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1. DiMeo TA, Anderson K, Phadke P, Fan C, Perou CM, Naber S, Kuperwasser C: A novel lung metastasis signature links Wnt signaling with cancer cell self-renewal and epithelial-mesenchymal transition in basal-like breast cancer. Cancer Res; 2009 Jul 1;69(13):5364-73
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  • [Title] A novel lung metastasis signature links Wnt signaling with cancer cell self-renewal and epithelial-mesenchymal transition in basal-like breast cancer.
  • In epithelial cancers, such as those of the breast, the epithelial-mesenchymal transition (EMT) is associated with basal-like breast cancers, generates cells with stem-like properties, and enables cancer cell dissemination and metastasis.
  • However, the molecular mechanism(s) that connects stem cell-like characteristics with EMT has yet to be defined.
  • Using an orthotopic model of human breast cancer metastasis to lung, we identified a poor prognosis gene signature, in which several components of the wnt signaling pathway were overexpressed in early lung metastases.
  • The wnt genes identified in this signature were strongly associated with human basal-like breast cancers.
  • Furthermore, inhibition of wnt signaling resulted in the reexpression of breast epithelial differentiation markers and repression of EMT transcription factors SLUG and TWIST.
  • Collectively, these results provide a molecular link between self-renewal, EMT, and metastasis in basal-like breast cancers.

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  • [ErratumIn] Cancer Res. 2009 Aug 1;69(15):6366. Feng, Chang [corrected to Fan, Cheng]
  • (PMID = 19549913.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA125554-02; United States / NCI NIH HHS / CA / R01 CA125554; United States / NCI NIH HHS / CA / R01 CA125554-02; United States / NCI NIH HHS / CA / R01CA12555
  • [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 / Nuclear Proteins; 0 / TWIST1 protein, human; 0 / Transcription Factors; 0 / Twist Transcription Factor; 0 / Wnt Proteins; 0 / snail family transcription factors
  • [Other-IDs] NLM/ NIHMS154900; NLM/ PMC2782448
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2. Graveel CR, DeGroot JD, Su Y, Koeman J, Dykema K, Leung S, Snider J, Davies SR, Swiatek PJ, Cottingham S, Watson MA, Ellis MJ, Sigler RE, Furge KA, Vande Woude GF: Met induces diverse mammary carcinomas in mice and is associated with human basal breast cancer. Proc Natl Acad Sci U S A; 2009 Aug 4;106(31):12909-14
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  • [Title] Met induces diverse mammary carcinomas in mice and is associated with human basal breast cancer.
  • Understanding the signaling pathways that drive aggressive breast cancers is critical to the development of effective therapeutics.
  • The oncogene MET is associated with decreased survival in breast cancer, yet the role that MET plays in the various breast cancer subtypes is unclear.
  • We describe a knockin mouse with mutationally activated Met (Met(mut)) that develops a high incidence of diverse mammary tumors with basal characteristics, including metaplasia, absence of progesterone receptor and ERBB2 expression, and expression of cytokeratin 5.
  • With gene expression and tissue microarray analysis, we show that high MET expression in human breast cancers significantly correlated with estrogen receptor negative/ERBB2 negative tumors and with basal breast cancers.
  • Few treatment options exist for breast cancers of the basal or trastuzumab-resistant ERBB2 subtypes.
  • We conclude from these studies that MET may play a critical role in the development of the most aggressive breast cancers and may be a rational therapeutic target.

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  • (PMID = 19567831.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / F32 CA105748; United States / NCI NIH HHS / CA / U01 CA114722; United States / NCI NIH HHS / CA / F32CA105748
  • [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 / Receptors, Progesterone; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2722304
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3. Van Laere SJ, Van den Eynden GG, Van der Auwera I, Vandenberghe M, van Dam P, Van Marck EA, van Golen KL, Vermeulen PB, Dirix LY: Identification of cell-of-origin breast tumor subtypes in inflammatory breast cancer by gene expression profiling. Breast Cancer Res Treat; 2006 Feb;95(3):243-55
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  • [Title] Identification of cell-of-origin breast tumor subtypes in inflammatory breast cancer by gene expression profiling.
  • Inflammatory breast cancer (IBC) is an aggressive form of locally advanced breast cancer with high metastatic potential.
  • Most patients have lymph node involvement at the time of diagnosis and 1/3 of the patients have distant metastases.
  • In a previous study, we demonstrated that IBC is a distinct form of breast cancer in comparison with non-IBC.
  • We identified the same cell-of-origin subtypes in IBC as those already described in non-IBC.
  • The robustness of this classification was assessed by an unsupervised hierarchical clustering with an alternative gene set of 141 genes related to the cell-of-origin subtypes, selected using a discriminating score and iterative random permutation testing.
  • The contribution of the different cell-of-origin subtypes to the IBC phenotype was investigated by principal component analysis.
  • Generally, the combined ErbB2-overexpressing and basal-like cluster was more expressed in IBC compared to non-IBC, whereas the combined luminal A, luminal B and normal-like cluster was more pronounced in non-IBC compared to IBC.
  • The presence of the same molecular cell-of-origin subtypes in IBC as in non-IBC does not exclude the specific molecular nature of IBC, since gene lists that characterize IBC and non-IBC are entirely different from gene lists that define the different cell-of-origin subtypes, as evidenced by principal component analysis.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / genetics. Breast Neoplasms / classification. Breast Neoplasms / genetics. Gene Expression Profiling
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma, Ductal, Breast / genetics. Carcinoma, Ductal, Breast / metabolism. Female. Humans. Immunoenzyme Techniques. Oligonucleotide Array Sequence Analysis


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4. Donnenberg VS, Donnenberg AD, Zimmerlin L, Landreneau RJ, Bhargava R, Wetzel RA, Basse P, Brufsky AM: Localization of CD44 and CD90 positive cells to the invasive front of breast tumors. Cytometry B Clin Cytom; 2010 Sep;78(5):287-301
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  • [Title] Localization of CD44 and CD90 positive cells to the invasive front of breast tumors.
  • BACKGROUND: A variety of markers have been proposed to identify breast cancer stem cells.
  • METHODS: Cytokeratin, CD44, and CD90 were localized to primary breast cancer and normal breast (NB) tissue by immunohistostaining and related to CD117 and CD133 expression by flow cytometry.
  • RESULTS: NB basal cells coexpressed CD44 and CD90.
  • In breast tumors, basal-like CD44+/CD90+ cells were localized to the tumor periphery, adjacent to CD90+ stroma.
  • Immunophenotyping (CD44/CD90/CD117/CD133) of cytokeratin+ cells revealed no significant difference in expression between tumors and tumor-free breast.
  • In both, CD133 was distributed approximately equally among CD44/CD90 subsets, whereas CD117 expression was highest in the basal-associated CD44+/CD90+ subset.
  • CONCLUSIONS: Our data demonstrate that all tumors contain a small population of CD44+/CD90+ cells, mimicking the phenotype of ductal-basal cells.
  • [MeSH-major] Adenocarcinoma / immunology. Antigens, CD44 / immunology. Antigens, Thy-1 / immunology. Breast Neoplasms / immunology. Neoplastic Stem Cells / immunology. Pleural Effusion, Malignant / immunology

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  • [Copyright] Copyright © 2010 International Clinical Cytometry Society.
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  • (PMID = 20533389.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA047904
  • [Publication-type] Journal Article; 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 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD44; 0 / Antigens, Thy-1; 0 / Biomarkers, Tumor; 0 / CD44 protein, human; 0 / Glycoproteins; 0 / Peptides; 68238-35-7 / Keratins; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ NIHMS626027; NLM/ PMC4165077
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5. Mejía W, Castro C, Umaña A, de Castro C, Riveros T, Sánchez-Gómez M: [Insulin-like growth factor receptor I signaling in a breast cancer cell line]. Biomedica; 2010 Oct-Dec;30(4):551-8
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  • [Title] [Insulin-like growth factor receptor I signaling in a breast cancer cell line].
  • INTRODUCTION: In vitro studies strongly suggest that proliferation, migration and cell survival of breast cancer cell lines are significantly affected by activation of the IGF type 1 receptor (IGF-IR).
  • OBJECTIVE: The phosphorylation by IGF-I of IGF-IR and the intracellular signaling molecules Akt (PI-3K pathway) and Erk1/2 (MAPK pathway) was characterized in a human breast cancer cell lines.
  • MATERIALS AND METHODS: The study compared a standard breast adenocarcinoma line (MCF-7) cell line with a line (CSC 1595) derived from an infiltrating ductal breast cancer in a Colombian patient.
  • The CSC 1595 and MCF-7 cell lines were cultured in DMEM supplemented with 10% fetal bovine serum, 2 mM glutamine, 100 U/ml penicillin, and 100 µg/ml streptomycin and grown at 37 °C in 5% CO₂ atmosphere and 95% humidity.
  • Cell extracts were prepared, followed by immunoprecipitation and immunoblotting with specific anti-pIGF-IR, anti-pERK1/2 and anti-pAkt antibodies.
  • RESULTS: After 5 minute stimulation with IGF-I, 70% of the IGF-IR was phosphorylated in the cell line CSC 1595 and 25% in MCF-7.
  • Basal and stimulated levels of phosphorylated ERK1/2 were substantially higher compared to those in the MCF-7 cell line.
  • CONCLUSIONS: The IGF-IR and MAPK kinase pathway involving proteins ERK1/2 showed more significant phosphorylation in the 1,595 cells compared to the observed in the MCF-7 cell line.
  • Since the IGF-IR is the major activator of this pathway it may play an important role in ductal infiltrating breast cancer tumor growth and metastases.
  • [MeSH-major] Breast Neoplasms / physiopathology. Cell Line, Tumor. Receptor, IGF Type 1 / metabolism. Signal Transduction / physiology


6. Fadare O, Tavassoli FA: The phenotypic spectrum of basal-like breast cancers: a critical appraisal. Adv Anat Pathol; 2007 Sep;14(5):358-73
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  • [Title] The phenotypic spectrum of basal-like breast cancers: a critical appraisal.
  • There are 2 well-recognized cell populations lining the mammary duct system: the epithelial cells lining the lumen and the myoepithelial cells surrounding them.
  • The mammary stem cell, a putative third cell type, has not yet been well characterized.
  • It is not established whether the putative stem cell expresses the full complement, a subset, or none of the markers of normal epithelial and/or myoepithelial cells.
  • All 3 cell types may theoretically undergo malignant transformation.
  • The advent of oligonucleotide and cDNA microarrays has facilitated gene expression profiling of breast cancers, revealing molecular subclasses that may be prognostically relevant.
  • One such subclass, the basal-like breast carcinomas, has been found in numerous independent datasets to be associated with a comparatively worse overall and disease-free survival.
  • These cancers show expression of molecules characteristic of the normal myoepithelial cell, such as basal cytokeratins, and reduced expression of estrogen receptor-related and Erb-B2-related genes and proteins.
  • The classifier genes that formed the basis for the delineation of basal-like carcinomas were derived from datasets that were composed predominantly of ductal type cancers.
  • Therefore, the clinical significance of a basal-like gene expression or immunohistochemical profile in the other breast cancer subtypes is presently unknown.
  • Herein, we evaluate in detail the current state of knowledge on the pathologic features of breast carcinomas classified as basal-like by immunohistochemical and/or gene expression profiling criteria, with an emphasis on their full phenotypic spectrum and also previously underemphasized areas of heterogeneity and ambiguity where present.
  • There seems to be a phenotypic and biologic spectrum of basal-like or myoepithelial-type carcinomas, just as there is a wide range among tumors of luminal epithelial derivation/differentiation.
  • [MeSH-major] Adenocarcinoma / pathology. Breast Neoplasms / pathology. Neoplasms, Basal Cell / pathology

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  • (PMID = 17717437.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 153
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7. Sitterding SM, Wiseman WR, Schiller CL, Luan C, Chen F, Moyano JV, Watkin WG, Wiley EL, Cryns VL, Diaz LK: AlphaB-crystallin: a novel marker of invasive basal-like and metaplastic breast carcinomas. Ann Diagn Pathol; 2008 Feb;12(1):33-40
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  • [Title] AlphaB-crystallin: a novel marker of invasive basal-like and metaplastic breast carcinomas.
  • Basal-like tumors are a newly recognized estrogen receptor (ER) negative and HER2 negative breast cancer subtype that express basal epithelial genes and are associated with poor survival.
  • Metaplastic carcinomas are thought to belong within the basal-like group.
  • We have recently demonstrated that the small heat shock protein alphaB-crystallin is commonly expressed in basal-like tumors and contributes to their aggressive phenotype.
  • The current study examined the rates and patterns of alphaB-crystallin expression in whole tissue sections of human breast, including normal tissue, proliferative lesions, in situ and invasive carcinomas (ER positive, HER2 positive, basal-like, and metaplastic cancers).
  • In normal breast tissue, proliferative lesions and in situ carcinomas, alphaB-crystallin expression was restricted to the myoepithelial cell compartment of ductal and lobular units.
  • Most basal-like and metaplastic carcinomas demonstrated cytoplasmic expression of alphaB-crystallin (81% and 86%, respectively).
  • Conversely, no staining for alphaB-crystallin was observed in nonbasal-like (ie, ER positive or HER2 positive) breast carcinomas.
  • Taken together, our results indicate that alphaB-crystallin is a sensitive (81%) and specific (100%) marker for basal-like breast carcinomas.
  • Moreover, the high rates of expression of alphaB-crystallin in metaplastic breast carcinomas (86%) suggest that these tumors may represent a histologically distinctive subset of basal-like breast tumors with a similar underlying molecular etiology.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Breast Neoplasms / metabolism. Neoplasm Proteins / metabolism. alpha-Crystallin B Chain / metabolism
  • [MeSH-minor] Breast Cyst / metabolism. Breast Cyst / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Cell Proliferation. Female. Fibrocystic Breast Disease / metabolism. Fibrocystic Breast Disease / pathology. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Metaplasia. Neoplasm Invasiveness. Predictive Value of Tests

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  • (PMID = 18164413.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA89018; United States / NCI NIH HHS / CA / R01CA097198
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / alpha-Crystallin B Chain
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8. Nalwoga H, Arnes JB, Wabinga H, Akslen LA: Expression of EGFR and c-kit is associated with the basal-like phenotype in breast carcinomas of African women. APMIS; 2008 Jun;116(6):515-25
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  • [Title] Expression of EGFR and c-kit is associated with the basal-like phenotype in breast carcinomas of African women.
  • Epidermal growth factor receptor (EGFR) and c-kit are tyrosine kinase growth factor receptors which are frequently expressed in basal-like breast carcinomas, and tyrosine kinase inhibition is now a promising strategy in treatment of breast cancer.
  • The aim of this study was to evaluate the expression of EGFR and c-kit in breast cancer with special focus on the basal-like phenotype (BLP) and other prognostic factors in an African population.
  • EGFR and/or c-kit were expressed in 55% of basal-like tumors.
  • In conclusion, there is a high expression of EGFR and/or c-kit in basal-like breast carcinoma in this series from Uganda and their expression is associated with features of poor prognosis.
  • More studies are required to assess the clinical significance of EGFR and c-kit in breast cancer patients in Uganda.
  • [MeSH-major] Adenocarcinoma, Mucinous / metabolism. Breast Neoplasms / metabolism. Carcinoma, Basal Cell / metabolism. Carcinoma, Ductal, Breast / metabolism. Proto-Oncogene Proteins c-kit / metabolism. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 18754326.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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9. Ihemelandu CU, Naab TJ, Mezghebe HM, Makambi KH, Siram SM, Leffall LD Jr, Dewitty RL Jr, Frederick WA: Basal cell-like (triple-negative) breast cancer, a predictor of distant metastasis in African American women. Am J Surg; 2008 Feb;195(2):153-8
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  • [Title] Basal cell-like (triple-negative) breast cancer, a predictor of distant metastasis in African American women.
  • BACKGROUND: The aim of this study was to evaluate the prognostic significance of the basal cell-like molecular breast cancer subtype with respect to locoregional recurrence and distant metastasis in African American women treated for breast cancer.
  • METHODS: A retrospective analysis was performed of the tumor registry database for all African American women diagnosed and treated for breast cancer from 1998 to 2005 who had assessable data for all 3 markers: estrogen, progesterone, and Her-2/neu.
  • Of these, 22 (6.1%) had locoregional recurrence, 35 (9.8%) had distant metastasis, and 301 (84.1%) had no evidence of breast tumor recurrence.
  • Compared with the other molecular subtypes the basal cell-like subtype showed a statistically significant association to distant metastasis: 15 (42.9%) vs 13 (37.1%), 4 (11.4%), and 3 (8.6%) (P < .001), respectively, for luminal A, Her-2/neu, and luminal B subtypes.
  • The basal cell-like subtype was an independent predictor of distant metastasis (odds ratio, 5.8; 95% confidence interval, 1.5-22.0, P = .009).
  • The molecular subtypes showed no statistically significant difference with respect to locoregional treatment administered and tumor stage at time of diagnosis.
  • CONCLUSIONS: The basal cell-like molecular breast cancer subtype is an independent predictor of distant metastasis in African American women.
  • [MeSH-major] Adenocarcinoma / ethnology. Adenocarcinoma / secondary. African Americans / genetics. Breast Neoplasms / ethnology. Breast Neoplasms / genetics. Neoplasm Recurrence, Local / genetics


10. Murakami A, Kawachi K, Sasaki T, Ishikawa T, Nagashima Y, Nozawa A: Sebaceous carcinoma of the breast. Pathol Int; 2009 Mar;59(3):188-92
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  • [Title] Sebaceous carcinoma of the breast.
  • Sebaceous carcinoma (SC) of the breast is a rare malignant tumor and only nine cases, including the present one, have been reported in the English-language literature.
  • Microscopically, lobules encircled by a fibrous envelope and cords or small cell nests in the stroma were noted.
  • In the lobules the gradual transitions from basal dark cells to central clear foamy cells and comedo-like necrosis were observed.
  • This is the first case of an androgen receptor-positive mammary SC to be reported, and therefore contributes to the understanding of the clinicopathological features of SC of the breast.
  • [MeSH-major] Adenocarcinoma, Sebaceous / pathology. Breast Neoplasms / pathology. Receptors, Androgen / metabolism. Sebaceous Gland Neoplasms / pathology

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  • (PMID = 19261098.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Receptors, Androgen
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11. Kantrow SM, Ivan D, Williams MD, Prieto VG, Lazar AJ: Metastasizing adenocarcinoma and multiple neoplastic proliferations arising in a nevus sebaceus. Am J Dermatopathol; 2007 Oct;29(5):462-6
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  • [Title] Metastasizing adenocarcinoma and multiple neoplastic proliferations arising in a nevus sebaceus.
  • Many neoplasms have been reported to arise in association with nevus sebaceus, most commonly trichoblastoma/basal cell carcinoma and syringocystadenoma papilliferum.
  • We report a case of a 66-year-old woman with an adenocarcinoma as well as multiple neoplastic proliferations arising in a long standing nevus sebaceus on the scalp, with subsequent occipital neck metastatic disease.
  • Most of the lesion was composed of an adenocarcinoma with areas showing ductal differentiation with decapitation secretion, well-formed papillae and focal cribriform structures.
  • Other portions demonstrated a high-grade neoplasm with prominent nuclear atypia and a solid pattern of growth resembling high-grade breast carcinoma.
  • A breast primary was ruled out by clinical and radiologic examination.
  • [MeSH-major] Adenocarcinoma / secondary. Head and Neck Neoplasms / secondary. Nevus / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Cell Proliferation. Female. Humans. Membrane Proteins / metabolism. Mucin-1 / metabolism. Receptor, ErbB-2 / metabolism


12. Singh B, Cook KR, Vincent L, Hall CS, Berry JA, Multani AS, Lucci A: Cyclooxygenase-2 induces genomic instability, BCL2 expression, doxorubicin resistance, and altered cancer-initiating cell phenotype in MCF7 breast cancer cells. J Surg Res; 2008 Jun 15;147(2):240-6
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  • [Title] Cyclooxygenase-2 induces genomic instability, BCL2 expression, doxorubicin resistance, and altered cancer-initiating cell phenotype in MCF7 breast cancer cells.
  • INTRODUCTION: Cyclooxygenase (COX2) expression in primary breast cancer correlates with a worse prognosis.
  • We reported previously that COX2 expression in MCF10A breast epithelial cells of basal subtype induces genomic instability.
  • To understand the role of COX2 in estrogen receptor-positive (non-basal) breast cancer, we transfected the MCF7 cell line with COX2 and analyzed its chromosomal profile, BCL2 protein expression, and resistance to doxorubicin.
  • We also analyzed cell cultures grown as mammospheres to determine whether COX2 expression affects the cancer-initiating ("stem") cell phenotype in MCF7 cells.
  • CONCLUSIONS: We found that COX2 expression in MCF7 breast cancer cells induced genomic instability, BCL2 expression, and doxorubicin resistance, thus making them significantly more tumorigenic.
  • This data suggests that COX-2 may be an important target for breast cancer treatment.
  • [MeSH-major] Adenocarcinoma / enzymology. Breast Neoplasms / enzymology. Cell Transformation, Neoplastic. Cyclooxygenase 2 / metabolism. Genomic Instability / physiology
  • [MeSH-minor] Antibiotics, Antineoplastic / administration & dosage. Cell Culture Techniques. Cell Line, Tumor. Colony-Forming Units Assay. Cytogenetic Analysis. DNA, Complementary. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm / physiology. Female. Humans. Phenotype. Proto-Oncogene Proteins c-bcl-2 / metabolism. Transfection

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  • (PMID = 18498876.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R21 DK067682
  • [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 / Antibiotics, Antineoplastic; 0 / DNA, Complementary; 0 / Proto-Oncogene Proteins c-bcl-2; 80168379AG / Doxorubicin; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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13. Iwase H, Kurebayashi J, Tsuda H, Ohta T, Kurosumi M, Miyamoto K, Yamamoto Y, Iwase T: Clinicopathological analyses of triple negative breast cancer using surveillance data from the Registration Committee of the Japanese Breast Cancer Society. Breast Cancer; 2010 Apr;17(2):118-24
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  • [Title] Clinicopathological analyses of triple negative breast cancer using surveillance data from the Registration Committee of the Japanese Breast Cancer Society.
  • BACKGROUND: Triple negative (TN) breast cancer is defined as a subtype that is negative for estrogen receptor (ER), progesterone receptor (PgR), and human epidermal growth factor receptor 2 (HER2).
  • To clarify the characteristics of TN breast cancer, surveillance data of the Registration Committee of the Japanese Breast Cancer Society were analyzed.
  • Mucinous, tubular, or secretary carcinomas were frequently found in the hormone receptor positive/HER2 negative subtype, while squamous cell carcinoma, spindle cell carcinoma, and metaplastic carcinoma with bone/cartilage metaplasia were very frequently found in the TN group.
  • CONCLUSIONS: Although TN types are similar to basal-like breast tumor, as determined by gene profiling, their diagnosis needs verification by determination of the level of epidermal growth factor receptor or cytokeratin 5/6 expression.
  • [MeSH-major] Breast Neoplasms / pathology. Receptor, Epidermal Growth Factor / metabolism. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma, Scirrhous / metabolism. Adenocarcinoma, Scirrhous / pathology. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Female. Humans. Japan. Middle Aged. Prognosis. Receptor, ErbB-2 / metabolism. Registries. Societies, Medical / statistics & numerical data. Young Adult


14. Graziani G, Tentori L, Muzi A, Vergati M, Tringali G, Pozzoli G, Navarra P: Evidence that corticotropin-releasing hormone inhibits cell growth of human breast cancer cells via the activation of CRH-R1 receptor subtype. Mol Cell Endocrinol; 2007 Jan 29;264(1-2):44-9
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  • [Title] Evidence that corticotropin-releasing hormone inhibits cell growth of human breast cancer cells via the activation of CRH-R1 receptor subtype.
  • It has been previously shown that corticotropin-releasing hormone (CRH) exerts antiproliferative activity on an estrogen-dependent tumor cell line, i.e. human endometrial adenocarcinoma Ishikawa (IK) cells.
  • Here we have investigated the effects of CRH on another estrogen-dependent tumor cell line, human breast cancer MCF7 cells.
  • In this paradigm, CRH given at a fixed concentration of 100 nM significantly inhibited cell growth induced by 100 nM estradiol (E2) after 48 and 72 h of incubation.
  • CRH inhibition of cell proliferation was counteracted in a concentration-dependent manner by the non-selective CRH receptor antagonist, astressin, as well as by a CRH-R1 selective receptor antagonist, antalarmin.
  • RNase protection assays carried out on MCF7 under basal conditions showed that these cells express in a constitutive manner the CRH-R1 receptor subtype.
  • We have also investigated the putative source of CRH acting on breast cancer cells; we found that MCF7 cells express CRH mRNA under basal conditions and secrete sizable amounts of immunoreactive CRH, which leads to postulate the existence of paracrine-autocrine inhibitory mechanism operated by CRH in breast cancer cells.
  • [MeSH-major] Autocrine Communication / drug effects. Cell Proliferation / drug effects. Corticotropin-Releasing Hormone / pharmacology. Hormones / pharmacology. Paracrine Communication / drug effects. Receptors, Corticotropin-Releasing Hormone / agonists
  • [MeSH-minor] Breast Neoplasms. Cell Line, Tumor. Dose-Response Relationship, Drug. Estradiol / pharmacology. Female. Humans. Pyrimidines / pharmacology. Pyrroles / pharmacology

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  • (PMID = 17097220.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CRF receptor type 1; 0 / Hormones; 0 / Pyrimidines; 0 / Pyrroles; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / antalarmin; 4TI98Z838E / Estradiol; 9015-71-8 / Corticotropin-Releasing Hormone
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15. Wei B, Bu H, Chen HJ, Zhang HY, Li XJ: [Clinicopathologic study of solid papillary carcinoma of breast]. Zhonghua Bing Li Xue Za Zhi; 2006 Oct;35(10):589-93
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  • [Title] [Clinicopathologic study of solid papillary carcinoma of breast].
  • OBJECTIVE: To study the clinicopathologic features and immunophenotype of solid papillary carcinoma (SPC) of breast.
  • Immunohistochemical study showed that the tumor cells expressed CK8 but not basal cell cytokeratin.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Papillary / pathology
  • [MeSH-minor] Actins / metabolism. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Mucinous / surgery. Adult. Aged. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Carcinoma, Ductal, Breast / surgery. Chromogranin A / metabolism. Female. Follow-Up Studies. Humans. Immunohistochemistry. Keratin-8 / metabolism. Mastectomy / methods. Middle Aged. Synaptophysin / metabolism

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  • (PMID = 17134565.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ACTA2 protein, human; 0 / Actins; 0 / Chromogranin A; 0 / Keratin-8; 0 / Synaptophysin
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16. Abdel-Fatah TM, Powe DG, Hodi Z, Reis-Filho JS, Lee AH, Ellis IO: Morphologic and molecular evolutionary pathways of low nuclear grade invasive breast cancers and their putative precursor lesions: further evidence to support the concept of low nuclear grade breast neoplasia family. Am J Surg Pathol; 2008 Apr;32(4):513-23
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  • [Title] Morphologic and molecular evolutionary pathways of low nuclear grade invasive breast cancers and their putative precursor lesions: further evidence to support the concept of low nuclear grade breast neoplasia family.
  • We have previously provided evidence showing an association between some precursor lesions with low nuclear grade breast carcinomas (LNGBCs).
  • Precursor lesions including columnar cell lesions, atypical ductal hyperplasia, ductal carcinoma in situ, usual epithelial hyperplasia, and lobular neoplasia were compared with matching "morphologically normal" terminal lobular duct units and matching invasive carcinoma.
  • The epithelial cells in the putative precursor flat epithelial atypia, atypical ductal hyperplasia, lobular neoplasia, ductal carcinoma in situ lesions, and their coexisting LNGBC were negative for basal and myoepithelial markers, but positive for CK19/18/8, estrogen receptor (ER)-alpha, Bcl-2, and cyclin D1.
  • The ER-alpha/ER-beta expression ratio increased during carcinogenesis, as did expression of cyclin D1 and Bcl-2. p53 immunopositivity was found 3% in LNGBC versus 43% in high nuclear grade breast carcinoma (HNGBC), whereas ataxia telangiectasia mutated expression was absent or reduced in 22% of LNGBC versus 53% of HNGBC cases.
  • These may represent a family of precursor, in situ and invasive neoplastic lesions belonging to the luminal "A" subclass of breast cancer.
  • Ataxia telangiectasia mutated may be one of the alternative regulatory mechanisms to TP53 mutation or dysfunction in low-grade and high-grade breast carcinoma.
  • Our findings support the concept that progression of LNGBC to HNGBC (basal-like or HER2+) phenotype is an unlikely biologic phenomenon.
  • [MeSH-major] Breast Neoplasms / chemistry. Breast Neoplasms / pathology. Mammary Glands, Human / chemistry. Mammary Glands, Human / pathology. Precancerous Conditions / chemistry. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / chemistry. Adenocarcinoma / pathology. Ataxia Telangiectasia Mutated Proteins. Carcinoma, Intraductal, Noninfiltrating / chemistry. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Lobular / chemistry. Carcinoma, Lobular / pathology. Cell Cycle Proteins / analysis. Cyclin D. Cyclins / analysis. DNA-Binding Proteins / analysis. Estrogen Receptor alpha / analysis. Estrogen Receptor beta / analysis. Evolution, Molecular. Female. Humans. Hyperplasia. Immunohistochemistry. Keratin-18 / analysis. Keratin-19 / analysis. Keratin-8 / analysis. Neoplasm Invasiveness. Neoplasm Staging. Phenotype. Protein-Serine-Threonine Kinases / analysis. Proto-Oncogene Proteins c-bcl-2 / analysis. Tissue Array Analysis. Tumor Suppressor Protein p53 / analysis. Tumor Suppressor Proteins / analysis

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  • (PMID = 18223478.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclin D; 0 / Cyclins; 0 / DNA-Binding Proteins; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / KRT18 protein, human; 0 / KRT8 protein, human; 0 / Keratin-18; 0 / Keratin-19; 0 / Keratin-8; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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17. Newill H, Loske R, Wagner J, Johannes C, Lorenz RL, Lehmann L: Oxidation products of stigmasterol interfere with the action of the female sex hormone 17beta-estradiol in cultured human breast and endometrium cell lines. Mol Nutr Food Res; 2007 Jul;51(7):888-98
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  • [Title] Oxidation products of stigmasterol interfere with the action of the female sex hormone 17beta-estradiol in cultured human breast and endometrium cell lines.
  • Therefore, the estrogenic and antiestrogenic activities of a mixture of six oxidation products of stigmasterol (oxy-StOL) were determined at the following endpoints: (i) the affinity to isolated human estrogen receptors (ER), (ii) the basal and 17beta-estradiol (E2)-induced expression of the alkaline phosphatase (AlP) in human endometrial adenocarcinoma (Ishikawa) cells, and (iii) the basal and E2-induced proliferation of human breast adenocarcinoma (MCF-7) cells.
  • [MeSH-minor] Alkaline Phosphatase / genetics. Breast Neoplasms. Cell Division / drug effects. Cell Line, Tumor. Endometrial Neoplasms. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Female. Gene Expression / drug effects. Humans. Oxidation-Reduction. RNA, Messenger / analysis. Recombinant Proteins / metabolism

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  • (PMID = 17579897.001).
  • [ISSN] 1613-4125
  • [Journal-full-title] Molecular nutrition & food research
  • [ISO-abbreviation] Mol Nutr Food Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Messenger; 0 / Recombinant Proteins; 4TI98Z838E / Estradiol; 99WUK5D0Y8 / Stigmasterol; EC 3.1.3.1 / Alkaline Phosphatase
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18. Chen CH, Rowlands C, Sengupta SK, George RL, Parulekar W, Thain K, O'Malley F, Isotalo PA: Primary basaloid carcinoma of the nipple with associated squamous cell carcinoma in situ. Breast J; 2009 Jul-Aug;15(4):409-13
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  • [Title] Primary basaloid carcinoma of the nipple with associated squamous cell carcinoma in situ.
  • We describe a primary invasive adenocarcinoma of the nipple with extensive basaloid features that was also associated with squamous cell carcinoma (SCC) in situ and an aggressive behavior.
  • A 69-year-old woman without a history of breast neoplasia presented with right nipple pain.
  • The differential diagnosis included a primary basaloid adenocarcinoma of the nipple, basal cell carcinoma of the nipple, neuroendocrine carcinoma, melanoma, basaloid variant of adenoid cystic carcinoma and metastatic disease.
  • Immunohistochemical profile of this tumor supported a primary basaloid adenocarcinoma of the nipple.
  • Although the initial sentinel lymph node biopsy was negative, within a year of diagnosis, the patient developed ipsilateral axillary node and pulmonary metastases.
  • [MeSH-major] Carcinoma in Situ / pathology. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / pathology. Nipples / pathology

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  • (PMID = 19601946.001).
  • [ISSN] 1524-4741
  • [Journal-full-title] The breast journal
  • [ISO-abbreviation] Breast J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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19. Michelucci A, Di Cristofano C, Lami A, Collecchi P, Caligo A, Decarli N, Leopizzi M, Aretini P, Bertacca G, Porta RP, Ricci S, Della Rocca C, Stanta G, Bevilacqua G, Cavazzana A: PIK3CA in breast carcinoma: a mutational analysis of sporadic and hereditary cases. Diagn Mol Pathol; 2009 Dec;18(4):200-5
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  • [Title] PIK3CA in breast carcinoma: a mutational analysis of sporadic and hereditary cases.
  • The PI3K-Akt cascade is a key signaling pathway involved in cell proliferation, survival, and growth.
  • Activating PIK3CA mutations have been reported in breast carcinoma (BC).
  • The PIK3CA mutation seems to characterize the luminal-type BC, in both sporadic and BRCA2 mutated forms, and is absent in the basal-type BC, in both the sporadic and BRCA1 mutated forms.
  • [MeSH-major] Adenocarcinoma / genetics. Breast Neoplasms / genetics. DNA Mutational Analysis. Germ-Line Mutation. Mutation, Missense / genetics. Phosphatidylinositol 3-Kinases / genetics
  • [MeSH-minor] Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / mortality. Adenocarcinoma, Mucinous / pathology. Apoptosis Regulatory Proteins. BRCA2 Protein / genetics. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma, Ductal, Breast / genetics. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / mortality. Carcinoma, Ductal, Breast / pathology. Carcinoma, Lobular / genetics. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / mortality. Carcinoma, Lobular / pathology. DNA, Neoplasm / analysis. Female. Humans. Italy / epidemiology. Kaplan-Meier Estimate. Lymph Nodes / pathology. Middle Aged. Survival Rate. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 19861897.001).
  • [ISSN] 1533-4066
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BLID protein, human; 0 / BRCA2 Protein; 0 / BRCA2 protein, human; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 6.3.2.- / BRAP protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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20. Martinez VG, Williams KJ, Stratford IJ, Clynes M, O'Connor R: Overexpression of cytochrome P450 NADPH reductase sensitises MDA 231 breast carcinoma cells to 5-fluorouracil: possible mechanisms involved. Toxicol In Vitro; 2008 Apr;22(3):582-8
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  • [Title] Overexpression of cytochrome P450 NADPH reductase sensitises MDA 231 breast carcinoma cells to 5-fluorouracil: possible mechanisms involved.
  • MDA 231 breast adenocarcinoma cells transfected with human P450R (MDA R4) or an empty vector (MDA EV) were exposed to a series of commonly used chemotherapeutic drugs.
  • Overexpression of P450R did not affect cell sensitivity to cisplatin, mitoxantrone, paclitaxel, docetaxel, vincristine or etoposide.
  • Levels of NADPH were considerably decreased in MDA R4 as compared to MDA EV cells, while reactive oxygen species (ROS) production was increased in MDA R4 cells in basal conditions, showing no significant further increase after treatment with mitomycin C or 5-fluorouracil.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Breast Neoplasms / drug therapy. Fluorouracil / pharmacology. NADPH-Ferrihemoprotein Reductase / biosynthesis
  • [MeSH-minor] Antibiotics, Antineoplastic / metabolism. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / metabolism. Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Survival. Female. Glutathione / metabolism. Humans. Microsomes / metabolism. Mitomycin / metabolism. Mitomycin / pharmacology. NADP / metabolism. Reactive Oxygen Species / metabolism. Transfection. Vincristine / metabolism. Vincristine / pharmacology

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  • (PMID = 18191533.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G0500366; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Reactive Oxygen Species; 50SG953SK6 / Mitomycin; 53-59-8 / NADP; 5J49Q6B70F / Vincristine; EC 1.6.2.4 / NADPH-Ferrihemoprotein Reductase; GAN16C9B8O / Glutathione; U3P01618RT / Fluorouracil
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21. Roy JW, Cowley EA, Blay J, Linsdell P: The intermediate conductance Ca2+-activated K+ channel inhibitor TRAM-34 stimulates proliferation of breast cancer cells via activation of oestrogen receptors. Br J Pharmacol; 2010 Feb 1;159(3):650-8
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  • [Title] The intermediate conductance Ca2+-activated K+ channel inhibitor TRAM-34 stimulates proliferation of breast cancer cells via activation of oestrogen receptors.
  • We have investigated the effects of specific K(+) channel inhibitors on basal and oestrogen-stimulated proliferation of breast cancer cells.
  • EXPERIMENTAL APPROACH: Using the mammary adenocarcinoma cell line MCF-7 we assayed cell proliferation by radiolabelled thymidine incorporation in the absence or presence of various K(+) channel inhibitors with or without 17beta-oestradiol.
  • KEY RESULTS: Inhibitors of K(v)10.1 and K(Ca)3.1 K(+) channels suppressed basal proliferation of MCF-7 cells, but not oestrogen-stimulated proliferation.
  • TRAM-34, a specific inhibitor of K(Ca)3.1 channels increased or decreased cell proliferation depending on the concentration.
  • At intermediate concentrations (3-10 microM) TRAM-34 increased cell proliferation, whereas at higher concentrations (20-100 microM) TRAM-34 decreased cell proliferation.
  • The enhancement of cell proliferation caused by TRAM-34 was blocked by the oestrogen receptor antagonists ICI182,780 and tamoxifen.
  • CONCLUSIONS AND IMPLICATIONS: Our results demonstrate that K(+) channels K(v)10.1 and K(Ca)3.1 play a role in basal, but not oestrogen-stimulated MCF-7 cell proliferation.
  • TRAM-34, as well as inhibiting K(Ca)3.1, directly interacts with the oestrogen receptor and mimics the effects of 17beta-oestradiol on MCF-7 cell proliferation and gene modulation.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Estradiol / pharmacology. Potassium Channels, Calcium-Activated. Tamoxifen / pharmacology
  • [MeSH-minor] Calcium / metabolism. Calcium / pharmacology. Calcium / therapeutic use. Cell Line, Tumor. Cells / metabolism. Cells / pathology. Cellular Structures / metabolism. Cellular Structures / pathology. Estrogen Receptor alpha / metabolism. Estrogens / metabolism. Estrogens / pharmacology. Estrogens / therapeutic use. Female. Gene Expression / drug effects. Humans. Ion Transport / drug effects. Pyrazoles. RNA, Messenger / metabolism. RNA, Messenger / pharmacology. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism

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  • (PMID = 20050851.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Potassium Channels, Calcium-Activated; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / TRAM 34; 0 / estrogen receptor alpha, human; 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2828028
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22. Huss WJ, Gray DR, Greenberg NM, Mohler JL, Smith GJ: Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells. Cancer Res; 2005 Aug 1;65(15):6640-50
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  • [Title] Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells.
  • Putative prostate stem cells and prostate tumor stem cells in benign and malignant human prostate tissue, in primary human prostate xenografts, and in the transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model of prostate cancer, are defined by expression of breast cancer resistance protein (BCRP), a marker of pluripotent hematopoietic, muscle, and neural stem cells, and by an absence of androgen receptor (AR) protein.
  • Inhibition of BCRP-mediated efflux of dihydrotestosterone by novobiocin or fumitremorgin C in a rat prostate progenitor cell line that expresses BCRP and AR mRNAs, but minimal AR protein, results in stabilization and nuclear translocation of AR protein, providing a mechanism for lack of AR protein in BCRP-expressing stem cells.
  • In both benign and malignant human prostate tissue, the rare epithelial cells that express BCRP and lack AR protein are localized in the basal cell compartment, survive androgen deprivation, and maintain proliferative potential in the hypoxic, androgen-deprived prostate.

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  • (PMID = 16061644.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA84296; United States / NCI NIH HHS / CA / P01 CA077739; United States / NCI NIH HHS / CA / CA77739; United States / NCI NIH HHS / CA / CA64851; United States / NIEHS NIH HHS / ES / ES07017; United States / NCI NIH HHS / CA / CA64865
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / Androgens; 0 / Indoles; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; 17EC19951N / Novobiocin; CW5S8OP3VO / tryptoquivaline
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23. Fernandes RC, Bevilacqua JL, Soares IC, Siqueira SA, Pires L, Hegg R, Carvalho FM: Coordinated expression of ER, PR and HER2 define different prognostic subtypes among poorly differentiated breast carcinomas. Histopathology; 2009 Sep;55(3):346-52
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  • [Title] Coordinated expression of ER, PR and HER2 define different prognostic subtypes among poorly differentiated breast carcinomas.
  • AIMS: Histological grade is one of the most important prognostic factors in breast carcinomas, but poorly differentiated neoplasms still have quite heterogeneous biological behaviour, since they can be genetically classified as basal-like, HER2+ or even luminal.
  • The aim was to analyse the frequency of oestrogen receptor (ER), progesterone receptor (PR) and HER2 expression profiles among breast carcinomas with <10% tubular formation, and their correlation with classic prognostic factors.
  • The only difference was the expression of basal cytokeratins (basal CK), which was more frequent among triple-negative carcinomas.
  • Basal-CK expression defined a more aggressive group of tumours, according to the pathological features, regardless of the immunohistochemical profile.
  • Among poorly differentiated breast carcinomas, the classic profile associated with basal-CK identifies distinct subtypes equivalent to those seen by genetic classification.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Receptor, ErbB-2 / metabolism. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism
  • [MeSH-minor] Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Adult. Aged. Aged, 80 and over. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Cell Proliferation. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Keratins / metabolism. Middle Aged. Necrosis. Prognosis. Retrospective Studies. Tissue Array Analysis. Young Adult

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  • (PMID = 19723150.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 68238-35-7 / Keratins; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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24. Chung AC, Zhou S, Liao L, Tien JC, Greenberg NM, Xu J: Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Cancer Res; 2007 Jun 15;67(12):5965-75
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  • [Title] Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice.
  • Although the amplified-in-breast cancer 1 (AIB1; SRC-3, ACTR, or NCoA3) was defined as a coactivator for androgen receptor (AR) by in vitro studies, its role in AR-mediated prostate development and prostate cancer remained unexplored.
  • We report here that AIB1 is expressed in the basal and stromal cells but not in the epithelial cells of the normal mouse prostates.
  • Surprisingly, when prostate tumorigenesis was induced by the SV40 transgene in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice, AIB1 expression was observed in certain epithelial cells of the prostate intraepithelial neoplasia (PIN) and well-differentiated carcinoma and in almost all cells of the poorly differentiated carcinoma.
  • AIB1-/-/TRAMP prostates showed much lower cell proliferation than WT/TRAMP prostates.

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  • (PMID = 17575167.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK58242; United States / NIDDK NIH HHS / DK / DK058242-05; United States / NCI NIH HHS / CA / CA119689-03; United States / NCI NIH HHS / CA / CA112403; United States / NCI NIH HHS / CA / R01 CA112403-02; United States / NCI NIH HHS / CA / CA112403-02; United States / NIDDK NIH HHS / DK / R01 DK058242-05; United States / NCI NIH HHS / CA / R01 CA119689-03; United States / NCI NIH HHS / CA / CA119689; United States / NCI NIH HHS / CA / R01 CA112403; United States / NIDDK NIH HHS / DK / R01 DK058242; United States / NCI NIH HHS / CA / R01 CA119689
  • [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 / Receptors, Androgen; 0 / Trans-Activators; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / Ncoa3 protein, mouse; EC 2.3.1.48 / Nuclear Receptor Coactivator 3
  • [Other-IDs] NLM/ NIHMS50339; NLM/ PMC2898573
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25. Fassan M, Pizzi M, Battaglia G, Giacomelli L, Parente P, Bocus P, Ancona E, Rugge M: Programmed cell death 4 (PDCD4) expression during multistep Barrett's carcinogenesis. J Clin Pathol; 2010 Aug;63(8):692-6
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  • [Title] Programmed cell death 4 (PDCD4) expression during multistep Barrett's carcinogenesis.
  • AIM: To test the contribution of programmed cell death 4 (PDCD4) tumour suppressor gene in Barrett's carcinogenesis.
  • METHODS: PDCD4 immunohistochemical expression was assessed in 88 biopsy samples obtained from histologically proven long-segment Barrett's mucosa (BM; 25 non-intestinal columnar metaplasia, 25 intestinal metaplasia (IM), 16 low-grade intraepithelial neoplasia (LG-IEN), 12 high-grade IEN (HG-IEN) and 10 Barrett's adenocarcinoma (BAc)).
  • Normal basal squamous epithelial layers featured strong PDCD4 nuclear immunoreaction (mostly coexisting with weak-moderate cytoplasmic staining).
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biopsy. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Disease Progression. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. MicroRNAs / genetics. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis / methods. RNA, Neoplasm / genetics. Retrospective Studies

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  • (PMID = 20702469.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / MIRN21 microRNA, human; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / PDCD4 protein, human; 0 / RNA, Neoplasm; 0 / RNA-Binding Proteins
  • [Other-IDs] NLM/ PMC2976066
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26. Prayaga AK, Loya AC, Gottimukkala SR, Digumarti RR, Maddali LS, Challa S: Cytologic features of primary malignant tumors of skin and adnexae. Acta Cytol; 2008 Nov-Dec;52(6):702-9
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  • Melanoma was the most common (n=12), followed by squamous cell carcinoma (SCC) (n=5).
  • There were 3 basal cell carcinomas and 2 cases each of sebaceous carcinoma, Paget's disease of the breast and lymphoma.
  • There were single cases of eccrine carcinoma, malignant trichilemmal tumor, undifferentiated carcinoma and extramedullary myeloid cell tumor.
  • [MeSH-minor] Adenocarcinoma, Sebaceous / pathology. Breast Neoplasms / pathology. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / pathology. Cytodiagnosis. Humans. Lymphatic Metastasis. Medical Records. Melanoma / pathology. Paget's Disease, Mammary / pathology

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  • (PMID = 19068675.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Müller I, Wischnewski F, Pantel K, Schwarzenbach H: Promoter- and cell-specific epigenetic regulation of CD44, Cyclin D2, GLIPR1 and PTEN by methyl-CpG binding proteins and histone modifications. BMC Cancer; 2010;10:297
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  • [Title] Promoter- and cell-specific epigenetic regulation of CD44, Cyclin D2, GLIPR1 and PTEN by methyl-CpG binding proteins and histone modifications.
  • BACKGROUND: The aim of the current study was to analyze the involvement of methyl-CpG binding proteins (MBDs) and histone modifications on the regulation of CD44, Cyclin D2, GLIPR1 and PTEN in different cellular contexts such as the prostate cancer cells DU145 and LNCaP, and the breast cancer cells MCF-7.
  • METHODS: In DU145, LNCaP and MCF-7 cells mRNA expression levels of CD44, Cyclin D2, GLIPR1 and PTEN were determined by quantitative RT-PCR at the basal status as well as after treatment with demethylating agent 5-aza-2'-deoxycytidine and/or histone deacetylase inhibitor Trichostatin A.
  • RESULTS: Comparison of the different promoters showed that MeCP2 and MBD2a repressed promoter-specifically Cyclin D2 in all cell lines, whereas in MCF-7 cells MeCP2 repressed cell-specifically all methylated promoters.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Breast Neoplasms / genetics. Breast Neoplasms / pathology. Chromatin / genetics. Chromatin Immunoprecipitation. CpG Islands. DNA Methylation / drug effects. Enzyme Inhibitors / pharmacology. Epigenesis, Genetic. Female. Gene Silencing. Humans. Male. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 20565761.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CCND2 protein, human; 0 / CD44 protein, human; 0 / Chromatin; 0 / Cyclin D2; 0 / Enzyme Inhibitors; 0 / GLIPR1 protein, human; 0 / Histones; 0 / Methyl-CpG-Binding Protein 2; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2912262
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28. Brusevold IJ, Søland TM, Khuu C, Christoffersen T, Bryne M: Nuclear and cytoplasmic expression of Met in oral squamous cell carcinoma and in an organotypic oral cancer model. Eur J Oral Sci; 2010 Aug;118(4):342-9
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  • [Title] Nuclear and cytoplasmic expression of Met in oral squamous cell carcinoma and in an organotypic oral cancer model.
  • The aim of this study was to examine the pattern of Met expression and its value as a prognostic factor in oral squamous cell carcinomas (OSCCs).
  • The material consisted of 53 OSCCs and five healthy controls from normal oral mucosa supplied with cell lines, 10 organotypic models supplied with oral cancer cells, and three organotypic models supplied with normal keratinocytes.
  • Met expression was scarce and limited to the basal layer in normal oral mucosa, but was more extensive in the tumours.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Cell Nucleus / ultrastructure. Cytoplasm / ultrastructure. Mouth Neoplasms / pathology. Proto-Oncogene Proteins c-met / analysis
  • [MeSH-minor] Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Breast Neoplasms / pathology. Carcinoma / pathology. Cell Culture Techniques. Cell Line. Cells, Cultured. Coculture Techniques. Female. Fibroblasts / cytology. Gingiva / cytology. Humans. Keratinocytes / cytology. Keratins / analysis. Male. Middle Aged. Mouth Mucosa / cytology. Neoplasm Invasiveness. Prognosis. Skin Neoplasms / pathology. Tissue Scaffolds. Tongue Neoplasms / pathology. Up-Regulation


29. Xue LY, Zou SM, Zheng S, Xie YQ, Wen P, Liu XY, Lin DM, Lü N: [Expression of fascin and CK14 in different histological types of cancer and its differential diagnostic significance]. Zhonghua Zhong Liu Za Zhi; 2010 Nov;32(11):838-44
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  • OBJECTIVE: To investigate and analyze the expression of fascin and CK14 in multiple histological types of cancer and to explore the potential value of the two proteins as markers in diagnosis and differential diagnosis of various cancer types.
  • METHODS: Tissue microarray containing esophageal squamous cell carcinoma (SCC), lung SCC, larynx SCC, uterine cervical SCC, SCC of external genital organs, lung adenocarcinoma, gastric adenocarcinoma, colorectal adenocarcinoma, heptocellular carcinoma, pancreatic ductal adenocarcinoma, breast infiltrating ductal carcinoma, thyroid papillary carcinoma, uterine endometrioid adenocarcinoma, ovarian serous adenocarcinoma and renal clear cell carcinoma, 30 cases each, as well as corresponding normal controls was constructed.
  • RESULTS: In normal esophagus, bronchus, larynx, uterine cervix and skin, fascin was mainly expressed in the basal cells or reserve cells, but the expression was diffuse in esophageal SCC, lung SCC, larynx SCC, uterine cervical SCC and SCC of external genital organs, with a positive rate of 90.0%, 90.0%, 96.7%, 78.6% and 89.7%, respectively.
  • In the normal tissue of other organs, except breast and uterine endometrium, fascin was negative.
  • In lung adenocarcinoma, gastric adenocarcinoma, colorectal adenocarcinoma, hepatocellular carcinoma, pancreatic ductal adenocarcinoma, breast infiltrating dutal adenocarcinoma, thyroid papillary carcinoma, uterine endometrioid adenocarcinoma, ovarian serous adenocarcinoma and renal clear cell carcinoma, the positive rates were 38.0%, 23.3%, 14.3%, 10.3%, 73.3%, 13.3%, 6.7%, 60.0%, 66.7% and 10.0%, respectively.
  • CK14 was mainly expressed in the basal cells, reserve cells or myoepithelia of normal tissues.
  • It was weak and focal in lung adenocarcinoma, gastric adenocarcinoma, colorectal adenocarcinoma, hepatocellular carcinoma, pancreatic ductal adenocarcinoma, breast infiltrating dutal adenocarcinoma, thyroid papillary carcinoma, uterine endometrioid adenocarcinoma, ovarian serous adenocarcinoma, and renal clear cell carcinoma, with a positive rate of 13.3%, 13.3%, 20.7%, 41.4%, 46.7%, 6.7%, 40.0%, 13.3%, 20.0% and 6.7%, respectively.
  • Combination of fascin and CK14 should be a valuable marker in diagnosis and differential diagnosis of carcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. Carrier Proteins / metabolism. Keratin-14 / metabolism. Laryngeal Neoplasms / metabolism. Microfilament Proteins / metabolism
  • [MeSH-minor] Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Cystadenocarcinoma, Serous / metabolism. Cystadenocarcinoma, Serous / pathology. Diagnosis, Differential. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Female. Humans. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Male. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / pathology. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology. Uterine Cervical Neoplasms / metabolism. Uterine Cervical Neoplasms / pathology

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  • (PMID = 21223690.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Keratin-14; 0 / Microfilament Proteins; 146808-54-0 / fascin
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30. 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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  • 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

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  • (PMID = 21082595.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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31. Kim IM, Ackerson T, Ramakrishna S, Tretiakova M, Wang IC, Kalin TV, Major ML, Gusarova GA, Yoder HM, Costa RH, Kalinichenko VV: The Forkhead Box m1 transcription factor stimulates the proliferation of tumor cells during development of lung cancer. Cancer Res; 2006 Feb 15;66(4):2153-61
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  • The proliferation-specific Forkhead Box m1 (Foxm1 or Foxm1b) transcription factor (previously called HFH-11B, Trident, Win, or MPP2) regulates expression of cell cycle genes essential for progression into DNA replication and mitosis.
  • Expression of Foxm1 is found in a variety of distinct human cancers including hepatocellular carcinomas, intrahepatic cholangiocarcinomas, basal cell carcinomas, ductal breast carcinomas, and anaplastic astrocytomas and glioblastomas.
  • In this study, we show that human Foxm1 protein is abundantly expressed in highly proliferative human non-small cell lung cancers (NSCLC) as well as in mouse lung tumors induced by urethane.
  • Transient transfection experiments with A549 lung adenocarcinoma cells show that depletion of Foxm1 levels by short interfering RNA caused diminished DNA replication and mitosis and reduced anchorage-independent growth of cell colonies on soft agar.
  • Foxm1-depleted A549 cells exhibit reduced expression of cell cycle-promoting cyclin A2 and cyclin B1 genes.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Forkhead Transcription Factors / physiology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Alleles. Animals. Cell Adhesion. Cell Growth Processes / physiology. Cyclin A / biosynthesis. Cyclin A / genetics. Cyclin A2. Cyclin B / biosynthesis. Cyclin B / genetics. Cyclin B1. DNA Replication. DNA, Neoplasm / biosynthesis. Gene Deletion. Humans. Mice. Mice, Inbred C57BL. Mice, Transgenic. Mitosis. RNA, Small Interfering / genetics. Urethane

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  • (PMID = 16489016.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 54687-06
  • [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 / CCNA2 protein, human; 0 / CCNB1 protein, human; 0 / Ccnb1 protein, mouse; 0 / Cyclin A; 0 / Cyclin A2; 0 / Cyclin B; 0 / Cyclin B1; 0 / DNA, Neoplasm; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Foxm1 protein, mouse; 0 / RNA, Small Interfering; 3IN71E75Z5 / Urethane
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32. Wu XM, Liu X, Bu YQ, Sengupta J, Cui HJ, Yi FP, Liu T, Yuan CF, Shi YY, Song FZ: RNAi-mediated silencing of the Bmi-1 gene causes growth inhibition and enhances doxorubicin-induced apoptosis in MCF-7 cells. Genet Mol Biol; 2009 Oct;32(4):697-703
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  • Its expression is found to be greatly increased in a number of malignant tumors including breast cancer.
  • In this study, RNAi was introduced to down-regulate the expression of Bmi-1 in a highly malignant breast adenocarcinoma cell line, MCF-7.
  • The number of target cells was found to increase in phase G (0) /G (1) and decrease in the S phase, but no increase in the basal level of apoptosis was noticed.
  • Here, we report on a study regarding the RNAi-mediated silencing of the Bmi-1 gene in breast cancer.

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  • (PMID = 21637439.001).
  • [ISSN] 1678-4685
  • [Journal-full-title] Genetics and molecular biology
  • [ISO-abbreviation] Genet. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC3036904
  • [Keywords] NOTNLM ; Bmi-1 / RNA interference / breast cancer / doxorubicin / retrovirus vector
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33. Seo SI, Song SY, Kang MR, Kim MS, Oh JE, Kim YR, Lee JY, Yoo NJ, Lee SH: Immunohistochemical analysis of NF-kappaB signaling proteins IKKepsilon, p50/p105, p52/p100 and RelA in prostate cancers. APMIS; 2009 Aug;117(8):623-8
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  • A recent study revealed that IkappaB kinase epsilon (IKKepsilon), an activator of NF-kappaB, was overexpressed in breast cancers and acted as an oncogene.
  • We analyzed the expression of IKKepsilon, p50/105, p52/p100 and RelA in 107 prostate adenocarcinoma tissues by immunohistochemistry using a tissue microarray (TMA) method.
  • In the TMA, IKKepsilon is expressed in basal cells, but not in alveolar cells in normal prostate glands.
  • [MeSH-major] Adenocarcinoma / pathology. I-kappa B Kinase / biosynthesis. NF-kappa B p50 Subunit / biosynthesis. NF-kappa B p52 Subunit / biosynthesis. Prostatic Neoplasms / pathology. Transcription Factor RelA / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Signal Transduction. Tissue Array Analysis

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  • (PMID = 19664134.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / NF-kappa B p50 Subunit; 0 / NF-kappa B p52 Subunit; 0 / Transcription Factor RelA; EC 2.7.11.10 / I-kappa B Kinase
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34. Immonen E, Serpi R, Vähäkangas K, Myllynen P: Responses of PhIP (2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine) in MCF-7 cells are culture condition dependent. Chem Biol Interact; 2009 Nov 10;182(1):73-83
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  • Effects of PhIP and estradiol on cell viability and proliferation were determined by ATP analysis and Ki-67 immunocytochemistry.
  • Expression of estrogen receptor alpha, cell stress markers (p53 and ERK) and estrogen responsive proteins (c-myc and ERK) were immunoblotted.
  • All concentrations of estradiol induced cell proliferation, viability and changes in protein expression, typical for estrogenic responses.
  • No changes in protein expressions by PhIP were noted, not even when switching cells from steroid-containing to -deprived medium which down-regulated the expression of proteins at basal level.
  • [MeSH-major] Carcinogens / pharmacology. Cell Culture Techniques / methods. Estrogen Receptor alpha / metabolism. Imidazoles / pharmacology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenosine Triphosphate / metabolism. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Dose-Response Relationship, Drug. Estradiol / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Immunoblotting. Immunohistochemistry. Ki-67 Antigen / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19647730.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Estrogen Receptor alpha; 0 / Imidazoles; 0 / Ki-67 Antigen; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Tumor Suppressor Protein p53; 4TI98Z838E / Estradiol; 8L70Q75FXE / Adenosine Triphosphate; 909C6UN66T / 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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35. Young GS, Setayesh K: Spin-echo echo-planar perfusion MR imaging in the differential diagnosis of solitary enhancing brain lesions: distinguishing solitary metastases from primary glioma. AJNR Am J Neuroradiol; 2009 Mar;30(3):575-7
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  • [Title] Spin-echo echo-planar perfusion MR imaging in the differential diagnosis of solitary enhancing brain lesions: distinguishing solitary metastases from primary glioma.
  • [MeSH-minor] Adenocarcinoma / secondary. Adult. Aged. Astrocytoma / pathology. Breast Neoplasms / pathology. Carcinoma, Basal Cell / secondary. Colorectal Neoplasms / pathology. Diagnosis, Differential. Esophageal Neoplasms / pathology. Female. Humans. Lung Neoplasms / pathology. Male. Melanoma / secondary. Middle Aged. Models, Neurological. Prostatic Neoplasms / pathology. Retrospective Studies. Sensitivity and Specificity. Skin Neoplasms / pathology

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  • (PMID = 19095787.001).
  • [ISSN] 1936-959X
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
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36. Seigne C, Fontanière S, Carreira C, Lu J, Tong WM, Fontanière B, Wang ZQ, Zhang CX, Frappart L: Characterisation of prostate cancer lesions in heterozygous Men1 mutant mice. BMC Cancer; 2010;10:395
The Lens. Cited by Patents in .

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  • Using immunostaining for the androgen receptor and p63, a basal epithelial cell marker, we demonstrated that the menin-negative prostate cancer cells did not display p63 expression and that the androgen receptor was expressed but more heterogeneous in these lesions.
  • Furthermore, our data showed that the expression of the cyclin-dependent kinase inhibitor CDKN1B (p27), a Men1 target gene known to be inactivated during prostate cell tumorigenesis, was notably decreased in the prostate cancers that developed in the mutant mice.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Loss of Heterozygosity. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology. Proto-Oncogene Proteins / physiology


37. Gade P, Singh AK, Roy SK, Reddy SP, Kalvakolanu DV: Down-regulation of the transcriptional mediator subunit Med1 contributes to the loss of expression of metastasis-associated dapk1 in human cancers and cancer cells. Int J Cancer; 2009 Oct 1;125(7):1566-74
The Lens. Cited by Patents in .

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  • We have recently shown that CCAAT/Enhancer binding protein-beta (C/EBP-beta) is required for the basal and interferon gamma (IFN-gamma)-induced expression of dapk1 in many cell types.
  • C/EBP-beta interacts with the transcriptional Mediator, a multisubunit complex that couples enhancer bound transcription factors to the basal transcriptional machinery in an IFN-gamma dependent manner for regulating dapk1 expression.
  • We compared the relative occupancy of these factors at the dapk1 promoter at CRE/ATF sites in normal and cancer cell lines.
  • A significantly lower binding of these factors to the CRE/ATF site of dapk1 promoter occurred in human cancer cell lines than in normal cells.
  • Med1 levels were significantly lower in cancer cell lines than in normal controls.
  • Our studies reveal a critical parameter limiting dapk1 expression in cancer cell lines.

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  • (PMID = 19521987.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105005; United States / NIEHS NIH HHS / ES / ES11863; United States / NCI NIH HHS / CA / R01 CA105005; United States / NIEHS NIH HHS / ES / R01 ES011863; United States / NCI NIH HHS / CA / CA78282; United States / NCI NIH HHS / CA / R01 CA078282; United States / NHLBI NIH HHS / HL / HL66109; United States / NHLBI NIH HHS / HL / R01 HL066109; United States / NCI NIH HHS / CA / R01 CA078282-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / MED1 protein, human; 0 / Med1 protein, mouse; 0 / Mediator Complex Subunit 1; 0 / Transcription Factors; 82115-62-6 / Interferon-gamma; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Dapk1 protein, mouse; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ NIHMS137980; NLM/ PMC4010141
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38. de Ostrovich KK, Lambertz I, Colby JK, Tian J, Rundhaug JE, Johnston D, Conti CJ, DiGiovanni J, Fuchs-Young R: Paracrine overexpression of insulin-like growth factor-1 enhances mammary tumorigenesis in vivo. Am J Pathol; 2008 Sep;173(3):824-34
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  • Insulin-like growth factor-1 (IGF-1) stimulates proliferation, regulates tissue development, protects against apoptosis, and promotes the malignant phenotype in the breast and other organs.
  • Some epidemiological studies have linked high circulating levels of IGF-1 with an increased risk of breast cancer.
  • To study the role of IGF-1 in mammary tumorigenesis in vivo, we used transgenic mice in which overexpression of IGF-1 is under the control of the bovine keratin 5 (BK5) promoter and is directed to either the myoepithelial or basal cells in a variety of organs, including the mammary gland.
  • This model closely recapitulates the paracrine exposure of breast epithelium to stromal IGF-1 seen in women.

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  • (PMID = 18688034.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA037111; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA 104114; United States / NCI NIH HHS / CA / R01 CA104114; United States / NIEHS NIH HHS / ES / P30 ES007784; United States / NCI NIH HHS / CA / CA37111; United States / NIEHS NIH HHS / ES / ES07784
  • [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 / Keratin-5; 0 / Keratin-8; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 136601-57-5 / Cyclin D1; 67763-96-6 / Insulin-Like Growth Factor I
  • [Other-IDs] NLM/ PMC2527085
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39. 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
Hazardous Substances Data Bank. TAXOL .

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  • 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.
  • 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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  • (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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40. Tan KP, Kosuge K, Yang M, Ito S: NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity. Free Radic Biol Med; 2008 Dec 15;45(12):1663-73
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • Using in vitro cell and in vivo mouse models, we report that RA, specifically all-trans-RA (atRA) at concentrations implicated in toxicity, can activate NRF2 and induce NRF2 target genes, particularly the subunits of the rate-limiting enzyme of glutathione biosynthesis, glutamate cysteine ligase (GCLM/GCLC).
  • RNA interference-mediated silencing of NRF2, but not of retinoid X receptor-alpha and -beta, reduced basal and atRA-induced GCLM/GCLC gene expression.
  • Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA.
  • [MeSH-minor] Adenocarcinoma / metabolism. Aldehydes / metabolism. Animals. Antioxidants / metabolism. Breast Neoplasms / metabolism. Carcinoma, Hepatocellular / metabolism. Cells, Cultured. Glutamate-Cysteine Ligase / genetics. Glutamate-Cysteine Ligase / metabolism. Humans. Kidney / cytology. Kidney / drug effects. Kidney / metabolism. Lipid Peroxidation. Liver Neoplasms / metabolism. MAP Kinase Kinase 1 / antagonists & inhibitors. MAP Kinase Kinase 1 / metabolism. Male. Mice. Mitochondria / drug effects. Mitochondria / metabolism. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / metabolism. RNA, Small Interfering / pharmacology. Response Elements. Retinoid X Receptor alpha / metabolism. Retinoid X Receptor beta / metabolism

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  • (PMID = 18845239.001).
  • [ISSN] 0891-5849
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / NF-E2-Related Factor 2; 0 / RNA, Small Interfering; 0 / Retinoid X Receptor alpha; 0 / Retinoid X Receptor beta; 29343-52-0 / 4-hydroxy-2-nonenal; 5688UTC01R / Tretinoin; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 6.3.2.2 / Glutamate-Cysteine Ligase
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41. Mood NI, Eftekhar Z, Haratian A, Saeedi L, Rahimi-Moghaddam P, Yarandi F: A cytohistologic study of atypical glandular cells detected in cervical smears during cervical screening tests in Iran. Int J Gynecol Cancer; 2006 Jan-Feb;16(1):257-61
International Agency for Research on Cancer - Screening Group. diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas .

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  • Among them were cervical intraepithelial neoplasia, basal cell abnormality of undetermined significance, cervical adenocarcinoma, endometrial hyperplasia or adenocarcinoma, vaginal adenocarcinoma, endocervical glandular dysplasia, metastatic breast carcinoma, and simple nonvillous trophoblastic tissue.
  • The results of the current study underline the importance of follow-up for patients with the diagnosis of AGC.
  • To our knowledge, this is the first report in Iran showing the significance of AGC diagnosis.

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  • (PMID = 16445641.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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42. Carvalho J, Fullen D, Lowe L, Su L, Ma L: The expression of CD23 in cutaneous non-lymphoid neoplasms. J Cutan Pathol; 2007 Sep;34(9):693-8
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  • CD23 staining was seen in 42% (8/19) of microcystic adnexal carcinoma (MAC), while no staining was observed in tumor cells of desmoplastic trichoepithelioma, morpheaform basal cell carcinoma and syringoma.
  • In addition, CD23 reacted diffusely with cutaneous mucinous eccrine carcinoma in a manner similar to breast or colonic adenocarcinoma.

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  • (PMID = 17696916.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, IgE
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43. Escaff S, Fernández JM, González LO, Suárez A, González-Reyes S, González JM, Vizoso FJ: Study of matrix metalloproteinases and their inhibitors in prostate cancer. Br J Cancer; 2010 Mar 2;102(5):922-9
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Extracellular matrix metalloproteases (MMPs) have raised an extraordinary interest in cancer research because of their potential role in basal membrane and extracellular matrix degradation, consequently facilitating tumour invasion and metastases development.
  • [MeSH-major] Adenocarcinoma / metabolism. Matrix Metalloproteinases / metabolism. Prostatic Hyperplasia / metabolism. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Neoplasms / metabolism. Tissue Inhibitor of Metalloproteinases / metabolism

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  • (PMID = 20160732.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ PMC2833257
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44. Mrena J, Wiksten JP, Nordling S, Kokkola A, Ristimäki A, Haglund C: MMP-2 but not MMP-9 associated with COX-2 and survival in gastric cancer. J Clin Pathol; 2006 Jun;59(6):618-23
MedlinePlus Health Information. consumer health - Stomach Cancer.

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  • BACKGROUND AND AIM: Matrix metalloproteinases (MMPs) MMP-2 and MMP-9 can degrade type IV collagen of extracellular matrix and basal membranes.
  • [MeSH-major] Adenocarcinoma / enzymology. Biomarkers, Tumor / metabolism. Cyclooxygenase 2 / metabolism. Matrix Metalloproteinase 2 / metabolism. Stomach Neoplasms / enzymology

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  • (PMID = 16731602.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC1860392
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45. Lanoy E, Costagliola D, Engels EA: Skin cancers associated with HIV infection and solid-organ transplantation among elderly adults. Int J Cancer; 2010 Apr 1;126(7):1724-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The study comprised 29,926 skin cancer cases (excluding basal cell and squamous cell carcinomas) and 119,704 controls, frequency-matched by gender, age and calendar year (1987-2002).
  • Medicare claims identified solid-organ transplantation or HIV infection before cancer diagnosis/control selection.
  • As negative controls, we evaluated other medical conditions (e.g., hypertension and depression) and cancers (breast, colon and prostate) not linked to immunosuppression.
  • Solid-organ transplantation was also associated with increased risks of Merkel cell carcinoma (N = 1,286; OR [95%CI] 4.95 [2.62-9.34]) and other cutaneous sarcomas (N = 972; 4.19 [1.83-9.56]).
  • [MeSH-major] Adenocarcinoma / etiology. HIV Infections / complications. HIV Infections / therapy. HIV-1 / pathogenicity. Organ Transplantation / adverse effects. Skin Neoplasms / etiology


46. Puebla-Mora AG, Heras A, Cano-Valdez AM, Domínguez-Malagón H: Human telomerase and alpha-methylacyl-coenzyme A racemase in prostatic carcinoma. A comparative immunohistochemical study. Ann Diagn Pathol; 2006 Aug;10(4):205-8
MedlinePlus Health Information. consumer health - Prostate Cancer.

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  • Human telomerase detected by in situ hybridization has been demonstrated to be a useful tool for the diagnosis of malignancy and has also been tested by reverse transcriptase-polymerase chain reaction in several tumors such as hepatic cell carcinoma, melanoma, colonic carcinoma, gastric carcinoma, biliary carcinoma, breast carcinoma, mesothelioma, lung carcinoma, female tract carcinoma, and prostatic carcinoma.
  • Carcinomas of cervix, endometrium, and breast have been studied by this method, but its value in prostatic carcinoma has not been explored; for that reason, we studied benign and malignant prostatic lesions by immunohistochemistry using paraffin embedded tissue.
  • Fifty-five specimens of diverse prostatic lesions were selected for study (43 needle biopsies and 12 transurethral resections); there were 61 malignancies (47 infiltrating carcinomas and 14 high-grade prostatic intraepithelial neoplasias [PIN]) and 29 benign lesions (10 basal cell hyperplasias, 12 nodular hyperplasias, 4 chronic prostatitis, and 3 atrophic glands).
  • [MeSH-major] Adenocarcinoma / enzymology. DNA-Binding Proteins / metabolism. Immunoenzyme Techniques / methods. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Neoplasms / enzymology. Racemases and Epimerases / metabolism. Telomerase / metabolism

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  • (PMID = 16844561.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; EC 2.7.7.49 / Telomerase; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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47. Vesely DL: Cardiac and renal hormones: anticancer effects in vitro and in vivo. J Investig Med; 2009 Jan;57(1):22-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Four cardiovascular hormones, ie, vessel dilator, long-acting natriuretic peptide, kaliuretic peptide, and atrial natriuretic peptide each at 1 mmol/L, decrease up to 97% of human breast, ovarian, pancreatic, colon, kidney, and prostate adenocarcinoma cells, as well as small cell and squamous cell lung cancer cells within 24 hours.
  • Similarly, two thirds of human breast cancers in athymic mice can be eliminated without surgery with these cardiac hormones.
  • CONCLUSIONS: The cardiac hormones' anticancer mechanism of action(s) include a strong inhibition of mitogen (epidermal growth factor and insulin) activated extracellular signal-regulated kinases (ERK) 1/2 and as well as inhibition of basal extracellular-signal regulated kinase 1/2 and upstream MEK 1/2 phosphorylation.

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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 19092678.001).
  • [ISSN] 1081-5589
  • [Journal-full-title] Journal of investigative medicine : the official publication of the American Federation for Clinical Research
  • [ISO-abbreviation] J. Investig. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Natriuretic Peptides
  • [Number-of-references] 76
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