human papillomaviruses (HPVs) is detectable in nonmelanoma skin cancers, as well as in healthy skin, but the significance that the presence of these types of HPV DNA has for the pathogenesis of skin cancer remains unclear.
  • METHODS: We studied 349 nonimmunosuppressed patients with skin lesions (82 with squamous cell carcinomas, 126 with basal cell carcinomas, 49 with actinic keratoses, and 92 with benign lesions).
  • After superficial skin had been removed by tape, paired biopsy samples--from the lesion and from healthy skin from the same patient--were tested for HPV DNA.
  • RESULTS: Overall, 12% of healthy skin samples were positive for HPV DNA, compared with 26% of benign lesions, 22% of actinic keratoses, 18% of basal cell carcinomas, and 26% of squamous cell carcinomas.
  • HPV DNA was associated with sites extensively exposed to the sun, both for the lesions (odds ratio [OR], 4.45 [95% confidence interval {CI}, 2.44-8.11]) and for the healthy skin samples (OR, 3.65 [95% CI 1.79-7.44]).
  • HPV types of Beta-papillomavirus species 2 predominate in squamous cell carcinomas (OR, 4.40 [95% CI, 1.92-10.06]), whereas HPV types of Beta-papillomavirus species 1 are primarily found in benign lesions (OR, 3.47 [95% CI, 1.72-6.99]).
  • HPV types of Beta-papillomavirus species 2, but not of species 1, are associated with squamous cell carcinoma.
  • [MeSH-major] Betapapillomavirus / isolation & purification. Carcinoma, Squamous Cell / virology. Papillomaviridae / classification. Papillomaviridae / isolation & purification. Papillomavirus Infections / virology. Skin / virology. Skin Neoplasms / virology. Sunlight / adverse effects

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  • (PMID = 17703418.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 18990
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
  • [Other-IDs] NLM/ EMS55140; NLM/ PMC3795387
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46. Cernea CR, Ferraz AR, de Castro IV, Sotto MN, Logullo AF, Bacchi CE, Plopper C, Wanderlei F, de Carlucci D Jr, Hojaij FC: Perineural invasion in aggressive skin carcinomas of the head and neck. Potentially dangerous but frequently overlooked. ORL J Otorhinolaryngol Relat Spec; 2009;71(1):21-6
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  • [Title] Perineural invasion in aggressive skin carcinomas of the head and neck. Potentially dangerous but frequently overlooked.
  • INTRODUCTION: Perineural invasion is a well-recognized form of cancer dissemination.
  • However, it has been reported only in few papers concerning cutaneous carcinomas (basal cell, BCC, and squamous cell, SCC).
  • No paper was found in the literature looking for perineural invasion in very aggressive skin cancers with skull base extension, with immunohistochemical analysis.
  • METHODS: This is a retrospective review, including 35 very advanced skin carcinomas with skull base invasion (24 BCCs and 11 SCCs, operated on at a single institution from 1982 to 2000).
  • CONCLUSIONS: In this series, it was demonstrated that immunohistochemically detected perineural invasion was very prevalent in advanced skin carcinomas.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / pathology. Head and Neck Neoplasms / pathology. Skin Neoplasms / pathology. Skull Base / innervation. Skull Base / pathology

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18946230.001).
  • [ISSN] 1423-0275
  • [Journal-full-title] ORL; journal for oto-rhino-laryngology and its related specialties
  • [ISO-abbreviation] ORL J. Otorhinolaryngol. Relat. Spec.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / S100 Proteins
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47. Lee JH, Pyon JK, Kim DW, Lee SH, Nam HS, Kim CH, Kang SG, Lee YJ, Park MY, Jeong DJ, Cho MK: Elevated c-Src and c-Yes expression in malignant skin cancers. J Exp Clin Cancer Res; 2010;29:116
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  • [Title] Elevated c-Src and c-Yes expression in malignant skin cancers.
  • BACKGROUND: Src family kinases (SFKs) play an important role in cancer proliferation, survival, motility, invasiveness, metastasis, and angiogenesis.
  • Among the SFKs, c-Src and c-Yes are particularly over-expressed or hyper-activated in many human epithelial cancers.
  • However, only a few studies have attempted to define the expression and role of c-Src and c-Yes in cutaneous carcinomas.
  • OBJECTIVES: To investigate the expression of c-Src and c-Yes in cutaneous carcinomas to include malignant melanoma (MM), squamous cell carcinoma (SCC) and basal cell carcinoma (BCC).
  • METHODS: We examined 6 normal skin tissues and 18 malignant skin tumor tissues using western blotting for the expression of c-Src and c-Yes.
  • In another set, 16 specimens of MM, 16 SCCs and 16 BCCs were analyzed for the expression of c-Src and c-Yes using immunohistochemical staining.
  • RESULTS: Western blotting showed that c-Src was expressed in all malignant skin tumors, but not in normal skin, while c-Yes was expressed in MM and SCC, but not in BCC and normal skin.
  • Immunohistochemical staining results of c-Src and c-Yes in MM, SCC, and BCC mirrored those of the western blot analysis.
  • CONCLUSIONS: c-Src, rather than c-Yes, plays a key role in the proliferation and progression of malignant skin cancers.
  • [MeSH-major] Carcinoma, Basal Cell / enzymology. Carcinoma, Squamous Cell / enzymology. Melanoma / enzymology. Protein-Tyrosine Kinases / analysis. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins c-yes / analysis. Skin Neoplasms / enzymology

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  • (PMID = 20796316.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / Proto-Oncogene Proteins c-yes; EC 2.7.10.2 / YES1 protein, human; EC 2.7.10.2 / src-Family Kinases
  • [Other-IDs] NLM/ PMC2936336
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48. Sapijaszko MJ: Imiquimod 5% cream (Aldara) in the treatment of basal cell carcinoma. Skin Therapy Lett; 2005 Jul-Aug;10(6):2-5
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  • [Title] Imiquimod 5% cream (Aldara) in the treatment of basal cell carcinoma.
  • Skin cancer, the most common human cancer, is now a global epidemic.
  • The most prevalent form of nonmelanoma skin cancer is basal cell carcinoma (BCC), the incidence of which continues to increase prompting development of new treatment modalities designed to add or complement current therapies.
  • It enhances both the innate and acquired immune response, and has successfully treated both superficial and nodular basal cell carcinomas through the localized activation of elaborate immune response.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 16292452.001).
  • [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 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
  • [Number-of-references] 14
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49. Sneddon JB, Zhen HH, Montgomery K, van de Rijn M, Tward AD, West R, Gladstone H, Chang HY, Morganroth GS, Oro AE, Brown PO: Bone morphogenetic protein antagonist gremlin 1 is widely expressed by cancer-associated stromal cells and can promote tumor cell proliferation. Proc Natl Acad Sci U S A; 2006 Oct 3;103(40):14842-7
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  • [Title] Bone morphogenetic protein antagonist gremlin 1 is widely expressed by cancer-associated stromal cells and can promote tumor cell proliferation.
  • In this work, we used a genomic approach to identify factors produced by cells in the microenvironment of basal cell carcinoma (BCC) of the skin, one of the most common human cancers.
  • The global gene expression programs of stromal cell cultures derived from human BCCs showed consistent, systematic differences from those derived from nontumor skin.
  • The gene most consistently expressed at a higher level in BCC tumor stromal cells compared with those from nontumor skin was GREMLIN 1, which encodes a secreted antagonist of the bone morphogenetic protein (BMP) pathway.
  • BMPs and their antagonists are known to play a crucial role in stem and progenitor cell biology as regulators of the balance between expansion and differentiation.
  • Consistent with the hypothesis that BMP antagonists might have a similar role in cancer, we found GREMLIN 1 expression in the stroma of human BCC tumors but not in normal skin in vivo.
  • Our data suggest that BMP antagonists may be important constituents of tumor stroma, providing a favorable microenvironment for cancer cell survival and expansion in many cancers.

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  • (PMID = 17003113.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE5502
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077097; United States / NIAMS NIH HHS / AR / AR 046786; United States / NCI NIH HHS / CA / CA 77097; United States / NIAMS NIH HHS / AR / K08 AR 0008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BMP2 protein, human; 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / GREM1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC1578503
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50. Hoeflich KP, O'Brien C, Boyd Z, Cavet G, Guerrero S, Jung K, Januario T, Savage H, Punnoose E, Truong T, Zhou W, Berry L, Murray L, Amler L, Belvin M, Friedman LS, Lackner MR: In vivo antitumor activity of MEK and phosphatidylinositol 3-kinase inhibitors in basal-like breast cancer models. Clin Cancer Res; 2009 Jul 15;15(14):4649-64
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  • [Title] In vivo antitumor activity of MEK and phosphatidylinositol 3-kinase inhibitors in basal-like breast cancer models.
  • PURPOSE: The pathways underlying basal-like breast cancer are poorly understood, and as yet, there is no approved targeted therapy for this disease.
  • We investigated the role of mitogen-activated protein kinase kinase (MEK) and phosphatidylinositol 3-kinase (PI3K) inhibitors as targeted therapies for basal-like breast cancer.
  • EXPERIMENTAL DESIGN: We used pharmacogenomic analysis of a large panel of breast cancer cell lines with detailed accompanying molecular information to identify molecular predictors of response to a potent and selective inhibitor of MEK and also to define molecular mechanisms underlying combined MEK and PI3K targeting in basal-like breast cancer.
  • RESULTS: We found that basal-like breast cancer models have an activated RAS-like transcriptional program and show greater sensitivity to a selective inhibitor of MEK compared with models representative of other breast cancer subtypes.
  • We also showed that loss of PTEN is a negative predictor of response to MEK inhibition, that treatment with a selective MEK inhibitor caused up-regulation of PI3K pathway signaling, and that dual blockade of both PI3K and MEK/extracellular signal-regulated kinase signaling synergized to potently impair the growth of basal-like breast cancer models in vitro and in vivo.
  • CONCLUSIONS: Our studies suggest that single-agent MEK inhibition is a promising therapeutic modality for basal-like breast cancers with intact PTEN, and also provide a basis for rational combination of MEK and PI3K inhibitors in basal-like cancers with both intact and deleted PTEN.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Cluster Analysis. Dose-Response Relationship, Drug. Female. Flow Cytometry. Gene Expression Profiling. Humans. Immunoblotting. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / metabolism. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Inbred Strains. Mice, Nude. Mutation. Oligonucleotide Array Sequence Analysis. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / metabolism

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  • [CommentIn] Clin Cancer Res. 2009 Jul 15;15(14):4518-20 [19584146.001]
  • (PMID = 19567590.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 3.1.3.67 / PTEN Phosphohydrolase
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51. Campbell RM, Perlis CS, Malik MK, Dufresne RG Jr: Characteristics of Mohs practices in the United States: a recall survey of ACMS surgeons. Dermatol Surg; 2007 Dec;33(12):1413-8; discussion 1418
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  • RESULTS: Most respondents were part of a single speciality group, in a suburban or urban setting, performed between 501-1,000 cases per year, and had been in practice from 0-5 years.
  • The vast majority of Mohs excisions are for basal cell cancers and squamous cell cancers, followed by melanoma.
  • [MeSH-major] Mohs Surgery / statistics & numerical data. Professional Practice / statistics & numerical data. Skin Neoplasms / surgery

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  • [CommentIn] Dermatol Surg. 2010 Feb;36(2):194-7 [20039919.001]
  • (PMID = 18076605.001).
  • [ISSN] 1524-4725
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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52. Krajewska M, Olson AH, Mercola D, Reed JC, Krajewski S: Claudin-1 immunohistochemistry for distinguishing malignant from benign epithelial lesions of prostate. Prostate; 2007 Jun 15;67(9):907-10
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  • BACKGROUND: Claudins are a family of approximately 23 integral membrane tight junction (TJ) proteins that maintain cell polarity and paracellular barrier functions in epithelial and endothelial cells.
  • Although Claudin-1 was demonstrated to be typically downregulated in various cancers, the precise expression patterns of this protein in normal and neoplastic tissues remain poorly characterized.
  • The Claudin-1 expression pattern was compared with that of the basal cell-specific markers, p63, and HMW cytokeratin (34betaE12), by employing double-labeling techniques in conjunction with image analysis methods utilizing color deconvolution algorithms.
  • RESULTS: In benign prostatic epithelium, pronounced Claudin-1 expression was observed in the basal cell layer with no staining in luminal cells.

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  • (PMID = 17440968.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114810; United States / NCI NIH HHS / CA / CA114810-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / CLDN1 protein, human; 0 / Claudin-1; 0 / Membrane Proteins; 68238-35-7 / Keratins
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53. Laska MJ, Nexø BA, Vistisen K, Poulsen HE, Loft S, Vogel U: Polymorphisms in RAI and in genes of nucleotide and base excision repair are not associated with risk of testicular cancer. Cancer Lett; 2005 Jul 28;225(2):245-51
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  • [Title] Polymorphisms in RAI and in genes of nucleotide and base excision repair are not associated with risk of testicular cancer.
  • Testicular cancer has been suggested to be primed in utero and there is familiar occurrence, particularly brothers and sons of men with testicular cancer have increased risk.
  • Although no specific causative genotoxic agents have been identified, variations in DNA repair capacity could be associated with the risk of testicular cancer.
  • A case-control study of 184 testicular cancer cases and 194 population-based controls living in the Copenhagen Greater Area in Denmark was performed.
  • We found that neither polymorphisms in several DNA repair genes nor alleles of several polymorphisms in the chromosomal of region 19q13.2-3, encompassing the genes ASE, ERCC1, RAI and XPD, were associated with risk of testicular cancer in Danish patients.
  • This is in contrast to other cancers, where we reported strong associations between polymorphisms in ERCC1, ASE and RAI and occurrence of basal cell carcinoma, breast cancer and lung.
  • To our knowledge this is the first study of DNA repair gene polymorphisms and risk of testicular cancer.

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  • (PMID = 15885892.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Nucleotides; 0 / PPP1R13L protein, human; 0 / Repressor Proteins
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54. Biel M: Advances in photodynamic therapy for the treatment of head and neck cancers. Lasers Surg Med; 2006 Jun;38(5):349-55
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  • [Title] Advances in photodynamic therapy for the treatment of head and neck cancers.
  • Photodynamic therapy (PDT) is an FDA-approved minimally invasive medical treatment modality that utilizes light in the presence of oxygen to activate photosensitizing agents that are relatively selectively concentrated in abnormal or neoplastic cells resulting in cell death.
  • In the EU the above noted indications have also been approved in addition to the treatment of early head and neck cancers and palliative treatment of head and neck cancer using the photosensitizer Foscan; and treatment of basal and squamous cell skin cancers using the photosensitizer Metvix.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Ambulatory Care. Carcinoma, Squamous Cell / therapy. Combined Modality Therapy. Female. Humans. Male. Melanoma / therapy. Middle Aged. Minnesota / epidemiology. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / therapy. Papilloma / therapy. Retrospective Studies. Sarcoma, Kaposi / therapy

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16788923.001).
  • [ISSN] 0196-8092
  • [Journal-full-title] Lasers in surgery and medicine
  • [ISO-abbreviation] Lasers Surg Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 97067-70-4 / Dihematoporphyrin Ether
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55. Conscience I, Jovenin N, Coissard C, Lorenzato M, Durlach A, Grange F, Birembaut P, Clavel C, Bernard P: P16 is overexpressed in cutaneous carcinomas located on sun-exposed areas. Eur J Dermatol; 2006 Sep-Oct;16(5):518-22
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  • BACKGROUND: Recently, an increased expression of P16, a cell cycle regulatory tumor suppressor protein, has been demonstrated in cervical squamous neoplasms as a marker of malignancy.
  • In contrast, studies performed in skin carcinomas led to contradictory results.
  • OBJECTIVES: Our first aim was to evaluate P16 expression in different types of non-melanoma skin cancers compared with normal skin and benign tumors.
  • The second aim was to evaluate the relationship between P16 expression and the location of skin tumors (i.e. exposed versus non exposed sites).
  • Finally, we also studied Ki67 expression in skin carcinomas and control biopsies.
  • METHODS: Skin biopsy specimens with typical histologic features of squamous cell carcinoma (SCC; n = 30), Bowen's disease (BD; n = 17), basal cell carcinoma (BCC; n = 10), seborrheic keratosis (SK; n = 10) and normal human skin (NHS; n = 9) were obtained from 76 patients seen at our institution between 2001 and 2003.
  • Overexpression of P16 was associated with a high rate of Ki67 positive tumour cells in 23/57 malignant skin tumors (40%).
  • CONCLUSION: Our study demonstrated that the expression of P16 and Ki67 is associated with skin carcinomas.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Skin Neoplasms / metabolism. Ultraviolet Rays

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  • (PMID = 17101472.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Ki-67 Antigen
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56. Maufort JP, Williams SM, Pitot HC, Lambert PF: Human papillomavirus 16 E5 oncogene contributes to two stages of skin carcinogenesis. Cancer Res; 2007 Jul 1;67(13):6106-12
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  • [Title] Human papillomavirus 16 E5 oncogene contributes to two stages of skin carcinogenesis.
  • High-risk human papillomaviruses (HPVs), which cause the vast majority of cervical cancer, other anogenital cancers, and a subset of head and neck squamous cell carcinomas, encode three oncogenes: E5, E6, and E7.
  • To determine the oncogenic properties of HPV16 E5 in vivo, we previously generated K14E5 transgenic mice, in which expression of E5 was directed to the basal compartment of stratified squamous epithelia.
  • In these mice, E5 induced epidermal hyperplasia and spontaneous skin tumors.
  • In the current study, we determined how E5 contributes to tumor formation in the skin using a multistage model for skin carcinogenesis that specifies the role of genes in three stages: initiation, promotion, and malignant progression.
  • Thus, HPV16 E5 contributes to two stages of skin carcinogenesis: promotion and progression.

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  • (PMID = 17616666.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA022443; United States / NCI NIH HHS / CA / P01 CA022443-320006; United States / NCI NIH HHS / CA / R01 CA098428-05; United States / NIDCR NIH HHS / DE / R01 DE017315-03; United States / NCI NIH HHS / CA / CA098428; United States / NCI NIH HHS / CA / CA098428-05; United States / NCI NIH HHS / CA / R01 CA098428-04; United States / NIDCR NIH HHS / DE / DE017315; United States / NCI NIH HHS / CA / CA022443-320006; United States / NIDCR NIH HHS / DE / R01 DE017315-02; United States / NIDCR NIH HHS / DE / R01 DE017315; United States / NCI NIH HHS / CA / CA098428-04S1; United States / NIDCR NIH HHS / DE / R01 DE017315-01; United States / NCI NIH HHS / CA / R01 CA098428-04S1; United States / NCI NIH HHS / CA / P01 CA022443-310006; United States / NCI NIH HHS / CA / CA022443-300006; United States / NCI NIH HHS / CA / CA022443-310006; United States / NCI NIH HHS / CA / P01 CA022443-300006; United States / NCI NIH HHS / CA / CA098428-04; United States / NCI NIH HHS / CA / P01 CA022443; United States / NCI NIH HHS / CA / R01 CA098428
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Oncogene Proteins, Viral; 0 / oncogene protein E5, Human papillomavirus type 16; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 8002-74-2 / Paraffin; 9007-49-2 / DNA; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS193051; NLM/ PMC2858287
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57. Wienke D, Davies GC, Johnson DA, Sturge J, Lambros MB, Savage K, Elsheikh SE, Green AR, Ellis IO, Robertson D, Reis-Filho JS, Isacke CM: The collagen receptor Endo180 (CD280) Is expressed on basal-like breast tumor cells and promotes tumor growth in vivo. Cancer Res; 2007 Nov 1;67(21):10230-40
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  • [Title] The collagen receptor Endo180 (CD280) Is expressed on basal-like breast tumor cells and promotes tumor growth in vivo.
  • Tumor cell invasion into the surrounding stroma requires increased cell motility and extensive remodeling of the extracellular matrix.
  • Endo180 (CD280, MRC2, urokinase-type plasminogen activator receptor-associated protein) is a recycling endocytic receptor that functions in both these cellular activities by promoting cell migration and uptake of collagens for intracellular degradation.
  • The contrary observation that Endo180 is expressed on epithelial tumor cell lines that display a high invasive capacity suggested that up-regulation of this receptor may be an associated and functional component in the acquisition of a more aggressive phenotype by tumor cells in vivo.
  • Here, we show that high levels of Endo180 are found in a subset of basal-like breast cancers and that this expression is an independent prognostic marker for shorter disease-free survival.
  • First, it was shown that Endo180 can be transcriptionally up-regulated in vitro following transforming growth factor-beta treatment of breast cancer cells.
  • Together, these data argue that elevated expression of this receptor in tumor cells could have important consequences in subsets of basal-like carcinomas for which there is a current lack of effective treatment.
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Tissue Array Analysis

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  • (PMID = 17974964.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endo180; 0 / Receptors, Mitogen
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58. Weinstock MA: Controversies in the public health approach to keratinocyte carcinomas. Br J Dermatol; 2006 May;154 Suppl 1:3-4
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  • Keratinocyte carcinomas are very common cancers in fair-skinned populations throughout the world.
  • The term 'keratinocyte carcinoma' includes basal and squamous cell carcinoma of the skin, but not other cancers that may be included under the more ambiguous term 'nonmelanoma skin cancer'.
  • Incidence and mortality are important for assessing impact and recent research suggests that these cancers are increasing in incidence in young adults.
  • Ultimately, our aim is to reduce mortality and morbidity from these cancers, and to that end several large-scale trials of public health interventions have been conducted that may help point the way forward.
  • [MeSH-major] Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Skin Neoplasms / epidemiology

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  • (PMID = 16712708.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 1406-16-2 / Vitamin D
  • [Number-of-references] 12
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59. Chen J, Ruczinski I, Jorgensen TJ, Yenokyan G, Yao Y, Alani R, Liégeois NJ, Hoffman SC, Hoffman-Bolton J, Strickland PT, Helzlsouer KJ, Alberg AJ: Nonmelanoma skin cancer and risk for subsequent malignancy. J Natl Cancer Inst; 2008 Sep 3;100(17):1215-22
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  • [Title] Nonmelanoma skin cancer and risk for subsequent malignancy.
  • BACKGROUND: Individuals with a personal history of nonmelanoma skin cancer (NMSC) may have an increased risk of subsequent noncutaneous malignancies.
  • METHODS: In the CLUE (Give Us a Clue to Cancer and Heart Disease) II cohort, which was established in Washington County, MD, in 1989, the risk of new malignancies was compared among individuals with (n = 769) and without (n = 18,405) a personal history of NMSC (total n = 19,174) during a 16-year follow-up period.
  • Pathologically confirmed NMSC (and other malignancies) were ascertained from the Washington County Cancer Registry.
  • RESULTS: The crude incidence rate (per 10,000 person-years) of subsequent cancers other than NMSC among participants with a positive personal history of NMSC was 293.5 and with a negative history was 77.8.
  • Compared with persons with no personal history of NMSC, those with such a history had a statistically significantly increased risk of being diagnosed with a subsequent cancer other than NMSC (RR = 1.99, 95% CI = 1.70 to 2.33) after adjusting for age, sex, body mass index, smoking status, and educational level.
  • The association was observed for both basal cell carcinoma (multivariable-adjusted RR = 2.03, 95% CI = 1.70 to 2.42) and squamous cell carcinoma (multivariable-adjusted RR = 1.97, 95% CI = 1.50 to 2.59) of the skin.
  • NMSC was a statistically significantly stronger cancer risk factor in younger age groups than in older age groups (P for interaction = .022).
  • CONCLUSIONS: This community-based, prospective cohort study provides evidence for an association between an NMSC diagnosis and an increased risk of subsequent cancer, even after adjusting for individual-level risk factors.

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  • (PMID = 18728282.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA105069; United States / NCI NIH HHS / CA / CA105069
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2720713
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60. Saarinen NM, Bingham C, Lorenzetti S, Mortensen A, Mäkelä S, Penttinen P, Sørensen IK, Valsta LM, Virgili F, Vollmer G, Wärri A, Zierau O: Tools to evaluate estrogenic potency of dietary phytoestrogens:A consensus paper from the EU Thematic Network "Phytohealth" (QLKI-2002-2453). Genes Nutr; 2006 Sep;1(3-4):143-58
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  • These compounds have been suggested to provide beneficial effects on multiple menopause-related conditions as well as on development of hormone-dependent cancers, which has increased the interest in products and foods with high phytoestrogen content.
  • For reliable assessment of estrogenicity of dietary phytoestrogens in vivo, special emphasis should be focused on selection of the basal diet, route and doses of administration, and possible metabolic differences between the species used and humans.

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  • (PMID = 18850210.001).
  • [ISSN] 1555-8932
  • [Journal-full-title] Genes & nutrition
  • [ISO-abbreviation] Genes Nutr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC3454835
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61. De Argila D, Rodríguez-Nevado IM, Chaves A: [Regarding the variability of medical practice in skin cancers]. Actas Dermosifiliogr; 2005 Jan-Feb;96(1):66-7
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  • [Title] [Regarding the variability of medical practice in skin cancers].
  • [Transliterated title] Sobre la variabilidad de la práctica médica en los cánceres de piel.
  • [MeSH-major] Carcinoma, Basal Cell / therapy. Consensus. Dermatology / standards. Skin Neoplasms / therapy

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  • (PMID = 16476340.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Letter
  • [Publication-country] Spain
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62. Pires MM, Emmert D, Hrycyna CA, Chmielewski J: Inhibition of P-glycoprotein-mediated paclitaxel resistance by reversibly linked quinine homodimers. Mol Pharmacol; 2009 Jan;75(1):92-100
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  • P-glycoprotein (P-gp), an ATP-dependent drug efflux pump, has been implicated in multidrug resistance of several cancers as a result of its overexpression.
  • The designed agents were potent inhibitors of rhodamine 123 efflux in cultured cancer cell lines that display high levels of P-gp expression at the cell surface and in transfected cells expressing P-gp.
  • Further studies revealed that Q2 inhibited the efflux of a range of fluorescent substrates (rhodamine 123, doxorubicin, mitoxantrone, and BODIPY-FL-prazosin) from MCF-7/DX1 cells.
  • The reversibility of the tether was confirmed in experiments showing that Q2 was readily hydrolyzed by esterases in vitro (t(1/2) approximately 20 h) while demonstrating high resistance to nonenzymatic hydrolysis in cell culture media (t(1/2) approximately 21 days).
  • In addition, low concentrations of Q2 stimulated basal P-gp ATPase levels.

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  • Hazardous Substances Data Bank. QUININE .
  • Hazardous Substances Data Bank. VERAPAMIL HYDROCHLORIDE .
  • Hazardous Substances Data Bank. PRAZOSIN HYDROCHLORIDE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. TAXOL .
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  • (PMID = 18945821.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R21 EY018481; United States / NCI NIH HHS / CA / 2P30-CA23168; United States / NEI NIH HHS / EY / EY018481
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Affinity Labels; 0 / Fluorescent Dyes; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123; 80168379AG / Doxorubicin; A7V27PHC7A / Quinine; CJ0O37KU29 / Verapamil; EC 3.6.1.- / Adenosine Triphosphatases; P88XT4IS4D / Paclitaxel; XM03YJ541D / Prazosin
  • [Other-IDs] NLM/ PMC2685053
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63. Hong JW, Wu LC: ZAS3 represses NFκB-dependent transcription by direct competition for DNA binding. BMB Rep; 2010 Dec;43(12):807-12
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  • NFκB and ZAS3 are transcription factors that control important cellular processes including immunity, cell survival and apoptosis.
  • Although both proteins bind the κB-motif, they produce opposite physiological consequences; NFκB activates transcription, promotes cell growth and is often found to be constitutively expressed in cancer cells, while ZAS3 generally represses transcription, inhibits cell proliferation and is downregulated in some cancers.
  • Transient transfection studies show that N-terminal 645 amino acids is sufficient to repress transcription activated by NFκB, and that the identical region also possesses intrinsic repression activity to inhibit basal transcription from a promoter.

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  • (PMID = 21189157.001).
  • [ISSN] 1976-670X
  • [Journal-full-title] BMB reports
  • [ISO-abbreviation] BMB Rep
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30CA15058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / NF-kappa B; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / ZAS3 protein, human; 9007-49-2 / DNA
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64. Parsons CM, Muilenburg D, Bowles TL, Virudachalam S, Bold RJ: The role of Akt activation in the response to chemotherapy in pancreatic cancer. Anticancer Res; 2010 Sep;30(9):3279-89
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  • [Title] The role of Akt activation in the response to chemotherapy in pancreatic cancer.
  • The PI3K/Akt signaling pathway is constitutively activated in some pancreatic cancers; when activated, it inhibits chemotherapy-mediated apoptosis.
  • We examined whether Akt activity correlates with apoptotic resistance to chemotherapy in pancreatic cancer.
  • MATERIALS AND METHODS: A panel of human pancreatic cancer cells was evaluated for basal Akt activity as well as response to three chemotherapies.
  • Chemotherapy-induced cell death was evaluated following either up- or down-regulation of Akt activity.
  • RESULTS: There was a broad distribution among pancreatic cancer cell lines by Akt activity, as well as sensitivity to the three chemotherapeutic agents with no apparent correlation.
  • CONCLUSIONS: Basal Akt activity does not appear to be a useful predictor for selection of pancreatic cancers in targeting Akt to broadly induce chemosensitivity.

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  • (PMID = 20944098.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA093373; United States / NCI NIH HHS / CA / R03 CA123004; United States / NCI NIH HHS / CA / 1R03 CA123004
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor p21; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS719230; NLM/ PMC4557882
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65. Pan X, Arumugam T, Yamamoto T, Levin PA, Ramachandran V, Ji B, Lopez-Berestein G, Vivas-Mejia PE, Sood AK, McConkey DJ, Logsdon CD: Nuclear factor-kappaB p65/relA silencing induces apoptosis and increases gemcitabine effectiveness in a subset of pancreatic cancer cells. Clin Cancer Res; 2008 Dec 15;14(24):8143-51
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  • [Title] Nuclear factor-kappaB p65/relA silencing induces apoptosis and increases gemcitabine effectiveness in a subset of pancreatic cancer cells.
  • PURPOSE: Nuclear factor kappaB (NFkappaB) activity may increase survival and protect cancer cells from chemotherapy.
  • Therefore, NFkappaB activity may be prognostic, and inhibition of NFkappaB may be useful for pancreatic cancer therapy.
  • To test these hypotheses, we examined NFkappaB activity and the effects of inhibiting NFkappaB in several pancreatic cancer cell lines with differing sensitivities to gemcitabine.
  • EXPERIMENTAL DESIGN: The gemcitabine sensitivity of pancreatic cancer cell lines BxPC-3, L3.6pl, CFPAC-1, MPanc-96, PANC-1, and MIA PaCa-2 were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and fluorescence-activated cell sorting assays.
  • RESULTS: The cell lines L3.6pl, BxPC-3, and CFPAC-1 were sensitive, whereas MPanc-96, PANC-1, and MIA PaCa-2 were resistant to gemcitabine.
  • No significant correlation was observed between basal NFkappaB activity and gemcitabine sensitivity.
  • Silencing of p65/relA induced apoptosis and increased gemcitabine killing of all gemcitabine-sensitive pancreatic cancer cells.
  • No significant effects, however, were observed on gemcitabine-resistant pancreatic cancer cell lines either in vitro or in vivo.
  • Silencing of p65/relA was effective alone and in combination with gemcitabine in gemcitabine-sensitive but not gemcitabine-resistant pancreatic cancer cells.
  • Thus, NFkappaB may be a useful therapeutic target for a subset of pancreatic cancers.

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  • (PMID = 19088029.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA101936; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P20-CA101936
  • [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 / Antimetabolites, Antineoplastic; 0 / RNA, Small Interfering; 0 / Transcription Factor RelA; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Other-IDs] NLM/ NIHMS675289; NLM/ PMC4403242
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66. Nan H, Qureshi AA, Hunter DJ, Han J: Genetic variants in FGFR2 and FGFR4 genes and skin cancer risk in the Nurses' Health Study. BMC Cancer; 2009 Jun 06;9:172
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  • [Title] Genetic variants in FGFR2 and FGFR4 genes and skin cancer risk in the Nurses' Health Study.
  • Deregulation of the FGFR2 gene has been identified in a number of cancer sites.
  • Previous studies reported associations between genetic variants in the FGFR2 and FGFR4 genes and development of various cancers.
  • METHODS: We evaluated the associations of four genetic variants in the FGFR2 gene highly related to breast cancer risk and the three common tag-SNPs in the FGFR4 gene with skin cancer risk in a nested case-control study of Caucasians within the Nurses' Health Study (NHS) among 218 melanoma cases, 285 squamous cell carcinoma (SCC) cases, 300 basal cell carcinoma (BCC) cases, and 870 controls.
  • RESULTS: We found no evidence for associations between these seven genetic variants and the risks of melanoma and nonmelanocytic skin cancer.
  • CONCLUSION: Given the power of this study, we did not detect any contribution of genetic variants in the FGFR2 or FGFR4 genes to inherited predisposition to skin cancer among Caucasian women.

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  • (PMID = 19500394.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA122838; United States / NCI NIH HHS / CA / CA132175
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FGFR2 protein, human; EC 2.7.10.1 / FGFR4 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4
  • [Other-IDs] NLM/ PMC2699349
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67. Nitin N, Carlson AL, Muldoon T, El-Naggar AK, Gillenwater A, Richards-Kortum R: Molecular imaging of glucose uptake in oral neoplasia following topical application of fluorescently labeled deoxy-glucose. Int J Cancer; 2009 Jun 1;124(11):2634-42
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  • An alternative technology is optical molecular imaging, which allows for subcellular spatial resolution and can be effectively used with topical contrast agents for imaging epithelial derived cancers.
  • In normal epithelium, the uptake of 2-NBDG is limited to basal epithelial cells.
  • In contrast, high-grade dysplasia and cancers show uptake of 2-NBDG in neoplastic cells throughout the lesion.

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  • (PMID = 19173294.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA103830; United States / NCI NIH HHS / CA / R01 CA103830-05; United States / NCI NIH HHS / CA / R01CA103830
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose; 9G2MP84A8W / Deoxyglucose; EQF2794IRE / 4-Chloro-7-nitrobenzofurazan; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ NIHMS98197; NLM/ PMC2700039
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68. Wei X, Guo W, Wu S, Wang L, Huang P, Liu J, Fang B: Oxidative stress in NSC-741909-induced apoptosis of cancer cells. J Transl Med; 2010 Apr 16;8:37
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  • [Title] Oxidative stress in NSC-741909-induced apoptosis of cancer cells.
  • BACKGROUND: NSC-741909 is a novel anticancer agent that can effectively suppress the growth of several cell lines derived from lung, colon, breast, ovarian, and kidney cancers.
  • METHODS: The generation of ROS was measured by using the cell-permeable nonfluorescent compound H2DCF-DA and flow cytometry analysis.
  • Cell viability was determined by sulforhodamine B assay.
  • RESULTS: Treatment with NSC-741909 induced robust ROS generation and marked MAPK phosphatase-1 and -7 clustering in NSC-741909-sensitive, but not resistant cell lines, in a dose- and time-dependent manner.
  • The generation of ROS was detectable as early as 30 min and ROS levels were as high as 6- to 8-fold above basal levels after treatment.
  • CONCLUSION: Our results demonstrate that the increased ROS production was associated with NSC-741909-induced antitumor activity and that ROS generation and subsequent JNK activation is one of the primary mechanisms of NSC-741909-mediated antitumor cell activity.

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  • (PMID = 20398386.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA092487-08; United States / NCI NIH HHS / CA / R01 CA092487; United States / NCI NIH HHS / CA / R01 CA124951; United States / NCI NIH HHS / CA / R01 CA124951-01A2; United States / NCI NIH HHS / CA / R01 CA092487-08; United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / R01 CA 092487; United States / NCI NIH HHS / CA / CA124951-01A2; United States / NCI NIH HHS / CA / R01 CA 124951
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Indoles; 0 / NSC-741909; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / oncrasin-1; 7BO8G1BYQU / Masoprocol; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.1.3.- / Mitogen-Activated Protein Kinase Phosphatases; EC 3.1.3.48 / DUSP16 protein, human; EC 3.1.3.48 / Dual-Specificity Phosphatases; EC 3.4.22.- / Caspase 8
  • [Other-IDs] NLM/ PMC2873373
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69. Alles MC, Gardiner-Garden M, Nott DJ, Wang Y, Foekens JA, Sutherland RL, Musgrove EA, Ormandy CJ: Meta-analysis and gene set enrichment relative to er status reveal elevated activity of MYC and E2F in the "basal" breast cancer subgroup. PLoS One; 2009;4(3):e4710
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  • [Title] Meta-analysis and gene set enrichment relative to er status reveal elevated activity of MYC and E2F in the "basal" breast cancer subgroup.
  • BACKGROUND: Breast cancers lacking the estrogen receptor (ER) can be distinguished from other breast cancers on the basis of poor prognosis, high grade, distinctive histopathology and unique molecular signatures.
  • We used a cell model of estrogen and MYC action to define the interaction between estrogen and MYC transcriptional activity in breast cancer.
  • We found that the basal subgroup of ER- breast cancer showed a strong MYC transcriptional response that reproduced the indirect estrogen response seen in estrogen receptor positive (ER+) breast cancer cells.
  • CONCLUSIONS/SIGNIFICANCE: Increased transcriptional activity of MYC is a characteristic of basal breast cancers where it mimics a large part of an estrogen response in the absence of the ER, suggesting a mechanism by which these cancers achieve estrogen-independence and providing a potential therapeutic target for this poor prognosis sub group of breast cancer.
  • [MeSH-major] Breast Neoplasms / genetics. Carcinoma, Basal Cell / genetics. E2F Transcription Factors / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / physiology. Proto-Oncogene Proteins c-myc / genetics. Receptors, Estrogen / genetics

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  • (PMID = 19270750.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / E2F Transcription Factors; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, Estrogen
  • [Other-IDs] NLM/ PMC2650420
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70. Ho CM, Huang CC, Huang CJ, Cheng JS, Chen IS, Tsai JY, Jiann BP, Tseng PL, Kuo SJ, Jan CR: Effects of antrodia camphorata on viability, apoptosis, and [Ca2+]i in PC3 human prostate cancer cells. Chin J Physiol; 2008 Apr 30;51(2):78-84
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  • [Title] Effects of antrodia camphorata on viability, apoptosis, and [Ca2+]i in PC3 human prostate cancer cells.
  • Antrodia camphorata (AC) has been used as a health supplement in Asia to control different cancers; however, the cellular mechanisms of its effects are unclear.
  • The effect of AC on cultured human prostate cancer cells (PC3) has not been explored.
  • AC at concentrations of 5-50 microg/ml did not affect cell viability, but at 100-200 microg/ml decreased viability and induced apoptosis in a concentration-dependent manner.
  • AC at concentrations of 25-200 microg/ml did not alter basal [Ca2+]i, but at a concentration of 25 microg/ml decreased the [Ca2+]i increases induced by ATP, bradykinin, histamine and thapsigargin.
  • ATP, bradykinin and histamine increased cell viability whereas thapsigargin decreased it.
  • [MeSH-minor] Adenosine Triphosphate / antagonists & inhibitors. Bradykinin / antagonists & inhibitors. Cell Survival / drug effects. Histamine Antagonists / pharmacology. Humans. Male. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation / drug effects. Thapsigargin / antagonists & inhibitors. Tumor Cells, Cultured

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  • [ErratumIn] Chin J Physiol. 2008 Jun 30;51(3):196
  • (PMID = 18666710.001).
  • [ISSN] 0304-4920
  • [Journal-full-title] The Chinese journal of physiology
  • [ISO-abbreviation] Chin J Physiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histamine Antagonists; 67526-95-8 / Thapsigargin; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; S8TIM42R2W / Bradykinin; SY7Q814VUP / Calcium
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71. Wietfeldt ED, Thiele J: Malignancies of the anal margin and perianal skin. Clin Colon Rectal Surg; 2009 May;22(2):127-35
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  • [Title] Malignancies of the anal margin and perianal skin.
  • Malignancies of the anal margin and perianal skin are relatively uncommon lesions, comprising 3 to 4% of all anorectal malignancies.
  • Commonly included in this group of cancers are Bowen's disease (intraepithelial squamous cell cancer), perianal Paget's disease (intraepithelial adenocarcinoma), invasive squamous cell cancer, basal cell cancer, and malignant melanoma.

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  • (PMID = 20436838.001).
  • [ISSN] 1530-9681
  • [Journal-full-title] Clinics in colon and rectal surgery
  • [ISO-abbreviation] Clin Colon Rectal Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2780245
  • [Keywords] NOTNLM ; Anal margin cancer / diagnosis / local excision / radiation therapy / treatment options
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72. Lonsdorf AS, Becker MR, Stockfleth E, Schäkel K, Ulrich C: [Primary and secondary prevention of skin cancer in organ transplant recipients]. Hautarzt; 2010 Mar;61(3):195-206
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  • [Title] [Primary and secondary prevention of skin cancer in organ transplant recipients].
  • Skin cancer constitutes the most frequently reported post-transplant malignancy in solid organ transplant recipients (OTR) worldwide.
  • Whereas the risk for malignant melanoma is only moderately increased, non-melanoma skin cancers (NMSC) seem to thrive on chronic immunosuppression and account for up to 95% of post-transplant cutaneous malignancies.
  • Compared to the general population cutaneous squamous cell carcinoma (SCC) and actinic keratoses (AK) characteristically show even higher incidences than basal cell carcinoma (BCC) and act as an indicator for the development of multiple primary cutaneous neoplasias and locally recurrent cancers (field cancerization).
  • Early diagnosis and therapy of pre-malignant cutaneous lesions is crucial for the secondary prophylaxis of further invasive and highly aggressive skin cancers.
  • High quality interdisciplinary care and prophylactic modalities, including consistent and sufficient UV protection, topical immunmodulatory therapies of UV-damaged skin areas, retinoid chemoprevention as well as tapering immunosuppressive treatment or the selection of immunosuppressants with proposed antiangiogenic properties like mTor-inhibitors may help to reduce the multiplicity of subsequent primary skin cancers in high-risk patients.
  • Apart from the continuous need for educational intervention of OTR in the primary prophylaxis of post-transplant skin cancers, dermatologic care occupies a central position within the field of transplantation medicine in terms of pre- and post-transplantation dermatologic evaluation and therapy as well as the implication of timely and effective secondary preventive approaches in the management of this high-risk patient population.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Immunosuppressive Agents / administration & dosage. Organ Transplantation / adverse effects. Primary Prevention / methods. Secondary Prevention / methods. Skin Neoplasms / etiology. Skin Neoplasms / prevention & control

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  • (PMID = 20177652.001).
  • [ISSN] 1432-1173
  • [Journal-full-title] Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete
  • [ISO-abbreviation] Hautarzt
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents
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73. Marchini C, Montani M, Konstantinidou G, Orrù R, Mannucci S, Ramadori G, Gabrielli F, Baruzzi A, Berton G, Merigo F, Fin S, Iezzi M, Bisaro B, Sbarbati A, Zerani M, Galiè M, Amici A: Mesenchymal/stromal gene expression signature relates to basal-like breast cancers, identifies bone metastasis and predicts resistance to therapies. PLoS One; 2010;5(11):e14131
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  • [Title] Mesenchymal/stromal gene expression signature relates to basal-like breast cancers, identifies bone metastasis and predicts resistance to therapies.
  • 1) significantly relates to basal-like breast cancer subtypes;.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cluster Analysis. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Drug Resistance, Neoplasm / genetics. Epithelial Cells / metabolism. Female. Humans. Mesenchymal Stromal Cells / metabolism. Mice. Neoadjuvant Therapy / methods. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction

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  • (PMID = 21152434.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2994727
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74. Stoff B, Salisbury C, Parker D, O'Reilly Zwald F: Dermatopathology of skin cancer in solid organ transplant recipients. Transplant Rev (Orlando); 2010 Oct;24(4):172-89
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  • [Title] Dermatopathology of skin cancer in solid organ transplant recipients.
  • Skin cancers occur more frequently in solid organ transplant recipients relative to the general population.
  • Transplant recipients are at particularly high risk of squamous cell carcinoma, with up to a 100-fold increase in the relative risk when compared to the nontransplanted population.
  • This compares with a 10- to 16-fold increase in basal cell carcinoma for renal transplant recipients.
  • Other types of skin cancer associated with immunosuppression in transplant patients include Kaposi sarcoma, Merkel cell carcinoma, and posttransplant lymphoproliferative disorder.
  • In addition, the contribution of viral induced carcinogenesis with respect to Kaposi sarcoma, Merkel cell carcinoma, and posttransplant lymphoproliferative disorder is discussed.
  • [MeSH-major] Kidney Transplantation / adverse effects. Organ Transplantation / adverse effects. Skin / pathology. Skin Neoplasms / epidemiology. Skin Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Basal Cell / etiology. Carcinoma, Merkel Cell / etiology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Humans. Keratosis, Actinic / etiology. Lymphoproliferative Disorders / etiology. Porokeratosis / epidemiology. Porokeratosis / etiology. Risk Assessment. Sarcoma, Kaposi / epidemiology

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20709518.001).
  • [ISSN] 1557-9816
  • [Journal-full-title] Transplantation reviews (Orlando, Fla.)
  • [ISO-abbreviation] Transplant Rev (Orlando)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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75. Roh JL, Moon BJ, Kim JS, Lee JH, Cho KJ, Choi SH, Nam SY, Lee BJ, Kim SY: Use of 18F-fluorodeoxyglucose positron emission tomography in patients with rare head and neck cancers. Clin Exp Otorhinolaryngol; 2008 Jun;1(2):103-9
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  • [Title] Use of 18F-fluorodeoxyglucose positron emission tomography in patients with rare head and neck cancers.
  • OBJECTIVES: The clinical utility of (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET) has been demonstrated in major head and neck cancers (HNCs) but is unclear in rare HNCs.
  • METHODS: FDG PET and CT/MRI scanning were performed at the initial staging and/or the follow-up in 24 patients with rare HNCs, 10 with melanoma, 9 with sarcoma, 3 with olfactory neuroblastomas, and 2 with basal cell carcinoma.

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  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2671791
  • [Keywords] NOTNLM ; Fluorodeoxyglucose / Head and neck neoplasms / Neoplasm staging / Positron-emission tomography / Surveillance
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76. Stang A, Lampert T, Uhlemann T, Trocchi P: Skin cancer mortality in Germany before and after the post-communist transition. Int J Dermatol; 2009 Apr;48(4):363-70
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  • [Title] Skin cancer mortality in Germany before and after the post-communist transition.
  • BACKGROUND AND OBJECTIVES: Until now mortality trends of melanoma and nonmelanoma skin cancer (NMSC) in Germany have been studied only in West Germany.
  • METHODS: We analyzed mortality data of skin melanoma and NMSC of West and East Germany (1980-2005).
  • RESULTS: Age-standardized skin melanoma mortality rates tended to be lower in East Germany than West Germany before reunification.
  • CONCLUSIONS: Even 15 years after reunification, mortality of NMSC is still higher in East than West Germany, although incidence rates of squamous cell cancers of the skin are not higher in East Germany.
  • Differences in the participation in early cancer detection and health care utilization in West and East Germany do not sufficiently explain our findings.
  • [MeSH-major] Carcinoma, Basal Cell / mortality. Carcinoma, Squamous Cell / mortality. Communism / statistics & numerical data. Melanoma / mortality. Skin Neoplasms / mortality

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  • (PMID = 19335420.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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77. Asplund A, Gustafsson AC, Wikonkal NM, Sela A, Leffell DJ, Kidd K, Lundeberg J, Brash DE, Pontén F: PTCH codon 1315 polymorphism and risk for nonmelanoma skin cancer. Br J Dermatol; 2005 May;152(5):868-73
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  • [Title] PTCH codon 1315 polymorphism and risk for nonmelanoma skin cancer.
  • BACKGROUND: The PTCH tumour suppressor gene is involved in the development of nearly all basal cell carcinomas (BCCs) of the skin and a fraction of squamous cell carcinomas (SCCs).
  • A nonconservative Pro/Leu nucleotide polymorphism within PTCH exon 23 at codon 1315 was recently reported to be potentially important for the development of breast epithelial cell cancers.
  • Objectives Accordingly, the status of PTCH codon 1315 was analysed for a possible association with the development of nonmelanoma skin cancers (NMSCs) in a pilot study.
  • Because skin cancer risk is affected by specific population-dependent phenotypes such as skin and hair colour, codon 1315 was also analysed for normal allele frequency variation in human populations having differing extents of eumelanin vs. phaeomelanin.
  • During development of a tumour, the effect of Pro may be magnified by loss of the Leu allele.
  • [MeSH-major] Genetic Predisposition to Disease. Neoplasm Proteins / genetics. Polymorphism, Single Nucleotide. Receptors, Cell Surface / genetics. Skin Neoplasms / genetics
  • [MeSH-minor] Carcinoma, Basal Cell / genetics. Carcinoma, Squamous Cell / genetics. Codon / genetics. Genotype. Hair Color / genetics. Humans. Loss of Heterozygosity. Pilot Projects. Polymerase Chain Reaction / methods. Skin Pigmentation / genetics

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  • (PMID = 15888139.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Codon; 0 / Neoplasm Proteins; 0 / Receptors, Cell Surface; 0 / patched receptors
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78. Tischkowitz MD, Foulkes WD: The basal phenotype of BRCA1-related breast cancer: past, present and future. Cell Cycle; 2006 May;5(9):963-7
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  • [Title] The basal phenotype of BRCA1-related breast cancer: past, present and future.
  • Many BRCA1-related tumors have a distinct histological characteristics which together have been called "basal-like."
  • These characteristics can be used to predict which breast cancers are most likely to be associated with germline BRCA1 mutations which has important implications for breast pathologists.
  • Moreover, BRCA1-related breast cancers generally have a poorer prognosis which may paradoxically be more pronounced in node negative cancers.
  • Conversely, BRCA1-related tumors may respond better to neoadjuvant chemotherapy and their characteristic molecular signature may provide opportunities to develop specific molecular targeted therapies akin to traztuzumab in HER2+ cancers.
  • Finally, many of the phenotypic features of BRCA1-related tumors might also be found in putative breast stem cells and therefore characterization of the BRCA1 breast cancer phenotype will improve our understanding of sporadic breast carcinogenesis.


79. Matsuhashi S, Narisawa Y, Ozaki I, Mizuta T: Expression patterns of programmed cell death 4 protein in normal human skin and some representative skin lesions. Exp Dermatol; 2007 Mar;16(3):179-84
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  • [Title] Expression patterns of programmed cell death 4 protein in normal human skin and some representative skin lesions.
  • Expression of a tumor suppressor gene, programmed cell death 4 (PDCD4), was investigated at the protein level in the human skin.
  • Immunohistochemically, PDCD4 protein expressed mainly in suprabasal layers, while PDCD4-positive and -negative areas were observed discontinuously in the basal cell layer of the epidermis.
  • In hair follicles, the suprabulbar area including the hair and inner root sheath was immunoreactive, while the bulbar area, containing germinative cells which were strongly proliferating cell nuclear antigen (PCNA)-positive, was not or less.
  • PDCD4-positive cells were localized in the inside layers while PCNA-positive cells were located in the basal layer in the outer root sheath of hair follicles.
  • PDCD4 expression was found to be suppressed in the epidermis overlying an adult T-cell lymphoma (ATL), possibly reflecting a paracrine effect of factors produced by ATL cells.
  • PDCD4 expression was suppressed in the keratinocyte cell line HaCaT by exposure of cultures to epidermal growth factor, transforming growth factor-beta1 or hepatocyte growth factor.
  • Immunohistochemically, various skin cancers tended to show less PDCD4 expression than normal skin.
  • Promotion of expression might prove useful in preventing or treating certain skin cancers.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. RNA-Binding Proteins / metabolism. Skin / cytology. Skin / metabolism. Skin Diseases / metabolism
  • [MeSH-minor] Cell Line. Cell Nucleus / metabolism. Hair Follicle / immunology. Hair Follicle / metabolism. Humans. Immunohistochemistry. Keratinocytes / cytology. Keratinocytes / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Sebaceous Glands / cytology. Sebaceous Glands / metabolism. Sweat Glands / cytology. Sweat Glands / metabolism

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  • (PMID = 17286809.001).
  • [ISSN] 0906-6705
  • [Journal-full-title] Experimental dermatology
  • [ISO-abbreviation] Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / PDCD4 protein, human; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA-Binding Proteins
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80. Asuquo ME, Ngim O, Ugare G, Omotoso J, Ebughe G: Major dermatologic malignancies encountered in a teaching hospital surgical department in South Nigeria. Am J Clin Dermatol; 2008;9(6):383-7
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  • BACKGROUND: Dermatologic malignancies are among the most common form of cancer.
  • However, dark-skinned individuals of African descent are said to be far less likely than fair-skinned individuals to develop skin cancer.
  • Significant differences in the pattern of skin malignancy have also been observed in different regions of Africa.
  • RESULTS: There were 63 histologically diagnosed dermatologic cancers, comprising 10% of all histologically diagnosed cancers at the University of Calabar Teaching Hospital during the study period.
  • Squamous cell carcinoma (SCC) was the most common (n = 23; 37%), followed by Kaposi sarcoma (KS) [n = 17; 27%].
  • Other malignancies included basal cell carcinoma (BCC), melanoma, and dermatofibrosarcoma protuberans (DFSP) [n = 5; 8% each].
  • The peak age varied with the type of cancer but none was found in patients in the first decade of life.
  • [MeSH-major] Skin Neoplasms / pathology. Skin Neoplasms / surgery
  • [MeSH-minor] Africa / epidemiology. African Continental Ancestry Group. Carcinoma, Basal Cell / pathology. Carcinoma, Basal Cell / surgery. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Female. Hospitals, Teaching / statistics & numerical data. Humans. Male. Melanoma / pathology. Melanoma / surgery. Neoplasm Metastasis. Nigeria. Retrospective Studies. Sarcoma, Kaposi / pathology. Sarcoma, Kaposi / surgery

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  • (PMID = 18973404.001).
  • [ISSN] 1175-0561
  • [Journal-full-title] American journal of clinical dermatology
  • [ISO-abbreviation] Am J Clin Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
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81. Wilson LA, Gemin A, Espiritu R, Singh G: ets-1 is transcriptionally up-regulated by H2O2 via an antioxidant response element. FASEB J; 2005 Dec;19(14):2085-7
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  • Expression of the transcription factor Ets-1 is increasingly associated with the progression of several human cancers.
  • Ets-1 expression in response to H2O2 was examined in an ovarian carcinoma cell model, and the genes promoter region was analyzed in order to identify putative elements involved in redox responsiveness.
  • This study has delineated