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1. Montironi R, Mazzucchelli R, Lopez-Beltran A, Cheng L, Scarpelli M: Mechanisms of disease: high-grade prostatic intraepithelial neoplasia and other proposed preneoplastic lesions in the prostate. Nat Clin Pract Urol; 2007 Jun;4(6):321-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of disease: high-grade prostatic intraepithelial neoplasia and other proposed preneoplastic lesions in the prostate.
  • High-grade prostatic intraepithelial neoplasia (HGPIN) is the most likely precursor of prostatic adenocarcinoma according to virtually all available evidence.
  • This lesion is characterized by cellular proliferations within pre-existing ducts and acini, with nuclear and nucleolar enlargements similar to those seen in prostate cancer, although unlike cancer HGPIN retains a basal-cell layer.
  • The recognition of HGPIN is clinically important because of the strong association between this disease and prostatic carcinoma.
  • The predictive value for cancer of an initial diagnosis of HGPIN on needle biopsy has substantially declined, with values falling from 36% to 21%.
  • Other possible findings in the prostate might indicate premalignant disease (low-grade prostatic intraepithelial neoplasia, atrophy, malignancy-associated changes, and atypical adenomatous hyperplasia or adenosis), but the data for these premalignant diseases are much less convincing than those for HGPIN.
  • [MeSH-major] Precancerous Conditions. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biopsy, Needle. Humans. Male. Predictive Value of Tests

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  • (PMID = 17551536.001).
  • [ISSN] 1743-4289
  • [Journal-full-title] Nature clinical practice. Urology
  • [ISO-abbreviation] Nat Clin Pract Urol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 78
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2. Lal DR, Clark I, Shalkow J, Downey RJ, Shorter NA, Klimstra DS, La Quaglia MP: Primary epithelial lung malignancies in the pediatric population. Pediatr Blood Cancer; 2005 Oct 15;45(5):683-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We reviewed the Memorial Sloan-Kettering Cancer Center experience with these tumors to better understand their histology, time to diagnosis, treatment, and outcome.
  • PROCEDURE: A retrospective review was performed on all patients 21 years of age or younger at diagnosis, treated for primary epithelial lung malignancies at Memorial Sloan-Kettering Cancer Center between 1980 and 2001.
  • The median age at diagnosis was 19 (range: 12-21) years.
  • The most common radiographic abnormality was a mass (55%) on chest imaging.
  • Seven patients (64%) were initially diagnosed as having pneumonia which contributed to a delay in diagnosis.
  • Final pathologic diagnoses included adenocarcinoma (four), carcinoid tumor (three typical, one atypical), basaloid carcinoma (two), and mucoepidermoid carcinoma (one).
  • A majority of patients presented with advanced disease (two stage III, four stage IV).
  • Patients with localized disease were treated with surgical resection and all but one remains disease free with a median follow-up of 60 months (range: 13-286).
  • Patients with either advanced locoregional or distant metastatic disease were treated with multimodal therapy and a majority had rapid progression of disease.
  • CONCLUSIONS: When children and adolescents present with primary epithelial lung malignancy a majority will have advanced disease and experience a delay in diagnosis.
  • Patients with carcinoid tumors seem to have the best prognosis, followed by adenocarcinoma.
  • [MeSH-major] Carcinoma / diagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Adolescent. Adult. Carcinoid Tumor / diagnosis. Carcinoid Tumor / pathology. Carcinoma, Basal Cell / diagnosis. Carcinoma, Basal Cell / pathology. Child. Diagnostic Errors. Female. Humans. Male. Pneumonia / diagnosis

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  • (PMID = 15714450.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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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4. Adley BP, Yang XJ: Alpha-methylacyl coenzyme A racemase immunoreactivity in partial atrophy of the prostate. Am J Clin Pathol; 2006 Dec;126(6):849-55
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  • In addition, 82 (67.2%) showed patchy to negative distribution of basal cells.
  • Compounding this problem, focal lack of basal cells may be seen.
  • However, the AMACR staining pattern of partial atrophy is usually comparable to that of adjacent benign glands and substantially different from adenocarcinoma.
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Adult. Aged. Atrophy / enzymology. Atrophy / pathology. Biomarkers / metabolism. Biopsy, Needle. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology

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  • (PMID = 17074684.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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5. Mukherjee S, Bhattacharya RK, Roy M: Targeting protein kinase C (PKC) and telomerase by phenethyl isothiocyanate (PEITC) sensitizes PC-3 cells towards chemotherapeutic drug-induced apoptosis. J Environ Pathol Toxicol Oncol; 2009;28(4):269-82
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  • [Title] Targeting protein kinase C (PKC) and telomerase by phenethyl isothiocyanate (PEITC) sensitizes PC-3 cells towards chemotherapeutic drug-induced apoptosis.
  • Telomerase, a reverse transcriptase, is highly activated in prostate cancer cells.
  • The present study investigates the effects of natural isothiocyanate phenethyl isothiocyanate (PEITC) in modulating the activities of PKC and telomerase in the androgen-independent human prostate adenocarcinoma (PC-3) cell line.
  • Basal level of PKC delta, a proapoptotic form, was very poor and its modulation was not significant.
  • Studies were conducted to measure the degree of apoptotic cell death induced either by PEITC alone or in combination with adriamycin or etoposide.
  • PEITC exhibited remarkable efficacy in sensitizing PC-3 cells to undergo cell death by adriamycin and etoposide, which might prove to be of considerable value in synergistic therapy of cancer.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Biomarkers, Tumor / metabolism. Caspases / metabolism. Cell Line, Tumor. Cytochromes c / metabolism. Down-Regulation / drug effects. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Etoposide / pharmacology. Humans. Male

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  • (PMID = 20102325.001).
  • [ISSN] 2162-6537
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Isothiocyanates; 6PLQ3CP4P3 / Etoposide; 6U7TFK75KV / phenethyl isothiocyanate; 80168379AG / Doxorubicin; 9007-43-6 / Cytochromes c; EC 2.7.11.13 / Protein Kinase C; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases
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6. Paquette J, Bessette B, Ledru E, Deal C: Identification of upstream stimulatory factor binding sites in the human IGFBP3 promoter and potential implication of adjacent single-nucleotide polymorphisms and responsiveness to insulin. Endocrinology; 2007 Dec;148(12):6007-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Functionality of these SNPs was further explored in hepatic adenocarcinoma-derived SK-HEP-1 cells using transient transfections of luciferase constructs driven by different haplotypes of the IGFBP3 promoter.
  • Basal luciferase activity revealed a significant haplotype-dependent transcriptional activity (at nucleotides -202 and -185, AC > CC, P < 0.001; AC > CT, P < 0.001; AC > AT, P < 0.001).
  • Chromatin immunoprecipitation with anti-USF-1/-2 showed an enrichment of IGFBP3 promoter in insulin-treated cells compared with unstimulated cells.
  • In summary, we report a methylation-dependent USF binding site influencing the basal and insulin-stimulated transcriptional activity of the IGFBP3 promoter.
  • [MeSH-minor] Base Sequence. Binding Sites / genetics. Cell Line, Tumor. Chromatin Immunoprecipitation. DNA Methylation. Electrophoretic Mobility Shift Assay. Haplotypes. Humans. Insulin-Like Growth Factor Binding Protein 3. Luciferases / genetics. Luciferases / metabolism. Molecular Sequence Data. Mutagenesis, Site-Directed. Mutation. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Transcription, Genetic / drug effects

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  • (PMID = 17823260.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IGFBP3 protein, human; 0 / Insulin; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Recombinant Fusion Proteins; 0 / Upstream Stimulatory Factors; EC 1.13.12.- / Luciferases
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7. Sanchis García JM, Dualde Beltrán D, Ramírez Sabio JB, Vera González A, Palmero da Cruz J: [Well-differentiated basal cell adenocarcinoma of the lacrimal sac: a case report]. Radiologia; 2007 May-Jun;49(3):201-4
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  • [Title] [Well-differentiated basal cell adenocarcinoma of the lacrimal sac: a case report].
  • [Transliterated title] Adenocarcinoma de células basales del saco lacrimal bien diferenciado. A propósito de un caso.
  • Basal cell adenocarcinoma is a rare tumor first considered to be a separate entity by the WHO in 1991.
  • We present a case of adenocarcinoma of the lacrimal sac diagnosed at histological study.
  • We discuss the differential diagnosis and treatment for this tumor.
  • [MeSH-major] Adenocarcinoma / diagnosis. Lacrimal Apparatus

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  • (PMID = 17524341.001).
  • [ISSN] 0033-8338
  • [Journal-full-title] Radiología
  • [ISO-abbreviation] Radiologia
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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8. Forest V, Campos L, Péoc'h M, Guyotat D, Vergnon JM: [Development of an experimental model for the study of the effects of cryotherapy on lung tumours]. Pathol Biol (Paris); 2005 May;53(4):199-203
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Adenocarcinomas are today the most frequent lung cancers.
  • MATERIALS AND METHODS: A xenograft system was used: cells from the A549 cell line were injected subcutaneously into SCID mice.
  • The histological study showed that these tumours faithfully reproduced the morphological features of adenocarcinoma, and developed an intratumoral neovascularization.
  • RESULTS: The basal expression of cleaved caspase-3 in untreated tumours (23%) increased after cryotherapy.
  • The increase was maximal eight hours after treatment (up to 47% of positive cells) and was less important with the first protocol, suggesting a lesser efficiency in the induction of apoptosis.
  • [MeSH-major] Adenocarcinoma / therapy. Cryotherapy. Lung Neoplasms / therapy. Neoadjuvant Therapy. Neoplasms, Experimental / therapy
  • [MeSH-minor] Animals. Cell Line, Tumor / transplantation. Humans. Male. Mice. Mice, SCID. Neoplasm Transplantation. Xenograft Model Antitumor Assays

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  • (PMID = 15850952.001).
  • [ISSN] 0369-8114
  • [Journal-full-title] Pathologie-biologie
  • [ISO-abbreviation] Pathol. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] France
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9. Li Y, Wo JM, Su RR, Ray MB, Jones W, Martin RC: Esophageal injury with external esophageal perfusion. J Surg Res; 2005 Nov;129(1):107-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: External esophageal perfusion (EEP) with the idea that esophageal perfusion can be controlled with a single ingredient at a constant rate and concentration, might be used to dissect the injurious role of gastro-duodenal secretions for the progression from esophagitis to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC).
  • Histological changes, cell proliferation, apoptosis, 8-hydroxy-deoxyguanosine (8-OH-dG) and Manganese superoxide dismutase (MnSOD) were observed after perfusion and compared.
  • RESULTS: The bile perfusion for 1 week, 2 weeks, and 4 weeks induced mucosa infiltration of inflammatory cells, basal cell hyperproliferation, and papillae hypertrophy in all animals.
  • Further studies are needed to induce Barrett's esophagus and esophageal adenocarcinoma.
  • [MeSH-minor] Animals. Apoptosis. Cell Division. Deoxyguanosine / analogs & derivatives. Deoxyguanosine / analysis. Gastric Juice / chemistry. Hypertrophy. Immunohistochemistry. In Situ Nick-End Labeling. Mucous Membrane / pathology. Rats. Rats, Sprague-Dawley. Superoxide Dismutase / analysis. Time Factors

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  • (PMID = 15921698.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; EC 1.15.1.1 / Superoxide Dismutase; G9481N71RO / Deoxyguanosine
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10. Quintyn-Ranty ML, Escourrou G, Guilbeau C, Rimailho J, Delisle MB: [Vaginal adenoid cystic carcinoma: a case report]. Ann Pathol; 2008 Apr;28(2):135-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Carcinome adénoïde kystique vaginal: à propos d'un cas.
  • Differential diagnosis includes adenoid basal carcinoma, polymorphous low-grade adenocarcinoma and basaloid squamous cell carcinoma.
  • Histological examination revealed nests of cells with peripheral palisading organisation and glandular lumina containing material produced by the tumor cells.
  • [MeSH-minor] Actins / analysis. Epithelial Cells / pathology. Female. Humans. Middle Aged. Papillomavirus Infections / pathology

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  • (PMID = 18675169.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Actins
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11. Teulière J, Faraldo MM, Deugnier MA, Shtutman M, Ben-Ze'ev A, Thiery JP, Glukhova MA: Targeted activation of beta-catenin signaling in basal mammary epithelial cells affects mammary development and leads to hyperplasia. Development; 2005 Jan;132(2):267-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted activation of beta-catenin signaling in basal mammary epithelial cells affects mammary development and leads to hyperplasia.
  • Wnt/beta-catenin signaling pathway is involved in the maintenance of the progenitor cell population in the skin, intestine and other tissues, and its aberrant activation caused by stabilization of beta-catenin contributes to tumorigenesis.
  • In the mammary gland, constitutive activation of Wnt/beta-catenin signaling in luminal secretory cells results in precocious lobuloalveolar differentiation and induces adenocarcinomas, whereas the impact of this signaling pathway on the function of the second major mammary epithelial cell lineage, the basal myoepithelial cells, has not been analyzed.
  • We have used the keratin (K) 5 promoter to target the expression of stabilized N-terminally truncated beta-catenin to the basal cell layer of mouse mammary epithelium.
  • Nulliparous transgenic females developed mammary hyperplasia that comprised undifferentiated basal (K5/14-positive, K8- and alpha-smooth muscle-actin-negative) cells.
  • Multiparous mice, in addition, developed invasive basal-type carcinomas.
  • Thus, activation of beta-catenin signaling in basal mammary epithelial cells affects the entire process of mammary gland development and induces amplification of basal-type cells that lack lineage markers, presumably, a subpopulation of mammary progenitors able to give rise to tumors.
  • [MeSH-major] Cytoskeletal Proteins / genetics. Cytoskeletal Proteins / metabolism. Epithelial Cells / metabolism. Gene Expression Regulation, Developmental. Mammary Glands, Animal / metabolism. Trans-Activators / genetics. Trans-Activators / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Animals. Blotting, Southern. Blotting, Western. Cell Differentiation. Cell Lineage. Cell Proliferation. DNA Primers / chemistry. Epithelium / pathology. Female. Hyperplasia / metabolism. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, Inbred C57BL. Mice, Transgenic. Microscopy, Fluorescence. Phosphoproteins / genetics. Polymerase Chain Reaction. Promoter Regions, Genetic. Protein Structure, Tertiary. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Time Factors. beta Catenin


12. Epstein JI: An update of the Gleason grading system. J Urol; 2010 Feb;183(2):433-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Since the introduction of the Gleason grading system more than 40 years ago many aspects of prostate cancer have changed, including prostate specific antigen testing, transrectal ultrasound guided prostate needle biopsy with greater sampling, immunohistochemistry for basal cells that changed the classification of prostate cancer and new prostate cancer variants.
  • The grading of variants and subtypes of acinar adenocarcinoma of the prostate, including cancer with vacuoles, foamy gland carcinoma, ductal adenocarcinoma, pseudohyperplastic carcinoma and small cell carcinoma have also been modified.

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  • [Copyright] Copyright 2010 American Urological Association. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20006878.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 43
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13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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


14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Met induces diverse mammary carcinomas in mice and is associated with human basal breast cancer.
  • 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.


15. Donadelli M, Dalla Pozza E, Scupoli MT, Costanzo C, Scarpa A, Palmieri M: Intracellular zinc increase inhibits p53(-/-) pancreatic adenocarcinoma cell growth by ROS/AIF-mediated apoptosis. Biochim Biophys Acta; 2009 Feb;1793(2):273-80
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  • [Title] Intracellular zinc increase inhibits p53(-/-) pancreatic adenocarcinoma cell growth by ROS/AIF-mediated apoptosis.
  • We show that treatment with non-toxic doses of zinc in association to the ionophore compound pyrrolidine dithiocarbamate (PDTC) inhibits p53(-/-) pancreatic cancer cell growth much more efficiently than gemcitabine, the gold standard chemotherapeutic agent for pancreatic cancer.
  • Both the metal chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine and the radical scavenger N-acetyl-l-cysteine are able to recover cell growth inhibition by Zn/PDTC, demonstrating that this effect depends on the increased levels of intracellular zinc and of reactive oxygen species (ROS).
  • Zn/PDTC treatment induces a strong apoptotic cell death that is associated to ROS-dependent nuclear translocation of the mitochondrial factor AIF, but not to the regulation of apoptotic genes and caspase activation.
  • Primary fibroblasts are more resistant than pancreatic cancer cells to Zn/PDTC treatment and exhibit a lower basal and Zn/PDTC-induced enhancement of intracellular zinc.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis. Apoptosis Inducing Factor / metabolism. Pancreatic Neoplasms / pathology. Reactive Oxygen Species / metabolism. Tumor Suppressor Protein p53 / deficiency. Zinc / metabolism
  • [MeSH-minor] Caspases / metabolism. Cell Line, Tumor. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cell Proliferation / drug effects. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Ethylenediamines / pharmacology. Fibroblasts / cytology. Fibroblasts / drug effects. Humans. Intracellular Space / drug effects. Intracellular Space / metabolism. Leupeptins / pharmacology. Mitochondria / drug effects. Mitochondria / enzymology. Models, Biological. Protein Transport / drug effects. Pyrrolidines / pharmacology. Thiocarbamates / pharmacology

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  • (PMID = 18951928.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Inducing Factor; 0 / Ethylenediamines; 0 / Leupeptins; 0 / Pyrrolidines; 0 / Reactive Oxygen Species; 0 / Thiocarbamates; 0 / Tumor Suppressor Protein p53; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 16858-02-9 / N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine; 25769-03-3 / pyrrolidine dithiocarbamic acid; EC 3.4.22.- / Caspases; J41CSQ7QDS / Zinc
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16. González-García R, Nam-Cha SH, Muñoz-Guerra MF, Gamallo-Amat C: Basal cell adenoma of the parotid gland. Case report and review of the literature. Med Oral Patol Oral Cir Bucal; 2006 Mar;11(2):E206-9
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  • [Title] Basal cell adenoma of the parotid gland. Case report and review of the literature.
  • Basal cell adenoma of the salivary glands is an uncommon type of monomorphous adenoma.
  • Histologically, isomorphic cells in nests and interlaced trabecules with a prominent basal membrane are observed.
  • In contrast to pleomorphic adenoma, it tends to be multiple and its recurrence rate after surgical excision is high.
  • Due to prognostic implications, differential diagnosis with basal cell adenocarcinoma, adenoid cystic carcinoma and basaloid squamous cell carcinoma is mandatory.
  • We describe a case of basal cell adenoma of the parotid gland.
  • We also review the literature and discuss the diagnosis and management of this rare entity.
  • [MeSH-major] Adenoma / pathology. Parotid Neoplasms / pathology

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  • (PMID = 16505803.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng; spa
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 21
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17. Fok JY, Mehta K: Tissue transglutaminase induces the release of apoptosis inducing factor and results in apoptotic death of pancreatic cancer cells. Apoptosis; 2007 Aug;12(8):1455-63
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  • [Title] Tissue transglutaminase induces the release of apoptosis inducing factor and results in apoptotic death of pancreatic cancer cells.
  • Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignant disease with poor long-term survival rates.
  • Major reason for poor disease outcome is the profound intrinsic resistance of PDAC cells to currently available treatment regimens.
  • We recently found that a great majority of PDAC tumors and tumor cell lines express high basal level of tissue transglutaminase (TG2), a multifunctional protein implicated in apoptosis, cell attachment, cell survival, and cell motility functions.
  • Based on these observations, we hypothesized that activation of endogenous TG2 can induce spontaneous apoptosis in PDAC cells.
  • The results obtained suggested that activation of endogenous TG2 by calcium ionophore A23187 induced rapid and spontaneous apoptosis in PDAC cells.
  • The release of AIF from mitochondria led to its translocation to the nucleus and subsequent apoptosis of PDAC cells in caspase-independent manner.
  • In conclusion, our results provide first evidence that TG2 can induce apoptosis in PDAC cells in an AIF-dependent and caspase-independent manner.
  • [MeSH-minor] Calcimycin / pharmacology. Calcium Channels / metabolism. Cell Death. Cell Differentiation. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Disease Progression. GTP-Binding Proteins. Gene Expression Regulation, Neoplastic. Humans. Ionophores / pharmacology. Models, Biological. Tumor Cells, Cultured

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  • (PMID = 17440814.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AIFM1 protein, human; 0 / Apoptosis Inducing Factor; 0 / Calcium Channels; 0 / Ionophores; 0W860991D6 / Deoxycytidine; 37H9VM9WZL / Calcimycin; B76N6SBZ8R / gemcitabine; EC 2.3.2.- / transglutaminase 2; EC 2.3.2.13 / Transglutaminases; EC 3.6.1.- / GTP-Binding Proteins
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18. Yazgan S, Gürsoy S, Yaldiz S, Basok O: Outcome of surgery for lung cancer in young and elderly patients. Surg Today; 2005;35(10):823-7
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  • We conducted this study to determine whether the basal characteristics and survival of young patients undergoing surgical resection of lung cancer differ from those of elderly patients.
  • The patients' medical records were reviewed with respect to age, gender, histological diagnosis, coexisting diseases, smoking history, postoperative staging, type of operation, and postoperative morbidity, mortality, and survival results.
  • However, the 5-year survival rates for patients who underwent surgery for non-small cell lung cancer did not differ between groups 1 and 2, at 33.3% versus 21.3%, respectively (P = 0.09).
  • CONCLUSIONS: The incidence of adenocarcinoma was higher in the young patients, whose prognosis was slightly better than that of the elderly patients.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / mortality. Carcinoma, Non-Small-Cell Lung / surgery. Carcinoma, Small Cell / mortality. Carcinoma, Small Cell / surgery. Lung Neoplasms / mortality. Lung Neoplasms / surgery

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  • (PMID = 16175462.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
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19. Pires MM, Emmert D, Hrycyna CA, Chmielewski J: Inhibition of P-glycoprotein-mediated paclitaxel resistance by reversibly linked quinine homodimers. Mol Pharmacol; 2009 Jan;75(1):92-100
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  • The designed agents were potent inhibitors of rhodamine 123 efflux in cultured cancer cell lines that display high levels of P-gp expression at the cell surface and in transfected cells expressing P-gp.
  • Further studies revealed that Q2 inhibited the efflux of a range of fluorescent substrates (rhodamine 123, doxorubicin, mitoxantrone, and BODIPY-FL-prazosin) from MCF-7/DX1 cells.
  • The reversibility of the tether was confirmed in experiments showing that Q2 was readily hydrolyzed by esterases in vitro (t(1/2) approximately 20 h) while demonstrating high resistance to nonenzymatic hydrolysis in cell culture media (t(1/2) approximately 21 days).
  • In addition, low concentrations of Q2 stimulated basal P-gp ATPase levels.
  • Finally, Q2 was shown to inhibit the transport of radiolabeled paclitaxel (Taxol) in MCF-7/DX1 cells, and it completely reversed the P-gp-mediated paclitaxel resistance phenotype.

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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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20. Vasudev P, Boutross-Tadross O, Radhi J: Basaloid squamous cell carcinoma: two case reports. Cases J; 2009;2:9351
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  • [Title] Basaloid squamous cell carcinoma: two case reports.
  • Basaloid squamous cell carcinoma (BSCC) is a rare and aggressive variant of squamous cell carcinoma (SCC) that occurs preferentially in the upper aerodigestive tract.
  • BSCC of the head and neck should be distinguished from adenoid cystic carcinoma, small cell neuroendocrine carcinoma, basal cell adenocarcinoma, adenosquamous carcinoma, squamous cell carcinoma, spindle cell squamous carcinoma, mucoepidermoid carcinoma, and adenoid cystic carcinoma.

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  • (PMID = 20062602.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2804002
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21. Liu YL, Matsuzaki T, Nakazawa T, Murata S, Nakamura N, Kondo T, Iwashina M, Mochizuki K, Yamane T, Takata K, Katoh R: Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues. Hum Pathol; 2007 Jan;38(1):171-8
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  • To investigate the expression of AQP3 in normal and neoplastic lung tissues, we studied a series of 149 lung carcinoma tissues and 2 cell lines by immunohistochemistry, Western blotting, and reverse transcriptase-polymerase chain reaction.
  • In normal lung tissues, immunohistochemical expression of AQP3 was demonstrated in bronchial basal cells, alveolar type II cells, bronchiolar epithelial cells, and secretory cells of submucosal glands.
  • In lung carcinomas, AQP3 expression was observed in 59 (70.2%) of 84 adenocarcinomas.
  • Squamous cell carcinoma and large cell carcinoma had rather low positive ratios (35.8% and 13.4%, respectively).
  • No AQP3 expression was demonstrated in small cell carcinoma, pleomorphic carcinoma, or metastatic colon adenocarcinoma.
  • In adenocarcinomas, AQP3 was detected in all tumors of bronchioloalveolar subtype.
  • Papillary subtype also showed a higher positive ratio of AQP3 compared with that in acinar and solid with mucin subtypes.
  • In addition, AQP3 expression was related to tumor differentiation and clinical stage in adenocarcinomas.
  • Western blotting and reverse transcriptase-polymerase chain reaction analyses confirmed the expression of AQP3 protein and messenger RNA in cell lines and tissues of lung adenocarcinoma.
  • In addition, lung carcinomas, especially adenocarcinomas, can produce AQP3, possibly in connection with their functional and/or biological nature, although the detailed mechanism of AQP3 expression in lung carcinomas remains to be clarified.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Blotting, Western. Cell Line, Tumor. Female. Gene Expression. Humans. Immunohistochemistry. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17056099.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 158801-98-0 / Aquaporin 3
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22. Wei J, Yan W, Li X, Chang WC, Tai HH: Activation of thromboxane receptor alpha induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells. Biochem Pharmacol; 2007 Sep 1;74(5):787-800
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  • [Title] Activation of thromboxane receptor alpha induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells.
  • Human lung adenocarcinoma A549 cells stably transfected with TPalpha (A549-TPalpha) were used to study agonist I-BOP-induced expression of cyclooxygenase-2 (COX-2) and the related mechanisms of induced expression.
  • I-BOP, a TP agonist, induced a time- and dose-dependent expression of COX-2 in A549-TPalpha cells.
  • Distal NF-kappaB site is essential for the basal induction of the COX-2 transcription, whereas CRE and proximal NF-kappaB sites are important for the induced transcription.

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  • (PMID = 17632087.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL046296-11; United States / NHLBI NIH HHS / HL / R01 HL046296-07; United States / NHLBI NIH HHS / HL / R01 HL046296; United States / NHLBI NIH HHS / HL / HL046296-06; United States / NHLBI NIH HHS / HL / HL046296-07; United States / NHLBI NIH HHS / HL / HL-46296; United States / NHLBI NIH HHS / HL / R01 HL046296-09; United States / NHLBI NIH HHS / HL / HL046296-08; United States / NHLBI NIH HHS / HL / R01 HL046296-11; United States / NHLBI NIH HHS / HL / R01 HL046296-08; United States / NHLBI NIH HHS / HL / HL046296-09; United States / NHLBI NIH HHS / HL / R01 HL046296-10; United States / NHLBI NIH HHS / HL / HL046296-10; United States / NHLBI NIH HHS / HL / R01 HL046296-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bicyclo Compounds, Heterocyclic; 0 / Fatty Acids, Unsaturated; 0 / Protein Isoforms; 0 / Receptors, Thromboxane; 0 / Receptors, Thromboxane A2, Prostaglandin H2; 124924-85-2 / 7-(3-(3-hydroxy-4-(4'-iodophenoxy)-1-butenyl)-7-oxabicyclo(2.2.1)heptan-2-yl)-5-heptenoic acid; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ NIHMS28713; NLM/ PMC1995664
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23. Uphoff J, Woziwodzki J, Schattka SO, Kollias A: [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis]. Aktuelle Urol; 2008 Sep;39(5):373-7
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  • [Title] [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis].
  • Metastases in the penis only occur at an advanced state of the tumour and with a high dedifferentiation, e. g., ductal adenocarcinoma.
  • Changes in the morphology of the prostate carcinoma are specially known for the occurrence of small-cell neuroendocrine and undifferentiated carcinomas.
  • At this state of the disease, there is only the possibility of a palliative therapy with a poor prognosis.
  • [MeSH-major] Adenocarcinoma / secondary. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Basal Cell / secondary. Carcinoma, Transitional Cell / secondary. Cell Transformation, Neoplastic / pathology. Diphosphonates / therapeutic use. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Neoplasms, Multiple Primary / drug therapy. Penile Neoplasms / secondary. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy. Bone Neoplasms / drug therapy. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Bone Neoplasms / surgery. Combined Modality Therapy. Cystectomy. Diagnosis, Differential. Disease Progression. Humans. Lymphatic Metastasis. Male. Neoplasm Staging. Penis / pathology. Penis / surgery. Prostate / pathology. Prostate / surgery. Prostatectomy

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  • (PMID = 18798127.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Diphosphonates; 33515-09-2 / Gonadotropin-Releasing Hormone
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24. Peng Y, Jiang Y, Chuang ST, Yang XJ: Computer-aided detection of prostate cancer on tissue sections. Appl Immunohistochem Mol Morphol; 2009 Oct;17(5):442-50
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  • The first set of images consisted of 20 training images (10 malignant) used for developing the computer technique and 15 test images (7 malignant) used for testing and optimizing the technique.
  • The second set of images consisted of 299 images (114 malignant) used for evaluation of the performance of the computer technique.
  • The computer technique identified image segments of alpha-methylacyl-CoA racemase-labeled malignant epithelial cells (red), p63, and high-molecular-weight cytokeratin-labeled benign basal cells (brown), and secretory and stromal cells (blue) for identifying prostate cancer automatically.
  • If high-grade prostatic intraepithelial neoplasia, which is a precursor of cancer, and atypical cases were included, the sensitivity and specificity were 85% (97/114) and 89% (165/185), respectively.
  • These results show that the novel automated computer technique can accurately identify prostatic adenocarcinoma in the triple-antibody cocktail-stained prostate sections.

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  • (PMID = 19417626.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R21 EB006466; United States / NCI NIH HHS / CA / R21 CA97308; United States / NCI NIH HHS / CA / R21 CA097308-01; United States / NCI NIH HHS / CA / CA097308-02; United States / NCI NIH HHS / CA / R01 CA092361; United States / NCI NIH HHS / CA / CA097308-01; United States / NIBIB NIH HHS / EB / EB006466-02; United States / NIBIB NIH HHS / EB / EB006466-01A1; United States / NIBIB NIH HHS / EB / R21 EB006466-01A1; United States / NIBIB NIH HHS / EB / R21 EB006466-02; United States / NCI NIH HHS / CA / R21 CA097308; United States / NCI NIH HHS / CA / R21 CA097308-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS100571; NLM/ PMC2836393
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25. Koshimizu TA, Fujiwara Y, Sakai N, Shibata K, Tsuchiya H: Oxytocin stimulates expression of a noncoding RNA tumor marker in a human neuroblastoma cell line. Life Sci; 2010 Mar 13;86(11-12):455-60
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  • [Title] Oxytocin stimulates expression of a noncoding RNA tumor marker in a human neuroblastoma cell line.
  • AIMS: A noncoding RNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), is upregulated in several malignant tumors.
  • The aim of this study is to clarify how MALAT1 gene expression is altered by extracellular signals in the SK-N-SH neuroblastoma cell line and to define its proximal promoter in order to study the mechanism of MALAT1 gene expression.
  • Although the expression of immediate early genes returned to basal levels after 3h, MALAT1 transcript levels peaked 6-24h after stimulation.
  • SIGNIFICANCE: The expression of the tumor marker MALAT1 ncRNA is sensitive to cell surface receptor activation by oxytocin in a neuroblastoma cell line.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Oxytocin / pharmacology. RNA, Neoplasm / biosynthesis
  • [MeSH-minor] Brain Neoplasms / metabolism. Calcium / metabolism. Cell Line, Tumor. Cyclic AMP Response Element-Binding Protein / biosynthesis. Cyclic AMP Response Element-Binding Protein / genetics. Humans. Informatics. Neuroblastoma / metabolism. Oligonucleotide Array Sequence Analysis. Receptors, Oxytocin / agonists. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20149803.001).
  • [ISSN] 1879-0631
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclic AMP Response Element-Binding Protein; 0 / RNA, Neoplasm; 0 / Receptors, Oxytocin; 50-56-6 / Oxytocin; SY7Q814VUP / Calcium
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26. Colucci R, Blandizzi C, Ghisu N, Florio T, Del Tacca M: Somatostatin inhibits colon cancer cell growth through cyclooxygenase-2 downregulation. Br J Pharmacol; 2008 Sep;155(2):198-209
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  • [Title] Somatostatin inhibits colon cancer cell growth through cyclooxygenase-2 downregulation.
  • BACKGROUND AND PURPOSE: Cyclooxygenase-2 (COX-2) is expressed in colonic neoplasms, where it supports cell proliferation via prostaglandin E(2) (PGE(2)) production.
  • This study investigated the effects of somatostatin-14 on COX-2 expression, PGE(2) production and proliferation in colon cancer cells.
  • EXPERIMENTAL APPROACH: Human colon adenocarcinoma cell lines Caco-2, HT-29 and HCT116 were used.
  • The following techniques were employed: colourimetric assay for cell growth; 5-bromo-2'-deoxyuridine assay for DNA synthesis; enzyme immunoassay for PGE(2); COX-2 mRNA silencing; RT-PCR or Western blot for somatostatin receptor subtypes, cyclooxygenase isoforms, phosphorylated-ERK-1/ERK-2 and phosphorylated-Akt.
  • KEY RESULTS: HT-29 and Caco-2 cells expressed COX-2 and somatostatin receptors (sst(3/4/5) and sst(3/5), respectively).
  • HCT116 cells did express somatostatin receptors (sst(2/3/5)), but not COX-2.
  • Somatostatin-14 inhibited basal COX-2 expression, PGE(2) production, DNA synthesis and growth in Caco-2 cells and these effects were prevented by BN81658 (sst(3) receptor antagonist).
  • Basal proliferation of HT-29, HCT116 and COX-2-silenced Caco-2 cells was not affected by somatostatin-14.
  • Stimulation of HT-29 cells with gastrin-17 elicited increments of ERK-1/ERK-2 and Akt phosphorylation, COX-2 expression, PGE(2) production, DNA synthesis and cell growth, which were all counteracted by somatostatin-14.
  • CONCLUSIONS AND IMPLICATIONS: Somatostatin decreases COX-2 expression and function in colon cancer cells via activation of sst(3) or sst(5) receptors, and these effects contribute to the inhibitory action of somatostatin on cell proliferation.
  • [MeSH-major] Cell Proliferation / drug effects. Colonic Neoplasms / pathology. Cyclooxygenase 2 / metabolism. Cyclooxygenase 2 Inhibitors / pharmacology. Somatostatin / pharmacology
  • [MeSH-minor] Caco-2 Cells. Colon / pathology. Down-Regulation / drug effects. Down-Regulation / physiology. Gastrins / metabolism. HT29 Cells. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Oligopeptides / metabolism. Protein Kinase C / metabolism. Protein Tyrosine Phosphatases / metabolism

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  • (PMID = 18587421.001).
  • [ISSN] 0007-1188
  • [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 / BIM 23056; 0 / Cyclooxygenase 2 Inhibitors; 0 / Gastrins; 0 / Oligopeptides; 51110-01-1 / Somatostatin; 60748-06-3 / gastrin 17; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Other-IDs] NLM/ PMC2538699
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27. Seethala RR, Pasha TL, Raghunath PN, Livolsi VA, Zhang PJ: The selective expression of CD43 in adenoid cystic carcinoma. Appl Immunohistochem Mol Morphol; 2008 Mar;16(2):165-72
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  • CD43, a sialoglycoprotein expressed on hematopoietic cells, has only rarely been reported in nonhematopoietic tumors, mostly of colon.
  • CD43 immunoreactivity with 2 different antibodies was detected mainly in ACC but also 1 membranous type basal cell adenocarcinoma and 1 colonic adenocarcinoma.

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  • (PMID = 18227725.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD43; 0 / RNA, Messenger; 0 / UN1 sialoglycoprotein, human
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28. Devaney KO, Boschman CR, Willard SC, Ferlito A, Rinaldo A: Tumours of the external ear and temporal bone. Lancet Oncol; 2005 Jun;6(6):411-20
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  • The external ear can be the site of development of squamous carcinomas and basal-cell carcinomas; the middle ear and inner ear can host metastatic deposits, and primary squamous carcinomas and adenocarcinomas.
  • Most auricular malignant diseases occur in adulthood; only the rhabdomyosarcomas of the middle ear arise in children.
  • Most malignant diseases of the auricular apparatus are treated by a combination of surgery (commonly including radical excision of temporal bone), radiotherapy, and chemotherapy.
  • [MeSH-major] Ear Neoplasms / diagnosis. Ear Neoplasms / therapy. Ear, External. Skull Neoplasms / diagnosis. Skull Neoplasms / therapy. Temporal Bone

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  • (PMID = 15925819.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 76
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29. Osunkoya AO, Hansel DE, Sun X, Netto GJ, Epstein JI: Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases. Am J Surg Pathol; 2008 Mar;32(3):461-7
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  • [Title] Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases.
  • Aberrant diffuse expression of p63 in prostate carcinoma cells is a rare and poorly understood phenomenon.
  • The presence of p63 positive atypical glands with an infiltrative pattern and perineural invasion on radical prostatectomy confirmed the needle biopsy diagnosis of carcinoma.
  • Rarely, prostate cancer can aberrantly express diffuse p63 staining in a nonbasal cell distribution leading to the erroneous diagnosis of atrophy or atypical basal cell proliferation.
  • The diagnosis of prostate cancer is based on the morphology and confirmed by the absence of high molecular weight cytokeratin staining and positivity for alpha-methylacyl-CoA racemase in the atypical glands.
  • Pathologists need to be aware of this rare and unusual phenomenon, which is a potential pitfall in prostate cancer diagnosis.
  • [MeSH-major] Adenocarcinoma / chemistry. Biopsy, Needle. Membrane Proteins / analysis. Prostatectomy. Prostatic Neoplasms / chemistry

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  • (PMID = 18300803.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / Membrane Proteins
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30. Kurvinen K, Rantanen V, Syrjänen S, Johansson B: Radiation-induced effects on telomerase in gynecological cancer cell lines with different radiosensitivity and repair capacity. Int J Radiat Biol; 2006 Dec;82(12):859-67
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  • [Title] Radiation-induced effects on telomerase in gynecological cancer cell lines with different radiosensitivity and repair capacity.
  • PURPOSE: Telomerase activation in response to irradiation might enhance the radioresistance of cells.
  • Thus, we have investigated radiation-induced effects on telomerase in six gynecological cancer cell lines, with different intrinsic radiosensitivity and capacity for sublethal damage repair (SLDR).
  • MATERIALS AND METHODS: Three endometrial adenocarcinoma (UM-EC-1, UT-EC-2B and UT-EC-3) and three vulvar squamous cell carcinoma (A431, UM-SCV-2 and UM-SCV-7) cell lines were irradiated with doses of 5, 10 and 25 Gy and the effects on telomerase were evaluated at 0.5, 6, 24 and 48 h post-irradiation.
  • RESULTS: The most radioresistant cell line A431 had the strongest stimulatory effects (approximately 2.0 - 2.5-fold) on telomerase activity 24 and 48 h post-irradiation with the highest radiation doses.
  • In contrast to that, telomerase activities in the highly radiosensitive cell line UT-EC-2B remained below the basal level throughout the 48-h period of post-irradiation with the highest doses, and even a decline to approximately 50% of the basal level was found 24 h after exposure.
  • In other cell lines being either moderately or highly radiation resistant, telomerase activity levels in response to irradiation remained mainly at the basal level or gradually increased.
  • However, no correlation was found between the radiation-induced effects on telomerase and the sublethal damage repair capacity of the cells.
  • [MeSH-major] DNA Repair. DNA, Neoplasm / radiation effects. Genital Neoplasms, Female / enzymology. Genital Neoplasms, Female / genetics. Radiation Tolerance. Telomerase / metabolism. Telomerase / radiation effects
  • [MeSH-minor] Cell Line, Tumor. DNA Damage. Dose-Response Relationship, Radiation. Enzyme Activation / radiation effects. Female. Humans. Radiation Dosage

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  • (PMID = 17178626.001).
  • [ISSN] 0955-3002
  • [Journal-full-title] International journal of radiation biology
  • [ISO-abbreviation] Int. J. Radiat. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.7.49 / Telomerase
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31. Final report on the safety assessment of capsicum annuum extract, capsicum annuum fruit extract, capsicum annuum resin, capsicum annuum fruit powder, capsicum frutescens fruit, capsicum frutescens fruit extract, capsicum frutescens resin, and capsaicin. Int J Toxicol; 2007;26 Suppl 1:3-106
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  • Weanling rats fed basal diets supplemented with whole red pepper at concentrations up to 5.0% for up to 8 weeks had no pathology of the large intestines, livers, and kidneys, but destruction of the taste buds and keratinization and erosion of the gastrointestinal (GI) tract were noted in groups fed 0.5% to 5.0% red pepper.
  • A rabbit skin irritation test of Capsicum Annuum Fruit Extract at concentrations ranging from 0.1% to 1.0% produced no irritation, but Capsicum Frutescens Fruit Extract induced concentration-dependent (at 25 to 500 microg/ml) cytotoxicity in a human buccal mucosa fibroblast cell line.
  • Adenocarcinoma of the abdomen was observed in 7/20 mice fed 100 mg red chilies per day for 12 months; no tumors were seen in control animals.
  • Other feeding studies evaluated the effect of red chili peppers on the incidence of stomach tumors produced by N-methyl-N'-nitro-N-nitrosoguanidine, finding that red pepper had a promoting effect.
  • Capsaicin inhibits protein synthesis in Vero kidney cells and human neuroblastoma SHSY-5Y cells in vitro, and inhibits growth of E. coli, Pseudomonas solanacearum, and Bacillus subtilis bacterial cultures, but not Saccharomyces cerevisiae.

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  • (PMID = 17365137.001).
  • [ISSN] 1091-5818
  • [Journal-full-title] International journal of toxicology
  • [ISO-abbreviation] Int. J. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cosmetics; 0 / Plant Extracts; 0 / Resins, Plant; S07O44R1ZM / Capsaicin
  • [Number-of-references] 462
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32. Trauzold A, Röder C, Sipos B, Karsten K, Arlt A, Jiang P, Martin-Subero JI, Siegmund D, Müerköster S, Pagerols-Raluy L, Siebert R, Wajant H, Kalthoff H: CD95 and TRAF2 promote invasiveness of pancreatic cancer cells. FASEB J; 2005 Apr;19(6):620-2
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  • [Title] CD95 and TRAF2 promote invasiveness of pancreatic cancer cells.
  • Pancreatic adenocarcinoma represents a tumor type with extremely poor prognosis.
  • High apoptosis resistance and a strong invasive and early metastatic potential contribute to its highly malignant phenotype.
  • Using immunohistochemistry and Western blot analysis we found TRAF2 overexpressed in 34 of 36 pancreatic tumor samples as well as in pancreatic tumor cell lines resistant to CD95-mediated apoptosis.
  • Introduction of a TRAF2 expression vector in CD95-sensitive Colo357 cells resulted in (i) resistance to CD95-induced apoptosis;.
  • (ii) increased constitutive NF-kappaB and AP-1 activity; and (iii) higher basal secretion of matrix metalloproteinases (MMPs), urokinase-type plasminogen activator (uPA), and IL-8, leading to increased invasiveness.
  • Stimulation of TRAF2-overexpressing cells with CD95 ligand led to induction of NF-kappaB and AP-1, enhanced IL-8- and uPA-secretion, and a further increased invasiveness.
  • [MeSH-major] Adenocarcinoma / pathology. Antigens, CD95 / physiology. Neoplasm Invasiveness. Pancreatic Neoplasms / pathology. TNF Receptor-Associated Factor 2 / physiology
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Electrophoretic Mobility Shift Assay. Gene Expression. Humans. In Situ Hybridization, Fluorescence. Interleukin-8 / analysis. Mitogen-Activated Protein Kinase Kinases / metabolism. NF-kappa B / physiology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transfection. Urokinase-Type Plasminogen Activator / analysis

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  • (PMID = 15670977.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Interleukin-8; 0 / NF-kappa B; 0 / TNF Receptor-Associated Factor 2; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
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33. Trivunić S, Budakov P, Vucković N, Zivojinov M: [Morphological parameters of prostatic adenocarcinoma]. Med Pregl; 2007 Nov-Dec;60(11-12):549-52
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  • [Title] [Morphological parameters of prostatic adenocarcinoma].
  • The following histologic changes are associated with prostatic carcinomas. prostatic acini are close to one another and present with linear infiltrates in the fibromuscular tissue; cells lining the acini often consist of a single layer, and the basal cell layer is absent; prominent large eosinophilic nucleoli are usually present in malignant cells; nuclear hyperchromatism is rare and it depends on the quality of the tissue fixation; perineural invasion is often observed.
  • Immunohistochemistry is widely used in pathology and clinical diagnosis of prostatic carcinoma, metastases of prostatic origin in staging malignant tumors and in the prognosis.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 18666594.001).
  • [ISSN] 0025-8105
  • [Journal-full-title] Medicinski pregled
  • [ISO-abbreviation] Med. Pregl.
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
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34. Bozdogan O, Atasoy P, Bozdogan N, Erekul S, Batislam E, Yilmaz E, Başar MM: BAG-1 expression in hyperplastic and neoplastic prostate tissue: is there any relationship with BCL-related proteins and androgen receptor status? Tumori; 2005 Nov-Dec;91(6):539-45
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  • METHODS: Twenty-eight prostatic adenocarcinomas and 16 prostate hyperplasias were included in this retrospective study.
  • The M30 antibody was used to identify preapoptotic and apoptotic cells.
  • BAG-1 showed the same specific basal cell localization as BCL-2 in hyperplastic and normal glands.
  • BAG-1 in association with BCL-2 inhibits apoptosis and may prolong the life of neoplastic cells and give them a chance to gain new oncogenic features in early carcinogenesis.
  • [MeSH-major] Adenocarcinoma / chemistry. Biomarkers, Tumor / analysis. DNA-Binding Proteins / analysis. Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / chemistry. Receptors, Androgen / analysis. Transcription Factors / analysis


35. Zheng HC, Saito H, Masuda S, Wang ZG, Takano Y: Cytoplasmic and nuclear maspin expression in lung carcinomas: an immunohistochemical study using tissue microarrays. Appl Immunohistochem Mol Morphol; 2008 Oct;16(5):459-65
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  • Here, maspin expression was examined on tissue microarrays containing lung carcinoma (n=155) and adjacent noncancerous tissue (n=20) and also 4 lung carcinoma cell lines (LC-1/Sq, LC-IF, PC-14, and AoI) by immunohistochemistry.
  • Maspin expression showed positive nuclear staining in basal cells, LC-IF, and PC-14 cell lines, and also cytoplasmic immunoreactivity in secretory and ciliated cells, LC-1/Sq cell line.
  • Cytoplasmic staining was the lowest in adenocarcinoma (AD) and the highest in squamous cell carcinoma as compared with other types of lung carcinoma (P<0.05), and positively correlated with expression of p53 and caspase-3 (P<0.05).
  • The nuclear maspin expression gradually increased through squamous cell carcinoma, AD, large cell carcinoma to small cell carcinoma (P<0.05) and was also positively associated with the levels of vascular epithelial growth factor and extracellular matrix metalloproteinase inducer expression (P<0.05).
  • Kaplan-Meier analysis indicated that the cytoplasmic or nuclear maspin expression was not a good prognostic marker for lung carcinomas overall (P>0.05), but the cytoplasmic pattern pointed to good survival for AD cases (P<0.05).
  • The cytoplasmic maspin may play an important role in lung carcinomas by regulating apoptosis and thus is a favorable prognostic marker for AD patients, whereas the nuclear location may be linked to promotion of angiogenesis.

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  • (PMID = 18665036.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / SERPIN-B5; 0 / Serpins
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36. Wietfeldt ED, Thiele J: Malignancies of the anal margin and perianal skin. Clin Colon Rectal Surg; 2009 May;22(2):127-35
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  • Commonly included in this group of cancers are Bowen's disease (intraepithelial squamous cell cancer), perianal Paget's disease (intraepithelial adenocarcinoma), invasive squamous cell cancer, basal cell cancer, and malignant melanoma.
  • Proper diagnosis requires a high index of suspicion on the part of the surgeon.
  • Innocent local irritations will resolve in a short time with appropriate therapy; those that persist must be biopsied for tissue diagnosis.
  • All have met with a fair amount of success in controlling local disease; however, the number of patients treated in each instance is small, making it difficult to design an evidence-based treatment strategy.
  • Invasion and metastasis are relatively rare in this group of neoplasms; perianal Paget's disease has the highest risk of associated underlying neoplasm.

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  • (PMID = 20436838.001).
  • [ISSN] 1530-9681
  • [Journal-full-title] Clinics in colon and rectal surgery
  • [ISO-abbreviation] Clin Colon Rectal Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2780245
  • [Keywords] NOTNLM ; Anal margin cancer / diagnosis / local excision / radiation therapy / treatment options
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37. Pornpanich K, Chindasub P: Eyelid tumors in Siriraj Hospital from 2000-2004. J Med Assoc Thai; 2005 Nov;88 Suppl 9:S11-4
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  • RESULTS: There were 53 (17.8%) inflammatory conditions, 212 (71.4%) benign eyelid tumors and 32 (10.8%) malignant eyelid tumors.
  • These 32 malignant eyelid tumors included 13 sebaceous gland carcinomas, 12 basal cell carcinomas, 3 malignant melanomas, 2 squamous cell carcinomas, 1 apocrine adenocarcinoma and 1 metastatic carcinoma.
  • CONCLUSION: The majority of eyelid lesions were benign eyelid tumors while malignant eyelid tumors contributed 10.8% of the total eyelid lesions.
  • [MeSH-major] Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Eyelid Neoplasms / epidemiology. Sebaceous Gland Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Biopsy, Needle. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Incidence. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Risk Assessment. Sex Distribution. Thailand / epidemiology

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  • (PMID = 16681045.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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38. Yu N, Kozlowski JM, Park II, Chen L, Zhang Q, Xu D, Doll JA, Crawford SE, Brendler CB, Lee C: Overexpression of transforming growth factor β1 in malignant prostate cells is partly caused by a runaway of TGF-β1 auto-induction mediated through a defective recruitment of protein phosphatase 2A by TGF-β type I receptor. Urology; 2010 Dec;76(6):1519.e8-13
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  • [Title] Overexpression of transforming growth factor β1 in malignant prostate cells is partly caused by a runaway of TGF-β1 auto-induction mediated through a defective recruitment of protein phosphatase 2A by TGF-β type I receptor.
  • OBJECTIVES: To elucidate the mechanism of transforming growth factor (TGF)-β1 overexpression in prostate cancer cells.
  • METHODS: Malignant (PC3, DU145) and benign (RWPE1, BPH1) prostate epithelial cells were used.
  • Blockade of TGF-β1 signaling in cells was accomplished either by using TGF-β-neutralizing monoclonal antibody or by transduction of a dominant negative TGF-β type II receptor retroviral vector.
  • RESULTS: Basal levels of TGF-β1 in malignant cells were significantly higher than those in benign cells.
  • Blockade of TGF-β signaling resulted in a significant decrease in TGF-β1 expression in malignant cells, but not in benign cells.
  • Upon TGF-β1 treatment (10 ng/mL), TGF-β1 expression was increased in malignant cells, but not in benign cells.
  • This differential TGF-β1 auto-induction between benign and malignant cells correlated with differential activation of extracellular signal-regulated kinase (ERK).
  • Following TGF-β1 treatment, the activity of serine/threonine phosphatase and recruitment of PP2A-Bα by TβRI increased in benign cells, but not in malignant cells.
  • Inhibition of PP2A in benign cells resulted in an increase in ERK activation and in TGF-β1 auto-induction after TGF-β1 (10 ng/mL) treatment.
  • CONCLUSIONS: These results suggest that TGF-β1 overexpression in malignant cells is caused, at least in part, by a runaway of TGF-β1 auto-induction through ERK activation because of a defective recruitment of PP2A-Bα by TβRI.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 21030067.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090386-06A2; United States / NCI NIH HHS / CA / P50 CA090386; United States / NCI NIH HHS / CA / P50 CA090386-06A2; United States / NCI NIH HHS / CA / P50CA90386
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / PPP2R2A protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.1.3.16 / Protein Phosphatase 2
  • [Other-IDs] NLM/ NIHMS194313; NLM/ PMC2997920
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39. Adamski H, Le Lan J, Chevrier S, Cribier B, Watier E, Chevrant-Breton J: Primary cutaneous cribriform carcinoma: a rare apocrine tumour. J Cutan Pathol; 2005 Sep;32(8):577-80
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  • This neoplasm is often located on the limbs.
  • The histopathological diagnosis is difficult, mainly because this tumour is exceptional.
  • The aggregations of neoplastic cells were interconnected and varied in size and shape.
  • The cells were arranged in solid nests or tubular structures.
  • In the lumina of tubules, some papillary protrusion of basophilic cells was seen.
  • The ductal elements were lined by cuboidal or cylindric cells with images of decapitation secretion.
  • The nuclei of the neoplastic cells were pleomorphic.
  • Differential diagnoses, including cutaneous metastasis of adenocarcinoma, adenoid basal cell carcinoma and adenoid cystic carcinoma, are discussed.
  • [MeSH-major] Adenocarcinoma / pathology. Apocrine Glands / pathology. Sweat Gland Neoplasms / pathology
  • [MeSH-minor] Adult. Carcinoma, Adenoid Cystic / diagnosis. Carcinoma, Basal Cell / diagnosis. Diagnosis, Differential. Humans. Male. Treatment Outcome

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  • (PMID = 16115058.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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40. Scholz N, Krugmann J, Scholtz A, Höllrigl A, Verdorfer I: Genetic alterations in a basal cell adenocarcinoma of the glandula submandibularis. Cancer Genet Cytogenet; 2007 Jan 1;172(1):87-9
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  • [Title] Genetic alterations in a basal cell adenocarcinoma of the glandula submandibularis.
  • [MeSH-major] Adenocarcinoma / genetics. Submandibular Gland Neoplasms / genetics

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  • (PMID = 17175388.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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41. Trevino JG, Gray MJ, Nawrocki ST, Summy JM, Lesslie DP, Evans DB, Sawyer TK, Shakespeare WC, Watowich SS, Chiao PJ, McConkey DJ, Gallick GE: Src activation of Stat3 is an independent requirement from NF-kappaB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells. Angiogenesis; 2006;9(2):101-10
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  • [Title] Src activation of Stat3 is an independent requirement from NF-kappaB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells.
  • Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-kappaB, a frequent occurrence in pancreatic adenocarcinoma.
  • Pharmacologic inhibition of NF-kappaB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-kappaB activity was not dependent on Src.
  • We therefore suggest that Src activation, through phosphorylation of STAT3, and NF-kappaB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Interleukin-8 / metabolism. NF-kappa B / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins pp60(c-src) / metabolism. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Cell Line, Tumor. Genes, Reporter. Humans. Immunohistochemistry. Luciferases / metabolism. Microscopy, Confocal. Phosphorylation. RNA, Small Interfering / metabolism

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  • (PMID = 16871430.001).
  • [ISSN] 0969-6970
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2R01-1 CA65527; United States / NCI NIH HHS / CA / T32 CA 09599; United States / NCI NIH HHS / CA / U54 CA 090810-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; EC 1.13.12.- / Luciferases; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
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42. Seo JO, Han SI, Lim SC: Role of CDK8 and beta-catenin in colorectal adenocarcinoma. Oncol Rep; 2010 Jul;24(1):285-91
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  • [Title] Role of CDK8 and beta-catenin in colorectal adenocarcinoma.
  • Colorectal adenocarcinoma is a major cause of morbidity and mortality.
  • CDK8 is a cyclin-dependent kinase (CDK) member of the mediator complex that couples transcriptional regulators to the basal transcriptional machinery, and is implicated in the transcriptional regulation of key pathways involved in colon cancers.
  • To determine the relationship between CDK8 and beta-catenin expressions, a population-based study was conducted for immunohistochemical staining analysis of tumor tissues, and Western blot analysis and CDK8 interference studies of colon cancer cell lines.
  • However, beta-catenin expression was not completely suppressed by CDK8 interference in the colon cancer cell lines HCT-116, HT-29 and SNU-C5.
  • [MeSH-major] Adenocarcinoma / metabolism. Colorectal Neoplasms / metabolism. Cyclin-Dependent Kinase 8 / physiology. beta Catenin / physiology
  • [MeSH-minor] Case-Control Studies. Drug Evaluation, Preclinical. Female. HCT116 Cells. HT29 Cells. Humans. Male. Prognosis. RNA, Small Interfering / pharmacology. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 20514474.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / beta Catenin; EC 2.7.11.22 / CDK8 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 8
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43. Epstein JI: Precursor lesions to prostatic adenocarcinoma. Virchows Arch; 2009 Jan;454(1):1-16
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  • [Title] Precursor lesions to prostatic adenocarcinoma.
  • High-grade prostatic intraepithelial neoplasia (PIN) is the one well-documented precursor to adenocarcinoma of the prostate.
  • Benign lesions that may be confused with high-grade PIN, including central zone histology, clear cell cribriform hyperplasia, and basal cell hyperplasia are described and illustrated.
  • High-grade PIN is also differentiated from invasive acinar (usual) and ductal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Precancerous Conditions / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Prostatic Hyperplasia / diagnosis. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Intraepithelial Neoplasia / pathology. Risk Factors

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  • (PMID = 19048290.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 85
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44. 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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  • 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).
  • Of these, the most prevalent (53.8%) was a hormone-responsive subtype with ER positive/PgR positive/HER2 negative, followed by TN subtype (15.5%).
  • RESULTS: The proportion of postmenopausal patients was relatively high in the TN subtype.
  • Morphologically, the TN subtype was more frequently classified as solid-tubular carcinoma.
  • 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-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


45. 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 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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46. McCormick DL, Rao KV, Johnson WD, Bosland MC, Lubet RA, Steele VE: Null activity of selenium and vitamin e as cancer chemopreventive agents in the rat prostate. Cancer Prev Res (Phila); 2010 Mar;3(3):381-92
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  • After stimulation of prostate epithelial cell proliferation by a sequential regimen of cyproterone acetate followed by testosterone propionate, male Wistar-Unilever rats received a single i.v. injection of N-methyl-N-nitrosourea (MNU) followed by chronic androgen stimulation via subcutaneous implantation of testosterone pellets.
  • At 1 week post-MNU, groups of carcinogen-treated rats (39-44/group) were fed either a basal diet or a basal diet supplemented with l-selenomethionine (3 or 1.5 mg/kg diet; study 1), dl-alpha-tocopherol (vitamin E, 4,000 or 2,000 mg/kg diet; study 2), l-selenomethionine + vitamin E (3 + 2,000 mg/kg diet or 3 + 500 mg/kg diet; study 3), or selenized yeast (target selenium levels of 9 or 3 mg/kg diet; study 4).

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  • (PMID = 20145190.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-95113; United States / NCI NIH HHS / CA / P30 CA016087; United States / NCI NIH HHS / CN / N01 CN095113; United States / NIEHS NIH HHS / ES / P30-ES-00260; United States / NCI NIH HHS / CN / N01 CN065120; United States / NIEHS NIH HHS / ES / P30 ES000260; United States / NCI NIH HHS / CA / P30-CA-16087; United States / NCI NIH HHS / CA / N01 CN35566; United States / NCI NIH HHS / CN / CN35566-02; United States / NCI NIH HHS / CN / N01-CN-65120; United States / NCI NIH HHS / CN / N01 CN35566-02; United States / NCI NIH HHS / CN / N01-CN-35566-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Androgens; 0 / Antioxidants; 0 / Selenium Compounds; 1406-18-4 / Vitamin E; 3XMK78S47O / Testosterone; 4KM2BN5JHF / Cyproterone Acetate; 684-93-5 / Methylnitrosourea; 964MRK2PEL / Selenomethionine; H4N855PNZ1 / alpha-Tocopherol
  • [Other-IDs] NLM/ NIHMS161245; NLM/ PMC2945242
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47. Leinonen T, Pirinen R, Böhm J, Johansson R, Rinne A, Weber E, Kosma VM: Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-cell lung cancer. J Clin Pathol; 2007 May;60(5):515-9
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  • [Title] Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-cell lung cancer.
  • BACKGROUND: Acid cysteine protease inhibitor (ACPI) is an intracellular protein, often linked to neoplastic changes in epithelium and thought to have an inhibitory role in malignant transformation.
  • AIM: To analyse the expression and prognostic role of ACPI in non-small-cell lung cancer (NSCLC).
  • RESULTS: A normal bronchial epithelium showed positive staining for ACPI in the basal cells, whereas the upper two-thirds of the dysplastic epithelium was ACPI positive.
  • High staining for ACPI was found in 74% (91/123) of squamous-cell carcinomas, whereas 16% (8/49) of adenocarcinomas and 30% of (8/27) large-cell carcinomas showed the high expression of ACPI (p<0.001).
  • Among squamous-cell carcinomas, low expression of ACPI was correlated with poor tumour differentiation (p=0.032).
  • In overall survival (OS) and disease-free survival (DFS) analyses, the histological type of the tumour (both p<0.001) and stage of the tumour (p=0.001, p=0.013, respectively) were related to patient outcome.
  • Low expression of ACPI in tumour cells was associated with poor OS and DFS (p<0.041, p=0.004, respectively).
  • CONCLUSIONS: ACPI expression is linked with the malignant transformation of the bronchial epithelium and predicts a risk of tumour recurrence as well as poor rate of survival for the patients.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Cystatins / metabolism. Cysteine Proteinase Inhibitors / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Follow-Up Studies. Humans. Immunoenzyme Techniques. Middle Aged. Neoplasm Staging. Precancerous Conditions / metabolism. Prognosis. Survival Analysis

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  • (PMID = 16790691.001).
  • [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; 0 / Cystatins; 0 / Cysteine Proteinase Inhibitors
  • [Other-IDs] NLM/ PMC1994551
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48. Xu XL, Li B, Sun XL, Li LQ, Ren RJ, Gao F: [Clinical and pathological analysis of 2639 cases of eyelid tumors]. Zhonghua Yan Ke Za Zhi; 2008 Jan;44(1):38-41
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  • The 5 leading eyelid malignant tumors were basal cell carcinoma, sebaceous gland carcinoma, lymphoma, squamous cell carcinoma and melanoma.
  • The mean age at diagnosis was 61 years for basal cell carcinoma and sebaceous gland carcinoma, 57 years and 52 years for squamous cell carcinoma and melanoma, respectively, and 48 years for lymphoma.
  • There was no significant sex predilection in basal cell carcinoma and sebaceous gland carcinoma.
  • Melanoma and lymphoma occurred more commonly in women, whereas squamous cell carcinoma occurred more commonly in men.
  • CONCLUSIONS: Basal cell carcinoma and sebaceous gland carcinoma were the most common malignant eyelid tumors, and lymphoma ranked third and had an increasing trend.
  • The malignant tumors occurred predominantly in the elderly of 60 years and above.
  • [MeSH-major] Adenocarcinoma, Sebaceous / pathology. Carcinoma, Basal Cell / pathology. Eyelid Neoplasms / pathology. Lymphoma / pathology

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  • (PMID = 18510241.001).
  • [ISSN] 0412-4081
  • [Journal-full-title] [Zhonghua yan ke za zhi] Chinese journal of ophthalmology
  • [ISO-abbreviation] Zhonghua Yan Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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49. Akrish S, Peled M, Ben-Izhak O, Nagler RM: Malignant salivary gland tumors and cyclo-oxygenase-2: a histopathological and immunohistochemical analysis with implications on histogenesis. Oral Oncol; 2009 Dec;45(12):1044-50
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  • [Title] Malignant salivary gland tumors and cyclo-oxygenase-2: a histopathological and immunohistochemical analysis with implications on histogenesis.
  • The classification system for malignant salivary gland tumors (MST) is largely dependent on its histogenesis.
  • The histogenesis is uncertain but the "bicellular theory of origin" has been accepted by most and states that malignant transformation of reserve cells from either the intercalated or excretory duct are responsible for the development of MST.
  • Fifty six primary major and minor gland MST were stained with anti-cox-2 antibody and rated with a combined score that added a scale of intensity to the percentage of tumor cells that overexpressed the cox-2 protein.
  • Strong cox-2 overexpression was noted in all MST of proposed excretory duct origin: salivary duct carcinoma (100%), mucoepidermoid carcinoma (MEC) (92%), and adenocarcinoma nos (AdC nos) (83%).
  • Primary squamous cell carcinoma (PSCC) was the exception.
  • Negative expression was noted in all tumors of proposed intercalated duct origin (adenoid cystic carcinoma, basal cell adenocarcinoma and acinic cell carcinoma) with the exception of one case of polymorphous low grade adenocarcinoma.
  • Strong cox-2 overexpression was noted in the epidermoid cells of MEC, abluminal duct cells surrounding the duct-like structures and ductal cells of AdC nos and salivary duct carcinoma.
  • Myoepithelial and acinar cells were unreactive.

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  • (PMID = 19729335.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.14.99.1 / Cyclooxygenase 2
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50. Deng J, Fujimoto J, Ye XF, Men TY, Van Pelt CS, Chen YL, Lin XF, Kadara H, Tao Q, Lotan D, Lotan R: Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis. Cancer Prev Res (Phila); 2010 Apr;3(4):424-37
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  • Examination of normal lung tissue and tumors from 51 Gprc5a(+/+) (adenoma incidence, 9.8%; adenocarcinoma, 0%) and 38 Gprc5a(-/-) mice (adenoma, 63%; adenocarcinoma, 21%) revealed macrophage infiltration into lungs of 45% of the Gprc5a(-/-) mice and 8% of Gprc5a(+/+) mice and the direct association of macrophages with 42% of adenomas and 88% of adenocarcinomas in the knockout mice.
  • Studies with epithelial cells cultured from tracheas of Gprc5a(-/-) and Gprc5a(+/+) mice revealed that Gprc5a loss is associated with increased cell proliferation, resistance to cell death in suspension, and increased basal, tumor necrosis factor alpha-induced, and lipopolysaccharide-induced NF-kappaB activation, which were reversed partially in Gprc5a(-/-) adenocarcinoma cells by reexpression of Gprc5a.
  • Compared with Gprc5a(+/+) cells, the Gprc5a(-/-) cells produced higher levels of chemokines and cytokines and their conditioned medium induced more extensive macrophage migration.
  • Silencing Gprc5a and the p65 subunit of NF-kappaB in Gprc5a(+/+) and Gprc5a(-/-) cells, respectively, reversed these effects.
  • Thus, Gprc5a loss enhances NF-kappaB activation in lung epithelial cells, leading to increased autocrine and paracrine interactions, cell autonomy, and enhanced inflammation, which may synergize in the creation of a tumor-promoting microenvironment.

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  • [Copyright] (c) 2010 AACR.
  • [CommentIn] Cancer Prev Res (Phila). 2010 Apr;3(4):403-5 [20354166.001]
  • (PMID = 20354164.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P30 CA16672
  • [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 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, G-Protein-Coupled
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51. Lin Z, Liu M, Li Z, Kim C, Lee E, Kim I: DeltaNp63 protein expression in uterine cervical and endometrial cancers. J Cancer Res Clin Oncol; 2006 Dec;132(12):811-6
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  • MATERIALS AND METHODS: DeltaNp63 protein expression was studied in a variety of 127 cases of uterine cervical lesions (20 non-neoplastic cervices, 43 cervical intraepithelial neoplasia [CIN], 54 squamous cell carcinomas (SCCs), 40 adenocarcinomas, and 13 other histologic types) and 30 endometrioid type of endometrial adenocarcinomas by using immunohistochemistry.
  • One SCC cell line (ME-180) and one adenocarcinoma cell line (HeLa) were also included.
  • RESULTS: In uterine cervix, the expression of DeltaNp63 was increased with progression of CIN, and positive in all SCCs, transitional cell carcinomas, and adenoid basal carcinoma, but negative in all adenocarcinomas.
  • Adenosquamous cell carcinoma and mixed neuroendocrine and squamous cell carcinoma were positive in squamous component, but not in adenocarcinoma and neuroendocrine carcinoma components.
  • ME-180 cell line was positive, whereas HeLa cell line was negative.
  • Endometrioid type of endometrial adenocarcinomas showed a positive staining in glandular (26.7%) and squamous component.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. DNA-Binding Proteins / biosynthesis. Endometrial Neoplasms / metabolism. Trans-Activators / biosynthesis. Tumor Suppressor Proteins / biosynthesis. Uterine Cervical Neoplasms / metabolism
  • [MeSH-minor] Antigens, Differentiation / biosynthesis. Cell Line, Tumor. Cervix Uteri / cytology. Cervix Uteri / metabolism. Female. HeLa Cells. Humans. Immunohistochemistry. Transcription Factors

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  • (PMID = 16804722.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / DNA-Binding Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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52. Shieh JJ, Liu KT, Huang SW, Chen YJ, Hsieh TY: Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in basal cell carcinoma cells. J Invest Dermatol; 2009 Oct;129(10):2497-506
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  • [Title] Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in basal cell carcinoma cells.
  • Myeloid cell leukemia-1 (Mcl-1, Mcl-1L) is an anti-apoptotic protein of the Bcl-2 family that acts as a critical molecule in apoptosis control.
  • In this study, we found an imbalance between the expression levels of Mcl-1L and Mcl-1S in the skin basal cell carcinoma (BCC) cell line when compared with primary keratinocytes.
  • We showed that overexpression of Mcl-1S induces apoptosis in BCC cells.
  • This shift increases the level of pro-apoptotic Mcl-1S and reduces the level of anti-apoptotic Mcl-1L, which induces apoptosis in BCC cells and AGS cells, a human gastric adenocarcinoma epithelial cell line.
  • [MeSH-major] Alternative Splicing / drug effects. Apoptosis / drug effects. Carcinoma, Basal Cell / pathology. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / genetics. Skin Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Line, Tumor. Humans. Keratinocytes / metabolism. Keratinocytes / pathology. Myeloid Cell Leukemia Sequence 1 Protein. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology

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  • (PMID = 19369967.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
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53. Guo RX, Wei LH, Zhao D, Wang JL, Li XP: [Effects of ICI182780 (Faslodex) on proliferation and apoptosis induced by 17beta-estradiol in endometrial carcinoma cells]. Beijing Da Xue Xue Bao; 2006 Oct 18;38(5):470-4
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  • [Title] [Effects of ICI182780 (Faslodex) on proliferation and apoptosis induced by 17beta-estradiol in endometrial carcinoma cells].
  • OBJECTIVE: To observe the influence of estrogen receptor, ICI182780, on proleferation, cell cycle progression and apoptosis in estrogen receptor (ER)-positive and ER-poor endometrial carcinoma cells and to explore the possible preliminary value of ICI182780 treating endometrial carcinoma.
  • METHODS: The effects of ICI182780 on proliferation, apoptosis and cell cycle distribution of endometrial cancer cells costimulated with 10(-6) mol/L E2 was detected by monotetrazolium (MTT) assay and fluorescence-activated cell sorting technique.
  • Cell cycle distribution analysis revealed that percentage of Ishikawa cells at G0-G1 phase decreased and percentage at S phase increased significantly, whereas that of HEC-1A cells did not show significant alteration.
  • In cotreatment of endometrial cancer cells with ICI182780, values of OD 570 nm and numbers of apoptotic cells of Ishikawa cells decreased to basal levels, G0-G1 phase proportion increased, percentage of S phase increased in a time or time-dependent manner.
  • But there was no such alteration in HEC-1A cells.
  • CONCLUSION: The specific ER antagonist, ICI182780, can inhibit Ishikawa cell propagation induced by E2, make cells apoptosis and block Ishikawa cells at the G1/S transition.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Estradiol / analogs & derivatives. Estradiol / pharmacology
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Endometrial Neoplasms / pathology. Endometrial Neoplasms / physiopathology. Estrogen Antagonists / pharmacology. Female. Flow Cytometry. Humans

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  • (PMID = 17068616.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol
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54. Gubbay O, Guo W, Rae MT, Niven D, Langdon SP, Hillier SG: Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas. Br J Cancer; 2005 May 23;92(10):1927-33
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  • [Title] Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas.
  • The process of ovulation is synonymous with inflammation and inflammatory cytokines such as interleukin-1alpha (IL-1alpha) have recently been shown to induce both inflammatory and anti-inflammatory responses in human OSE (HOSE) cells.
  • In this study we directly compared levels of IL-1alpha-induced gene expression by analysing the levels of 11beta-hydroxysteroid dehydrogenase (11betaHSD) types 1 (11betaHSD-1) and 2 (11betaHSD-2), cyclooxygenase-2 (COX-2), IL-1 receptor (IL-1R) and glucocorticoid receptor alpha (GRalpha) mRNA between normal HOSE cells and cell lines derived from poorly differentiated (SKOV-3, BG-1, PEO-4) and well-differentiated (PEO-14) ovarian adenocarcinoma.
  • In HOSE cell cultures, and to a lesser extent PEO-14 cells, the basal mRNA levels of COX-2 and 11betaHSD-1 were relatively high and further shown to be induced in response to IL-1alpha (for HOSE cells; >20-fold, P<0.05 and PEO-14 cells; >3fold, P<0.05).
  • However, whereas HOSE cells expressed a low level of 11betaHSD-2 mRNA that was only mildly responsive to IL-1alpha (1.3-fold, P<0.001), all cell lines exhibited a higher basal level of 11betaHSD-2 mRNA that was in some cases further stimulated in PEO-4 cells (five-fold; P<0.05) or suppressed in SKOV-3 cells (two-fold; P<0.01) in response to IL-1alpha.
  • All cells tested expressed IL-1R and, with the exception of BG-1, GRalpha.
  • These results indicate that cell lines derived from ovarian cancers have lost the ability to respond normally to inflammatory cytokines such as IL-1alpha.
  • The finding that normal OSE cells, in contrast to cell lines derived from patients with ovarian adenocarcinoma, abundantly express 11betaHSD-1 mRNA but are essentially devoid of 11betaHSD-2 mRNA supports the concept that the pattern of 11betaHSD isoform gene expression is a defining feature of neoplastic cellular transformation, which might have particular relevance to the ovary.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / immunology. Cytokines / biosynthesis. Cytokines / genetics. Gene Expression Regulation. Inflammation. Ovarian Neoplasms / genetics. Ovarian Neoplasms / immunology
  • [MeSH-minor] 11-beta-Hydroxysteroid Dehydrogenases / biosynthesis. Cell Differentiation. Cell Transformation, Neoplastic. Cyclooxygenase 2. Epithelial Cells. Female. Humans. Interleukin-1 / pharmacology. Membrane Proteins. Ovulation. Prostaglandin-Endoperoxide Synthases / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15870720.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1; 0 / Membrane Proteins; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Other-IDs] NLM/ PMC2361768
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55. Bi S, Liu JR, Li Y, Wang Q, Liu HK, Yan YG, Chen BQ, Sun WG: gamma-Tocotrienol modulates the paracrine secretion of VEGF induced by cobalt(II) chloride via ERK signaling pathway in gastric adenocarcinoma SGC-7901 cell line. Toxicology; 2010 Jul-Aug;274(1-3):27-33
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  • [Title] gamma-Tocotrienol modulates the paracrine secretion of VEGF induced by cobalt(II) chloride via ERK signaling pathway in gastric adenocarcinoma SGC-7901 cell line.
  • Hypoxia is a common characteristic feature of solid tumors, and carcinoma cells are known to secrete many growth factors.
  • In this study, the effect of gamma-tocotrienol, a natural product commonly found in palm oil and rice bran, on the accumulation of HIF-1alpha protein and the paracrine secretion of VEGF in human gastric adenocarcinoma SGC-7901 cell line induced by cobalt(II) chloride (as a hypoxia mimic) was investigated.
  • These results showed that cobalt(II) chloride induced the high expression of VEGF in SGC-7901 cells at dose of 150 micromol/L for 24h.
  • Both basal level and cobalt(II) chloride-induced HIF-1alpha protein accumulation and VEGF paracrine secretion were inhibited in SGC-7901 cells treated with gamma-tocotrienol at 60 micromol/L treatment for 24 h.
  • [MeSH-minor] Adenocarcinoma. Cell Line. Chromans. Cobalt / pharmacology. Guanylate Cyclase. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / pharmacology. Mitogen-Activated Protein Kinase 3 / metabolism. Mitogen-Activated Protein Kinase 3 / pharmacology. Neovascularization, Pathologic. Phosphorylation. Receptors, Cytoplasmic and Nuclear. Signal Transduction / drug effects. Vascular Endothelial Growth Factors / metabolism. Vascular Endothelial Growth Factors / pharmacology. Vitamin E / analogs & derivatives

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20452389.001).
  • [ISSN] 1879-3185
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chromans; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 1406-18-4 / Vitamin E; 3G0H8C9362 / Cobalt; 4382-43-8 / plastochromanol 8; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 4.6.1.2 / Guanylate Cyclase; EC 4.6.1.2 / soluble guanylyl cyclase
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56. Kong CS, Beck AH, Longacre TA: A panel of 3 markers including p16, ProExC, or HPV ISH is optimal for distinguishing between primary endometrial and endocervical adenocarcinomas. Am J Surg Pathol; 2010 Jul;34(7):915-26
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  • [Title] A panel of 3 markers including p16, ProExC, or HPV ISH is optimal for distinguishing between primary endometrial and endocervical adenocarcinomas.
  • Endometrial and endocervical adenocarcinomas may seem histologically identical and it can be difficult to determine primary site of origin based on morphology alone.
  • The TMA consisted of 214 endometrial carcinomas, 33 endocervical adenocarcinomas, and 36 problematic cases.
  • The endometrial and endocervical carcinomas represented usual endometrioid and mucinous types, and special variants (uterine serous carcinoma, uterine clear cell carcinoma, minimal deviation endocervical adenocarcinoma, cervical small cell carcinoma, adenoid basal cell carcinoma, mesonephric carcinoma).
  • Using a script written in R, the diagnostic accuracy of all possible combinations of markers was evaluated and it was shown that a 3 marker panel including vimentin, ER, or PR, and an HPV marker (p16, ProExC, or HPV ISH) is optimal for determining site of origin for usual endometrial and endocervical adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Cyclin-Dependent Kinase Inhibitor p16 / analysis. DNA, Viral / analysis. Endometrial Neoplasms / diagnosis. Papillomaviridae / genetics. Uterine Cervical Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Immunoenzyme Techniques. In Situ Hybridization. Papillomavirus Infections / diagnosis. Reproducibility of Results. Tissue Array Analysis. Vimentin / metabolism

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  • (PMID = 20534993.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NLM NIH HHS / LM / T15 LM007033
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Viral; 0 / Vimentin
  • [Other-IDs] NLM/ NIHMS775595; NLM/ PMC4847142
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57. Sanchez-Salazar AJ, Basler JW, Nicolas MM: Intraductal carcinoma of the prostate in the ejaculatory duct. Int J Surg Pathol; 2010 Aug;18(4):298-9
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  • Intraductal carcinoma of the prostate (IDCP) involving prostatic ducts and acini is a well-known phenomenon typically seen in a background of high-grade invasive prostatic adenocarcinoma.
  • The current case of prostatic adenocarcinoma with Gleason score of 9 (4 + 5) invades the ejaculatory ducts, left seminal vesicle, and extraprostatic tissue.
  • The tumor involving the left ejaculatory duct spans the lumen with preservation of native duct architecture, including basal cells, similar features described in IDCP involving prostatic ducts and acini.
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Humans. Male. Neoplasms, Multiple Primary. Prognosis. Prostatectomy. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Intraepithelial Neoplasia / surgery

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  • (PMID = 20444733.001).
  • [ISSN] 1940-2465
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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58. Luebke AM, Schlomm T, Gunawan B, Bonkhoff H, Füzesi L, Erbersdobler A: Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach. Virchows Arch; 2005 Mar;446(3):338-41
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  • [Title] Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach.
  • Basal cell tumours of the prostatic gland are rare, and the classification is difficult.
  • In the present case report, a large, tumour-like proliferation of atypical basaloid cells was found incidentally in a prostatectomy specimen that otherwise contained a conventional acinar adenocarcinoma.
  • The basaloid cells displayed a solid or adenoid-cystic growth pattern and strongly expressed high-molecular-weight cytokeratins and bcl-2.
  • A high Ki-67 index was recorded within the atypical basaloid cells, by far exceeding the one counted in the conventional adenocarcinoma.
  • However, there were no definite criteria for a malignant behaviour of the basal cell tumour.
  • Comparative genomic hybridisation from microdissected tumour cells yielded losses at the short arms of chromosomes 8 and 12 in the conventional adenocarcinoma and a normal karyotype in the basal cell tumour.
  • The pathological findings favoured the diagnosis of an atypical basal cell hyperplasia.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Carcinoma, Acinar Cell / pathology. Prostatic Hyperplasia / complications. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / complications. Prostatic Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasms, Basal Cell / genetics. Neoplasms, Basal Cell / pathology. Nucleic Acid Hybridization

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  • (PMID = 15726402.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
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59. Fleming JC, Linder JS, Karcioglu ZA: Orbital hyperostosis following exenteration. Ophthal Plast Reconstr Surg; 2008 Sep-Oct;24(5):378-82
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  • The histopathology revealed necrotic destruction of the trabeculae mixed with randomly distributed chronic inflammatory cells and fibrosis and inflamed overlying granulation tissue.
  • [MeSH-major] Adenocarcinoma, Sebaceous / surgery. Carcinoma, Basal Cell / surgery. Eyelid Neoplasms / surgery. Hyperostosis / etiology. Orbital Diseases / etiology. Postoperative Complications
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Recurrence, Local / surgery. Orbit / pathology. Orbit / radiography. Orbit Evisceration. Tomography, X-Ray Computed

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  • (PMID = 18806659.001).
  • [ISSN] 1537-2677
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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60. Mayes DC, Patterson JW, Ramnani DM, Mills SE: alpha-methylacyl coenzyme A racemase is immunoreactive in extramammary Paget disease. Am J Clin Pathol; 2007 Apr;127(4):567-71
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  • [Title] alpha-methylacyl coenzyme A racemase is immunoreactive in extramammary Paget disease.
  • alpha-Methylacyl-coenzyme A racemase (AMACR) has become a common tool in the diagnosis of morphologically difficult prostatic carcinoma and often is used in combination with the basal cell markers p63 and 34betaE12.
  • We report findings in 21 cases of extramammary Paget disease (EMPD), a neoplasm not previously reported to show AMACR immunoreactivity.
  • AMACR immunoreactivity is a common finding in EMPD in men and women.
  • [MeSH-major] Adenocarcinoma / complications. Biomarkers, Tumor / analysis. Paget Disease, Extramammary / complications. Paget Disease, Extramammary / metabolism. Prostatic Neoplasms / complications. Racemases and Epimerases / metabolism

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  • (PMID = 17369131.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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61. Nasir S, Aydin MA: Versatility of free SCIA/SIEA flaps in head and neck defects. Ann Plast Surg; 2010 Jul;65(1):32-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenocarcinoma / surgery. Adolescent. Adult. Aged. Bone Transplantation. Burns / surgery. Carcinoma, Basal Cell / surgery. Carcinoma, Squamous Cell / surgery. Child. Cicatrix / surgery. Facial Neoplasms / surgery. Female. Follow-Up Studies. Humans. Male. Maxilla / surgery. Maxillary Neoplasms / surgery. Middle Aged. Neck Injuries / surgery. Neoplasm Recurrence, Local / surgery. Reoperation. Scalp / surgery. Skin Neoplasms / surgery. Young Adult

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  • (PMID = 20574218.001).
  • [ISSN] 1536-3708
  • [Journal-full-title] Annals of plastic surgery
  • [ISO-abbreviation] Ann Plast Surg
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] United States
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62. Parashar P, Baron E, Papadimitriou JC, Ord RA, Nikitakis NG: Basal cell adenocarcinoma of the oral minor salivary glands: review of the literature and presentation of two cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2007 Jan;103(1):77-84
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  • [Title] Basal cell adenocarcinoma of the oral minor salivary glands: review of the literature and presentation of two cases.
  • Basal cell adenocarcinoma (BCA) is an unusual salivary gland malignancy that very rarely affects the minor glands.
  • [MeSH-major] Adenocarcinoma / pathology. Salivary Gland Neoplasms / pathology. Salivary Glands, Minor / pathology

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  • (PMID = 17178498.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 35
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63. 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
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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
  • [MeSH-minor] Age Distribution. Aged. Female. Humans. Lymphatic Metastasis. Male. Matrix Metalloproteinase 9 / metabolism. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Prognosis. Survival Analysis

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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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64. Fukui D, Bando G, Ishikawa Y, Kadota K: Adenosquamous carcinoma with cilium formation, mucin production and keratinization in the nasal cavity of a red fox (Vulpes vulpes schrencki). J Comp Pathol; 2007 Aug-Oct;137(2-3):142-5
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  • A diagnosis of adenosquamous carcinoma was made in an 11-year-old red fox.
  • The nasal and oral lesions were composed of adenocarcinomatous cells and squamous cells, the latter predominating in the oral lesions.
  • The marrow of the palatine bone also contained neoplastic tissue, which consisted of cysts and keratin masses surrounded by well-differentiated squamous cells.
  • Although inconspicuous in the oral cavity and marrow, ciliated cells with or without mucin were observed in the adenocarcinomatous and cystic elements.
  • Neoplastic basal cells and less-differentiated adenocarcinoma cells, which were identifiable by immunolabelling for cytokeratin 5 (CK5) and CK18, were considered to be pluripotential.
  • These cells, which lined tubular structures, were distinct from intermediate cells in mucoepidermoid carcinoma, which can differentiate into squamous and mucin-producing cells but have a nondescript appearance.

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  • (PMID = 17645890.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Keratin-18; 0 / Keratin-5; 0 / Mucins; 68238-35-7 / Keratins
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65. Aust S, Brucker B, Graf J, Klimpfinger M, Thalhammer T: Melatonin modulates acid/base transport in human pancreatic carcinoma cells. Cell Physiol Biochem; 2006;18(1-3):91-102
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  • [Title] Melatonin modulates acid/base transport in human pancreatic carcinoma cells.
  • To study whether pancreatic bicarbonate secretion is stimulated by melatonin, investigations were done in two human ductal pancreatic adenocarcinoma cell lines MIA PaCa-2 (MIA) and PANC-1 (PANC).
  • Using the fluorescence pH-sensor BCECF-AM, we monitored melatonin effects on basal intracellular pH (pH(i)), and on pH(i) recovery after intracellular alkalinization produced by the removal of extracellular HCO(3) (-)/CO(2).
  • Exposure to 1 microM melatonin for 24 hrs and presence of the indoleamine during the experiment increases the basal pH(i).
  • In summary, we show a stimulatory effect of melatonin on bicarbonate secretion in the pancreatic cancer cell lines which may help to prevent duodenal damage.
  • [MeSH-minor] Antiporters / genetics. Bicarbonates / metabolism. Biological Transport / drug effects. Cell Line, Tumor. Colforsin / pharmacology. Cyclic AMP / metabolism. Gene Expression / drug effects. Gene Expression / genetics. Humans. Hydrogen-Ion Concentration / drug effects. Models, Biological. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Melatonin, MT1 / genetics. Receptor, Melatonin, MT2 / genetics. Reverse Transcriptase Polymerase Chain Reaction. Symporters / genetics

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  • (PMID = 16914894.001).
  • [ISSN] 1015-8987
  • [Journal-full-title] Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
  • [ISO-abbreviation] Cell. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Acids; 0 / Antiporters; 0 / Bicarbonates; 0 / RNA, Messenger; 0 / Receptor, Melatonin, MT1; 0 / Receptor, Melatonin, MT2; 0 / Symporters; 1F7A44V6OU / Colforsin; E0399OZS9N / Cyclic AMP; JL5DK93RCL / Melatonin
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66. Hirsch DL, Miles C, Dierks E: Basal cell adenocarcinoma of the parotid gland: report of a case and review of the literature. J Oral Maxillofac Surg; 2007 Nov;65(11):2385-8
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  • [Title] Basal cell adenocarcinoma of the parotid gland: report of a case and review of the literature.
  • [MeSH-major] Adenocarcinoma / diagnosis. Parotid Neoplasms / diagnosis

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  • (PMID = 17954345.001).
  • [ISSN] 0278-2391
  • [Journal-full-title] Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons
  • [ISO-abbreviation] J. Oral Maxillofac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 6
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67. Shimizu Y, Yoshida T, Kato M, Hirota J, Ono S, Nakagawa M, Kobayashi T, Kubota K, Asaka M: Low-grade dysplasia component in early invasive squamous cell carcinoma of the esophagus. J Gastroenterol Hepatol; 2010 Feb;25(2):314-8
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  • [Title] Low-grade dysplasia component in early invasive squamous cell carcinoma of the esophagus.
  • If LGD progresses to squamous cell carcinoma, early carcinoma lesions that have such a natural history might contain a remaining LGD component.
  • METHODS: The lesions in the 68 patients with early invasive squamous cell carcinoma who underwent endoscopic mucosal resection were examined for the presence of an LGD component.
  • RESULTS: Histological examination of resected specimens confirmed LGD components in 43% of the squamous cell carcinoma lesions.
  • CONCLUSION: Our results indicate the possibility that the lesion was formed by a combination of small lesions that arose as a multicentric occurrence of squamous cell carcinoma and dysplasia.
  • However, the concept of 'basal cell layer type carcinoma in situ' may be suitable for squamous cell lesions with a high degree of cytological abnormalities confined to the lower half of the epithelium.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma in Situ / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Cell Transformation, Neoplastic / pathology. Disease Progression. Esophagoscopy. Female. Humans. Male. Middle Aged. Mucous Membrane / pathology. Neoplasm Invasiveness. Neoplasm Staging

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  • (PMID = 19968747.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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68. Matsuzaki K, Okazaki K: Transforming growth factor-beta during carcinogenesis: the shift from epithelial to mesenchymal signaling. J Gastroenterol; 2006 Apr;41(4):295-303
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  • While the TbetaRI/pSmad3C pathway inhibits growth of normal epithelial cells, JNK/pSmad3L-mediated signaling is involved in invasion by activated mesenchymal cells.
  • During sporadic human colorectal carcinogenesis, TGF-beta signaling confers a selective advantage on tumor cells by shifting from the TbetaRI/pSmad3C pathway characteristic of mature epithelial cells to the JNK/pSmad3L pathway, which is more characteristic of the state of flux shown by the activated mesenchymal cells.
  • JNK acts as a regulator of TGF-beta signaling by increasing the basal level of pSmad3L available for action in the nuclei of the invasive adenocarcinoma, in the meantime shutting down TGF-beta-dependent nuclear activity of pSmad3C.
  • From the viewpoint of TGF-beta signaling, a key therapeutic aim in cancer would be restoration of the lost tumor suppressor function observed in normal colorectal epithelial cells at the expense of effects promoting aggressive behavior of the adenocarcinoma.
  • [MeSH-minor] Disease Progression. Humans

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  • (PMID = 16741607.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor beta
  • [Number-of-references] 41
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69. 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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  • [Title] Cytologic features of primary malignant tumors of skin and adnexae.
  • STUDY DESIGN: Cases of primary malignant tumors of skin and adnexae diagnosed on cytology with histopathology confirmation were retrieved from case records of 1998-2005.
  • RESULTS: Thirty primary malignant tumors of skin and adnexae were analyzed.
  • 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.
  • CONCLUSION: Cytodiagnosis of primary malignant tumors of skin and adnexae is possible based on morphology and clinical presentation.
  • [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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70. Krajewska M, Olson AH, Mercola D, Reed JC, Krajewski S: Claudin-1 immunohistochemistry for distinguishing malignant from benign epithelial lesions of prostate. Prostate; 2007 Jun 15;67(9):907-10
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  • [Title] Claudin-1 immunohistochemistry for distinguishing malignant from benign epithelial lesions of prostate.
  • BACKGROUND: Claudins are a family of approximately 23 integral membrane tight junction (TJ) proteins that maintain cell polarity and paracellular barrier functions in epithelial and endothelial cells.
  • METHODS: Using immunohistochemistry, the expression of Claudin-1 was investigated in prostate tissue samples arranged in a tissue microarray (TMA) format and comprising elements of normal prostatic epithelium (n = 6), benign prostatic hyperplasia (BPH; n = 38), prostatic intraepithelial neoplasia (PIN; n = 11), and prostate adenocarcinoma (n = 48).
  • The Claudin-1 expression pattern was compared with that of the basal cell-specific markers, p63, and HMW cytokeratin (34betaE12), by employing double-labeling techniques in conjunction with image analysis methods utilizing color deconvolution algorithms.
  • RESULTS: In benign prostatic epithelium, pronounced Claudin-1 expression was observed in the basal cell layer with no staining in luminal cells.
  • Prostate adenocarcinoma specimens from 98% (47/48) patients lacked Claudin-1 immunostaining, and no cases contained >5% immunopositive tumor cells.
  • CONCLUSIONS: Claudin-1 immunohistochemistry should be considered for use as a new diagnostic tool for distinguishing malignant from benign lesions of the prostate.

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  • (PMID = 17440968.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114810; United States / NCI NIH HHS / CA / CA114810-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / CLDN1 protein, human; 0 / Claudin-1; 0 / Membrane Proteins; 68238-35-7 / Keratins
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71. Marci V, Volante M, Cappia S, Righi L, Novello C, Scagliotti GV, Brambilla E, Papotti M: Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma. Virchows Arch; 2007 Sep;451(3):729-36
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  • [Title] Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma.
  • The 2004 WHO classification of lung tumours recognised basaloid carcinoma as a variant of squamous and large cell carcinoma.
  • We report a unique case of primary pulmonary adenocarcinoma with a basaloid component.
  • The patient is disease-free 13 months after diagnosis.
  • The former was an adenocarcinoma with mucus containing spaces lined by columnar mucinous cells and basaloid cells.
  • The solid component was an organoid proliferation of basaloid-type cells, as in cutaneous basal cell carcinoma.
  • Basaloid cells, but not mucinous cells, were immunoreactive for high molecular weight cytokeratins (CK), CK 7 and, focally, for TTF-1.
  • (1) The solid areas resemble a conventional basaloid carcinoma, except for the presence of small mucin-containing spaces. (2) The mucinous adenocarcinoma areas contain two layers of columnar and basaloid cells. (3) Both components are neoplastic based on cell morphology, invasive properties and phenotypic profile.
  • These findings indicate that a basaloid variant of adenocarcinoma is also existing in the spectrum of basaloid carcinomas of the lung.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Aged, 80 and over. Carcinoma, Basal Cell. Humans. Keratins / analysis. Male. Mucins / analysis. Neoplasm Invasiveness. Phenotype. World Health Organization


72. Midi A, Tecimer T, Bozkurt S, Ozkan N: Differences in the structural features of atypical adenomatous hyperplasia and low-grade prostatic adenocarcinoma. Indian J Urol; 2008 Apr;24(2):169-77
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  • [Title] Differences in the structural features of atypical adenomatous hyperplasia and low-grade prostatic adenocarcinoma.
  • AIM: Atypical adenomatous hyperplasia (AAH) is a small glandular proliferation that has histological similarities with Gleason grade 1 and 2 prostatic adenocarcinoma (PACG1,2).
  • Basal cell-specific antikeratin was applied to these lesions.
  • We assumed that PACG1,2 lesions did have not basal cells and we grouped the lesions as AAH and PACG1,2 based on this assumption.
  • RESULTS: We found differences between AAH and PACG1,2 lesions for some parameters including the number of glands, structures such as the main ductus and basal cells.
  • We found similar properties in the two lesions for the following parameters: localization, multiplicity, diameter of the lesion, focus asymmetry, distance between glands, inflammatory cells in and out of the lesions, secretory cell shape on the luminal side, papillary projection towards the luminal side of gland, the shape of the outer gland, the infiltrative pattern of the gland, glandular pleomorphism, biggest gland diameter and median gland diameter.

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  • (PMID = 19468392.001).
  • [ISSN] 0970-1591
  • [Journal-full-title] Indian journal of urology : IJU : journal of the Urological Society of India
  • [ISO-abbreviation] Indian J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2684265
  • [Keywords] NOTNLM ; Adenosis / cancer / hyperplasia / low grade / proliferations / prostate / small glandular
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73. Sato T, Murakumo Y, Hagiwara S, Jijiwa M, Suzuki C, Yatabe Y, Takahashi M: High-level expression of CD109 is frequently detected in lung squamous cell carcinomas. Pathol Int; 2007 Nov;57(11):719-24
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  • [Title] High-level expression of CD109 is frequently detected in lung squamous cell carcinomas.
  • CD109 is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein, which is a member of the alpha2-macroglobulin/C3, C4, C5 family of thioester-containing proteins.
  • It has been reported that CD109 is expressed in a subset of hematopoietic cells, endothelial cells and several kinds of human tumors.
  • Herein it is reported that the CD109 protein is preferentially expressed in lung squamous cell carcinomas compared with other types of lung carcinoma including adenocarcinomas, large cell carcinomas and small cell carcinomas.
  • Immunohistochemical staining of surgically resected lung specimens using an anti-CD109 antibody detected CD109 expression in basal cells of bronchial and bronchiolar epithelia and myoepithelial cells of bronchial secretary glands, but not in bronchial and bronchiolar apical epithelial cells and alveolar epithelial cells.
  • Furthermore, the CD109 immunoreactivity was observed in squamous cell carcinomas at a high frequency compared with other types of lung carcinoma.
  • Although the detailed function of CD109 protein is unclear, these results suggest that CD109 expression may play a role in the development of lung squamous cell carcinoma.
  • [MeSH-major] Antigens, CD / metabolism. Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / metabolism. Lung Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Blotting, Western. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Small Cell / metabolism. Carcinoma, Small Cell / pathology. Female. GPI-Linked Proteins. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Small Interfering

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  • (PMID = 17922683.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / CD109 protein, human; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering
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74. Yoshino M, Ishiwata T, Watanabe M, Matsunobu T, Komine O, Ono Y, Yamamoto T, Fujii T, Matsumoto K, Tokunaga A, Naito Z: Expression and roles of keratinocyte growth factor and its receptor in esophageal cancer cells. Int J Oncol; 2007 Oct;31(4):721-8
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  • [Title] Expression and roles of keratinocyte growth factor and its receptor in esophageal cancer cells.
  • The keratinocyte growth factor receptor (KGFR), also known as FGFR2 IIIb, is mainly localized in epithelial cells and is activated by the keratinocyte growth factor (KGF) that is predominantly synthesized by mesenchymal cells.
  • In noncancerous esophageal tissues, KGFR was localized in epithelial cells from the basal region of the epithelium to the lower one-third of the epithelium, and KGF was weakly localized in the basal to parabasal epithelial cells.
  • On the other hand, Ki-67 was localized in the parabasal cells.
  • In EC tissues, KGFR and KGF were expressed in cancer cells in 22 and 37 of 54 patients, respectively.
  • The coexpression of KGFR and KGF in cancer cells was detected in 14 of 54 (26%) patients.
  • Clinicopathologically, KGFR expression correlated with the well-differentiated cell type of EC (p<0.001), and KGF expression correlated with lymphatic invasion and lymph node metastasis (p=0.004 and 0.021, respectively).
  • The coexpression of KGFR and KGF in cancer cells correlated with the well-differentiated cell type of EC (p=0.001).
  • In human EC cell lines (TE-1, TE-8 and TE-11), KGFR mRNA was expressed but no KGF mRNA was detected.
  • The KGFR mRNA level was highest in TE-1 cells, derived from well-differentiated SCC and lowest in TE-8 cells.
  • KGFR was detected in the cancer cell lines by Western blot analysis.
  • Recombinant human KGF significantly stimulated the growth of TE-8 and -11 cells, derived from moderately differentiated SCC, but had no effect on TE-1 cell growth.
  • These results suggest that KGFR expression correlates with the differentiation of a normal esophageal epithelium and the well-differentiated cell type of EC.
  • On the other hand, KGF may induce the growth of some EC cells in a paracrine manner and closely correlates with lymphatic invasion and lymph node metastasis.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Blotting, Western. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / secondary. Cell Differentiation. Epithelial Cells. Female. Humans. Ki-67 Antigen / metabolism. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 17786302.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 126469-10-1 / Fibroblast Growth Factor 7; EC 2.7.1.- / keratinocyte growth factor receptor; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2
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75. Uke M, Rekhi B, Ajit D, Jambhekar NA: The use of p63 as an effective immunomarker in the diagnosis of pulmonary squamous cell carcinomas on de-stained bronchial lavage cytological smears. Cytopathology; 2010 Feb;21(1):56-63
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  • [Title] The use of p63 as an effective immunomarker in the diagnosis of pulmonary squamous cell carcinomas on de-stained bronchial lavage cytological smears.
  • OBJECTIVES: A diagnosis in pulmonary onco-cytopathology primarily necessitates distinguishing small cell carcinoma (SCLC) from non-small cell carcinoma (NSCLC), which includes squamous cell carcinoma and adenocarcinoma.
  • Lately, p63 antibody has been used for distinguishing squamous cell carcinoma from SCLC and adenocarcinoma.
  • METHODS: A single Papanicolaou-stained conventional smear was de-stained and re-fixed with cold acetone and methanol for immunocytochemical staining with p63 antibody.
  • RESULTS: Out of 100 cases, 21 were cytologically diagnosed as squamous cell carcinoma.
  • Twenty of these showed 2+ or 3+ p63 positivity, whereas one, which was adenocarcinoma on histology, showed 1+ staining.
  • Of seven cases cytologically diagnosed as adenocarcinoma, six showed no p63 staining, whereas one, which was squamous cell carcinoma on histology, showed 1+ staining.
  • The former three were found to be SCLC on histology while the latter was squamous cell carcinoma.
  • The former eight were adenocarcinoma on histology and the latter two were squamous cell carcinoma.
  • The 10 cases that showed 1+ p63 staining were adenocarcinomas (n = 5), squamous cell carcinoma (n = 4) and NSCLC, not otherwise specified (n = 1).
  • Positive staining was seen in normal basal cells, which acted as an internal control.
  • Overall sensitivity of p63 for squamous cell carcinoma was 100% and specificity was 90.4%.
  • CONCLUSIONS: p63 immunostaining on processed cytology smears can be used to help identify squamous cell carcinoma.
  • Its diffuse expression was specific for squamous cell carcinoma while focal staining was also seen in adenocarcinoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Trans-Activators / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adult. Aged. Aged, 80 and over. Bronchoalveolar Lavage / methods. Bronchoalveolar Lavage Fluid / cytology. Carcinoma, Non-Small-Cell Lung / diagnosis. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Transcription Factors

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  • (PMID = 19744186.001).
  • [ISSN] 1365-2303
  • [Journal-full-title] Cytopathology : official journal of the British Society for Clinical Cytology
  • [ISO-abbreviation] Cytopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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76. Iczkowski KA, Montironi R: Adenoid cystic/basal cell carcinoma of the prostate strongly expresses HER-2/neu. J Clin Pathol; 2006 Dec;59(12):1327-30
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  • [Title] Adenoid cystic/basal cell carcinoma of the prostate strongly expresses HER-2/neu.
  • Adenoid cystic/basal cell carcinoma (ACBCC) is a rare neoplasm in the prostate.
  • Ten acinar adenocarcinomas of varying grades were also immunostained as controls.
  • Benign acini expressed HER-2/neu only in the basal layer.
  • The finding of strong, consistent HER-2/neu expression in ACBCC suggests that treatment with Herceptin (trastuzumab) may be effective in patients with this rare tumour.
  • [MeSH-major] Carcinoma, Adenoid Cystic / metabolism. Carcinoma, Basal Cell / metabolism. Mixed Tumor, Malignant / metabolism. Prostatic Neoplasms / metabolism. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Adult. Aged. Gene Expression. Humans. In Situ Hybridization. Male. Middle Aged. RNA, Messenger / genetics. RNA, Neoplasm / genetics


77. Zhang X: Simultaneous exposure to dietary acrylamide and corn oil developed carcinogenesis through cell proliferation and inhibition of apoptosis by regulating p53-mediated mitochondria-dependent signaling pathway. Toxicol Ind Health; 2009 Mar;25(2):101-9
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  • [Title] Simultaneous exposure to dietary acrylamide and corn oil developed carcinogenesis through cell proliferation and inhibition of apoptosis by regulating p53-mediated mitochondria-dependent signaling pathway.
  • Colonic aberrant crypt foci (ACF) and tumors, including adenomas and carcinomas, were examined at 12, 24, 36, 48 week post ACR-exposure.
  • Colonic apoptosis and cell proliferation, expression of Wild type (wt) p53, Bcl-2, Bax and caspase-3, were detected at 48 week post ACR-exposure.
  • Apoptosis was decreased and cell proliferation was increased in colonic mucosa in ACR-treated rats on dietary corn oil compared to vehicle rats on basal diet (P < 0.05).
  • [MeSH-major] Acrylamide / toxicity. Apoptosis / drug effects. Cell Proliferation / drug effects. Corn Oil / administration & dosage. Gene Expression Regulation, Neoplastic / drug effects. Precancerous Conditions / chemically induced. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / pathology. Adenoma / chemically induced. Adenoma / pathology. Animals. Carcinogenicity Tests. Cocarcinogenesis. Colon / drug effects. Colon / pathology. Colonic Neoplasms / chemically induced. Colonic Neoplasms / pathology. Diet. Injections, Intraperitoneal. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Male. Mitochondria / drug effects. Mitochondria / metabolism. Rats. Rats, Sprague-Dawley. Signal Transduction / drug effects

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  • (PMID = 19458132.001).
  • [ISSN] 0748-2337
  • [Journal-full-title] Toxicology and industrial health
  • [ISO-abbreviation] Toxicol Ind Health
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; 20R035KLCI / Acrylamide; 8001-30-7 / Corn Oil
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78. Lisovsky M, Dresser K, Baker S, Fisher A, Woda B, Banner B, Lauwers GY: Cell polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and adenocarcinoma: an immunohistochemical study. Mod Pathol; 2009 Jul;22(7):977-84
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  • [Title] Cell polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and adenocarcinoma: an immunohistochemical study.
  • The diagnosis of gastric epithelial dysplasia, a precursor lesion of gastric adenocarcinoma, is hindered by interobserver variability and by its resemblance to regenerative changes.
  • Loss of cell polarity, a histological feature of gastric epithelial dysplasia, may be difficult to ascertain, especially in the setting of inflammation or injury.
  • A biomarker of cell polarity could be useful in diagnosis of dysplasia, but has not been reported.
  • The Lethal giant larvae (lgl) gene controls apical-basal polarity of epithelial cells in Drosophila, and has properties of a tumor-suppressor gene.
  • The goal of our study was to test the hypothesis that Lgl2 protein expression and/or localization are disrupted in gastric epithelial dysplasia and adenocarcinoma.
  • Routinely processed pathology specimens including 94 benign mucosae of digestive organs, in addition to 36 reactive gastropathy, 57 gastric epithelial dysplasia, and 77 gastric adenocarcinomas, were immunostained for Lgl2 protein.
  • All but one case each of gastric epithelial dysplasia and adenocarcinoma showed either complete loss of anti-Lgl2 immunoreactivity or diffuse, mostly weak, cytoplasmic staining.
  • Complete loss of immunoreactivity was significantly more often observed in diffuse-type than in intestinal-type adenocarcinomas (79 vs 48%, respectively).
  • Our data suggest that Lgl2 expression is either aberrantly localized or lost in gastric epithelial dysplasia and adenocarcinoma, whereas it is maintained in reactive gastric mucosa.
  • We propose that Lgl2 may be a potential marker to rule out gastric epithelial dysplasia and adenocarcinoma in diagnostic specimens.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Cytoskeletal Proteins / metabolism. Gastric Mucosa / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Cell Polarity. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Male. Middle Aged. Young Adult

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  • (PMID = 19407852.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytoskeletal Proteins; 0 / Hugl-2 protein, human
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79. Hoffmann S, Wunderlich A, Lingelbach S, Musholt PB, Musholt TJ, von Wasielewski R, Zielke A: Expression and secretion of endostatin in thyroid cancer. Ann Surg Oncol; 2008 Dec;15(12):3601-8
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  • The aim of this study was to evaluate endostatin expression in archival TC specimens and its secretion following stimulation with thyrotropin (TSH) and epidermal growth factor (EGF) in TC cell lines.
  • In vitro, six differentiated (FTC133, FTC236, HTC, HTC-TSHr, XTC, and TPC1) and three anaplastic (C643, Hth74, Kat4.0) TC cell lines were evaluated for basal as well as TSH (1-100 mU/ml) and EGF stimulated (1-100 ng/ml) endostatin.
  • In vitro, basal endostatin secretion varied between 33 +/- 5 pg/ml (FTC236) and 549 +/- 65 pg/ml (TPC1) and was doubled in FTC, when the "primary" (FTC133) was compared with the metastasis (FTC236).
  • Some cell lines showed TSH-induced (e.g., 60% in XTC) or EGF-induced (e.g., 120% in TPC1) upregulation of endostatin secretion, while others did not, despite documented receptor expression.
  • In vitro, endostatin secretion of some cell lines is regulated by TSH and EGF, however the individual differences deserve further functional studies.
  • [MeSH-major] Adenocarcinoma, Follicular / metabolism. Angiogenesis Inhibitors / metabolism. Carcinoma / metabolism. Carcinoma, Papillary / metabolism. Endostatins / metabolism. Thyroid Gland / metabolism. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Cell Differentiation / drug effects. Enzyme-Linked Immunosorbent Assay. Epidermal Growth Factor / pharmacology. Humans. Immunoenzyme Techniques. Lymphatic Metastasis. Paraffin Embedding. Thyrotropin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 18818971.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Endostatins; 62229-50-9 / Epidermal Growth Factor; 9002-71-5 / Thyrotropin
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80. Segawa N, Tsuji M, Nishida T, Takahara K, Azuma H, Katsuoka Y: Basal cell carcinoma of the prostate: report of a case and review of the published reports. Int J Urol; 2008 Jun;15(6):557-9
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  • [Title] Basal cell carcinoma of the prostate: report of a case and review of the published reports.
  • Prostatic basal cell carcinoma (BCC), a distinctive variant of adenocarcinoma, is rare.
  • [MeSH-major] Carcinoma, Basal Cell. Prostatic Neoplasms

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  • (PMID = 18489650.001).
  • [ISSN] 1442-2042
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 10
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81. Sadok A, Bourgarel-Rey V, Gattacceca F, Penel C, Lehmann M, Kovacic H: Nox1-dependent superoxide production controls colon adenocarcinoma cell migration. Biochim Biophys Acta; 2008 Jan;1783(1):23-33
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  • [Title] Nox1-dependent superoxide production controls colon adenocarcinoma cell migration.
  • Recently, new homologues of the catalytic subunit of NADPH oxidase have been discovered in non-phagocytic cells.
  • Using Nox1 siRNA, we show that Nox1-dependent superoxide production affects the migration of HT29-D4 colonic adenocarcinoma cells on collagen-I.
  • An addition of arachidonic acid stimulated Nox1-dependent superoxide production and HT29-D4 cell migration.
  • Inhibition of 12-lipoxygenase decreased basal and arachidonic acid induced Nox1-dependent superoxide production and cell migration.
  • Protein kinase C delta inhibition by rottlerin (and also GO6983) prevented Nox1-dependent superoxide production and inhibited cell migration, while other protein kinase C inhibitors were ineffective.
  • We conclude that Nox1 activation by arachidonic acid metabolism occurs through 12-lipoxygenase and protein kinase C delta, and controls cell migration by affecting integrin alpha 2 subunit turn-over.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Movement. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. NADPH Oxidase / metabolism. Superoxides / metabolism
  • [MeSH-minor] Arachidonate 12-Lipoxygenase / metabolism. Arachidonic Acids / pharmacology. Cell Membrane / metabolism. HT29 Cells. Humans. Integrin alpha2beta1 / metabolism. Protein Kinase C-delta / metabolism

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  • (PMID = 18023288.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Arachidonic Acids; 0 / Integrin alpha2beta1; 11062-77-4 / Superoxides; EC 1.13.11.31 / Arachidonate 12-Lipoxygenase; EC 1.6.3.- / NOX1 protein, human; EC 1.6.3.1 / NADPH Oxidase; EC 2.7.11.13 / Protein Kinase C-delta
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82. Andreadis D, Nomikos A, Epivatianos A, Poulopoulos A, Barbatis C: Basaloid squamous cell carcinoma versus basal cell adenocarcinoma of the oral cavity. Pathology; 2005 Dec;37(6):560-3
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  • [Title] Basaloid squamous cell carcinoma versus basal cell adenocarcinoma of the oral cavity.
  • [MeSH-major] Carcinoma, Basosquamous / pathology. Carcinoma, Squamous Cell / pathology. Oropharyngeal Neoplasms / pathology. Salivary Gland Neoplasms / pathology. Salivary Glands, Minor / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Immunohistochemistry


83. National Toxicology Program: Toxicology and carcinogenesis studies of divinylbenzene-HP (Cas No. 1321-74-0) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2006 Nov;(534):1-290
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  • Incidences of degeneration of the olfactory epithelium in 200 and 400 ppm rats and basal cell hyperplasia of the olfactory epithelium in rats exposed to 100 ppm or greater were significantly increased.
  • Following combined analysis of single and step-section data, the incidences of renal tubule adenoma and adenoma or carcinoma (combined) were marginally higher in 200 and 400 ppm males, and the incidence of renal tubule hyperplasia was significantly increased in 400 ppm males.
  • The incidences of malignant glial cell tumors (malignant astrocytoma and oligodendroglioma) in the brain were slightly increased in 100 and 200 ppm males, and the incidence in the 200 ppm group exceeded the historical range for chamber controls.
  • The incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) in 100 ppm males were greater than chamber control incidences, but the incidences of adenoma or carcinoma (combined) were within the historical control range.
  • The incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) in all exposed groups of females were generally greater than those of the chamber controls; the incidences were at the upper end or exceeded the historical control ranges.
  • There was equivocal evidence of carcinogenic activity of divinylbenzene-HP in female B6C3F1 mice based on the incidences of alveolar/bronchiolar adenoma or carcinoma (combined) in the lung.

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  • (PMID = 17342197.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vinyl Compounds; IZ715T4SBU / divinyl benzene
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84. Kohno H, Suzuki R, Yasui Y, Miyamoto S, Wakabayashi K, Tanaka T: Ursodeoxycholic acid versus sulfasalazine in colitis-related colon carcinogenesis in mice. Clin Cancer Res; 2007 Apr 15;13(8):2519-25
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  • They are then maintained on a basal diet mixed with UDCA (0.016%, 0.08%, or 0.4%) or sulfasalazine (0.05%) for 17 weeks.
  • The immunohistochemical expression of the proliferating cell nuclear antigen labeling index in colonic epithelial malignancies was also assessed.
  • RESULTS: Feeding the mice with UDCA at all doses significantly inhibited the multiplicity of colonic adenocarcinoma.
  • The treatment also significantly lowered the proliferating cell nuclear antigen labeling index in the colonic malignancies.
  • Sulfasalazine caused a nonsignificant reduction in the incidence and multiplicity of colonic neoplasia and did not affect these mRNA expression.
  • [MeSH-minor] Animals. Anticarcinogenic Agents. Azoxymethane / toxicity. Cyclooxygenase 2 / genetics. Disease Models, Animal. Male. Mice. Mice, Inbred ICR. RNA, Messenger / genetics

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  • (PMID = 17438113.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / RNA, Messenger; 3XC8GUZ6CB / Sulfasalazine; 724L30Y2QR / Ursodeoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; MO0N1J0SEN / Azoxymethane
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85. Adley BP, Yang XJ: Application of alpha-methylacyl coenzyme A racemase immunohistochemistry in the diagnosis of prostate cancer: a review. Anal Quant Cytol Histol; 2006 Feb;28(1):1-13
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  • [Title] Application of alpha-methylacyl coenzyme A racemase immunohistochemistry in the diagnosis of prostate cancer: a review.
  • Alpha-methylacyl coenzyme A racemase (AMACR) is a recently discovered enzyme protein that has been shown to be increased at both the mRNA and protein levels in prostatic adenocarcinoma as compared with normal prostatic tissues.
  • Since its discovery, AMACR has gained wide acceptance for use in the diagnosis of prostatic adenocarcinoma in conjunction with morphology and immunohistochemical staining for basal cell markers.
  • This review focuses on AMACR expression in prostate cancer and its morphologic variants, high grade prostatic intraepithelial neoplasia, adenosis and benign conditions of the prostate.

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  • (PMID = 16566275.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  • [Number-of-references] 63
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86. Holcomb B, Yip-Schneider MT, Matos JM, Dixon J, Kennard J, Mahomed J, Shanmugam R, Sebolt-Leopold J, Schmidt CM: Pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies. J Gastrointest Surg; 2008 Feb;12(2):288-96
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  • [Title] Pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
  • We hypothesize that pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
  • MATERIALS AND METHODS: PANC-1, PaCa-2, and BxPC-3 cells were treated with curcumin, LY294002, or PD325901 alone or in combination with gemcitabine.
  • Proliferation was measured by cell counts and enzyme activity by Western blot and electrophoretic mobility shift assay.
  • All cells decreased NF-kappaB activity with curcumin(24 h) except PaCa-2, MEK activity with PD325901(24 h), and PI3Kinase with LY294002(3 h).
  • However, PI3K rebounded to(PaCa-2) or above (Panc-1,BxPC-3) basal in LY294002-treated cells (24 h).
  • LY294002 + gemcitabine was nearly synergistic in PaCa-2 cells, which showed a lower induction of PI3Kinase activity with LY294002.
  • CONCLUSIONS: These results demonstrate differences in treatment efficacy, which correlate with the cell's signaling response to treatment.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Chromones / administration & dosage. Curcumin / administration & dosage. Deoxycytidine / analogs & derivatives. Enzyme Inhibitors / administration & dosage. Morpholines / administration & dosage. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Blotting, Western. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Drug Therapy, Combination. Electrophoretic Mobility Shift Assay. Humans. MAP Kinase Signaling System / drug effects. NF-kappa B / drug effects. NF-kappa B / physiology. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / physiology. Tumor Cells, Cultured

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  • (PMID = 18049840.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / NF-kappa B; 0W860991D6 / Deoxycytidine; 31M2U1DVID / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; B76N6SBZ8R / gemcitabine; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; IT942ZTH98 / Curcumin
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87. Stewart J, Fleshner N, Cole H, Sweet J: Comparison of annexin II, p63 and alpha-methylacyl-CoA racemase immunoreactivity in prostatic tissue: a tissue microarray study. J Clin Pathol; 2007 Jul;60(7):773-80
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  • BACKGROUND: Current ancillary markers for diagnosis in prostate biopsies include p63 and alpha-methylacyl-CoA racemase (AMACR).
  • Staining was evaluated in benign and atrophic glands, high-grade prostatic intraepithelial neoplasia (HGPIN), and prostatic adenocarcinoma.
  • RESULTS: Diffuse cytoplasmic expression of ANXII correlated with p63 reactivity in basal cells.
  • CONCLUSIONS: Immunohistochemical staining for ANXII is a consistent and reliable marker of prostatic neoplasia.
  • [MeSH-major] Adenocarcinoma / metabolism. Annexin A2 / metabolism. Biomarkers, Tumor / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. DNA-Binding Proteins / metabolism. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Proteins / metabolism. Organ Size. Prostate / pathology. Prostatectomy. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Intraepithelial Neoplasia / surgery. Racemases and Epimerases / metabolism. Trans-Activators / metabolism. Transcription Factors. Tumor Suppressor Proteins / metabolism

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  • (PMID = 16916997.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A2; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  • [Other-IDs] NLM/ PMC1995785
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88. Domingo-Domenech J, Mellado B, Ferrer B, Truan D, Codony-Servat J, Sauleda S, Alcover J, Campo E, Gascon P, Rovira A, Ross JS, Fernández PL, Albanell J: Activation of nuclear factor-kappaB in human prostate carcinogenesis and association to biochemical relapse. Br J Cancer; 2005 Nov 28;93(11):1285-94
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  • Nuclear factor (NF)-kappaB/p65 regulates the transcription of a wide variety of genes involved in cell survival, invasion and metastasis.
  • We characterised by immunohistochemistry the expression of NF-kappaB/p65 protein in six histologically normal prostate, 13 high-grade prostatic intraepithelial neoplasia (PIN) and 86 prostate adenocarcinoma specimens.
  • Nuclear localisation of NF-kappaB was only seen in scattered basal cells in normal prostate glands.
  • In prostate adenocarcinomas, cytoplasmic NF-kappaB was detected in 57 (66.3%) specimens, and nuclear NF-kappaB (activated) in 47 (54.7%).
  • [MeSH-major] Adenocarcinoma / pathology. Cell Transformation, Neoplastic. NF-kappa B / biosynthesis. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Cell Nucleus. Cytoplasm / chemistry. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Neoplasm Recurrence, Local. Prognosis. Prostate-Specific Antigen. Risk Factors. Transcription Factor RelA / analysis. Transcription Factor RelA / biosynthesis. Transcription Factor RelA / pharmacokinetics

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  • (PMID = 16278667.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NF-kappa B; 0 / Transcription Factor RelA; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ PMC2361509
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89. Casas A, Battah S, Di Venosa G, Dobbin P, Rodriguez L, Fukuda H, Batlle A, MacRobert AJ: Sustained and efficient porphyrin generation in vivo using dendrimer conjugates of 5-ALA for photodynamic therapy. J Control Release; 2009 Apr 17;135(2):136-43
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  • In vivo, the porphyrin kinetics from ALA exhibited an early peak between 3 and 4 h in most tissues, whereas the dendrimer induced sustained porphyrin production for over 24 h and basal values were not reached until 48 h after administration.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Animals. Cell Line, Tumor. Cell Survival / drug effects. Coloring Agents / metabolism. Dose-Response Relationship, Drug. Injections, Subcutaneous. Male. Mammary Neoplasms, Experimental / drug therapy. Mice. Mice, Inbred BALB C. Molecular Structure. Molecular Weight. Protoporphyrins / biosynthesis. Structure-Activity Relationship. Tetrazolium Salts / metabolism. Thiazoles / metabolism. Time Factors. Xenograft Model Antitumor Assays

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  • (PMID = 19168101.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D011329/1; United Kingdom / Wellcome Trust / / 067062/Z/029/Z; United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Dendrimers; 0 / Photosensitizing Agents; 0 / Porphyrins; 0 / Protoporphyrins; 0 / Tetrazolium Salts; 0 / Thiazoles; 88755TAZ87 / Aminolevulinic Acid; C2K325S808 / protoporphyrin IX; EUY85H477I / thiazolyl blue
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90. Ou-Yang RJ, Hui P, Yang XJ, Zynger DL: Expression of glypican 3 in placental site trophoblastic tumor. Diagn Pathol; 2010;5:64
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  • BACKGROUND: Glypican-3 (GPC3) is a membrane-bound heparan sulfate proteoglycan that functions in embryonic cell growth and differentiation and is highly expressed in the placenta.
  • The purpose of this study was to investigate the immunohistochemical expression of GPC3 in placental site trophoblastic tumor (PSTT), a very rare gestational trophoblastic neoplasm which may be morphologically confused with non-trophoblastic tumors, and to assess its possible utility as a diagnostic marker.
  • METHODS: Fifteen cases of PSTT, as well as samples from placental site nodule (PSN) (n = 2), leiomyosarcoma (n = 1), leiomyoma (n = 1), invasive cervical squamous cell carcinoma (n = 7) and endometrial adenocarcinoma (n = 11) were examined.
  • Immunoreactivity was semi-quantitatively evaluated as negative (0, < 5% of cells stained), focally positive (1+, 5-10% of cells stained), positive (2+, 11-50% of cells stained) or diffusely positive (3+, > 50% of cells stained).
  • Staining intensity for each subtype was graded from 0 to 3 and a mean intensity was calculated.
  • Stronger, predominately cytoplasmic staining was seen in larger multi- and mononucleated cells with smaller mononucleate cells showing weak muddy cytoplasmic staining.
  • Both PSN cases were positive (1+, 50%; 2+, 50%) and two of nine invasive cervical squamous cell carcinomas showed staining (0, 57%; 1+, 29%; 2+, 14%), predominately in a basal distribution.

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  • (PMID = 20868507.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPC3 protein, human; 0 / Glypicans
  • [Other-IDs] NLM/ PMC2954974
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91. Leite KR, Srougi M, Sanudo A, Dall'oglio MF, Nesrallah A, Antunes AA, Cury J, Camara-Lopes LH: The use of immunohistochemistry for diagnosis of prostate cancer. Int Braz J Urol; 2010 Sep-Oct;36(5):583-90
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  • [Title] The use of immunohistochemistry for diagnosis of prostate cancer.
  • The use of antibodies to mark basal cells is currently a common practice, in order to avoid rebiopsies.
  • There has been no reported study that has reviewed characteristics of radical prostatectomies (RPs) when immunohistochemistry (IHC) was necessary for definitive diagnosis.
  • The results of surgical specimens of 27 patients treated by RP after the diagnosis of prostate cancer (PC) was made using IHC (Group 1) were compared with 1040 patients where IHC was not necessary (Group 2).
  • In Group 1, two (7.4%) adenocarcinomas were insignificant versus 29 (2.9%) for Group 2.
  • CONCLUSION: The use of IHC did not lead to diagnosis of insignificant tumors as illustrated by absence of differences in pathological stage or positive surgical margins in men submitted to RP.
  • [MeSH-major] Adenocarcinoma / pathology. Prostate / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biopsy. Cell Proliferation. Humans. Immunohistochemistry / methods. Male. Middle Aged

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  • (PMID = 21044375.001).
  • [ISSN] 1677-6119
  • [Journal-full-title] International braz j urol : official journal of the Brazilian Society of Urology
  • [ISO-abbreviation] Int Braz J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
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92. Morichetti D, Mazzucchelli R, Stramazzotti D, Santinelli A, Lopez-Beltran A, Scarpelli M, Bono AV, Cheng L, Montironi R: Immunohistochemical expression of somatostatin receptor subtypes in prostate tissue from cystoprostatectomies with incidental prostate cancer. BJU Int; 2010 Oct;106(7):1072-80
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  • MATERIALS AND METHODS: The five SSTRs (SSTR1-5) were evaluated in 'normal-looking' epithelium (NEp), high-grade prostatic intraepithelial neoplasia (HGPIN) and pT2a Gleason score 6 adenocarcinoma in 20 CyP specimens with incidental prostate cancer and 20 radical prostatectomy (RP) specimens with clinically detected prostate cancer.
  • RESULTS: For cytoplasm expression, the mean percentage of positive secretory cells with strong cytoplasmic staining increased from NEp to HGPIN and prostate cancer, being slightly lower in the CyP than in the RP specimens.
  • Both in the CyP and RP specimens SSTR4 was found in the highest percentage of cells.
  • There was membrane staining in the secretory cells for SSTR3 and SSTR4.
  • There was nuclear staining in the secretory cells for SSTR4 and SSTR5.
  • For SSTR1 and SSTR3 the mean proportions of positive basal cells were higher than for the other three subtypes, and greater in NEp than in HGPIN.
  • There were positive smooth muscle and endothelial cells for all five SSTR subtypes, the highest proportions being SSTR1 and the lowest SSTR5.
  • [MeSH-major] Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology. Receptors, Somatostatin / metabolism

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  • [Copyright] © 2010 THE AUTHORS. JOURNAL COMPILATION © 2010 BJU INTERNATIONAL.
  • (PMID = 20201837.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Somatostatin
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93. Went PT, Sauter G, Oberholzer M, Bubendorf L: Abundant expression of AMACR in many distinct tumour types. Pathology; 2006 Oct;38(5):426-32
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  • AIMS: Alpha-methylacyl-CoA racemase (AMACR), a mitochondrial and peroxisomal enzyme, is a valuable tool to confirm the diagnosis of prostate cancer, especially if combined with basal cell markers.
  • RESULTS: Microarray analysis revealed that tumours with prominent AMACR expression included adenocarcinomas of the prostate (72%), hepatocellular carcinomas (77%), papillary renal cell carcinomas (70%), and colorectal adenocarcinomas (71%).
  • AMACR expression was equally frequent in colorectal adenomas and carcinomas.
  • In the thyroid, AMACR expression was found in 42% of the follicular carcinomas but in only 16% of follicular adenomas.
  • However, a more detailed analysis on a thyroid tissue microarray did not confirm a significant difference of AMACR expression in follicular adenoma and carcinomas.
  • CONCLUSION: Taken together, the results indicate that AMACR is expressed in a wide variety of adenocarcinomas, and its diagnostic utility is restricted to specific areas.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Neoplasms / metabolism. Racemases and Epimerases / metabolism

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  • (PMID = 17008281.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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94. Wang GF, Lai MD, Yang RR, Chen PH, Su YY, Lv BJ, Sun LP, Huang Q, Chen SZ: Histological types and significance of bronchial epithelial dysplasia. Mod Pathol; 2006 Mar;19(3):429-37
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  • Squamous dysplasia and atypical adenomatous hyperplasia have been identified and classified as preinvasive lesions of squamous cell carcinoma and peripheral pulmonary adenocarcinoma, respectively.
  • By examining 114 resection lung specimens, we concluded that there are four histological patterns of bronchial epithelial dysplasia based on morphological features (basal cell dysplasia, columnar cell dysplasia, bronchial epithelial dysplasia with transitional differentiation, and squamous dysplasia).
  • Basal cell dysplasia was focally positive for cytokeratin (CK) 17 and 10/13; columnar cell dysplasia was generally positive for CK7, 8, and 18; bronchial epithelial dysplasia with transitional differentiation had a heterogeneous immunoprofile, while squamous dysplasia was positive for CK10/13 and focally positive for CK17.
  • (1) bronchial epithelium can develop various patterns of dysplasia with abnormal/ambiguous cell differentiation and abnormal expressions of p53 and Ki-67.
  • [MeSH-minor] Adult. Aged. Bronchial Neoplasms / metabolism. Bronchial Neoplasms / pathology. Carcinoma, Bronchogenic / metabolism. Carcinoma, Bronchogenic / pathology. Cell Differentiation. Epithelial Cells / chemistry. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Keratins / analysis. Ki-67 Antigen / analysis. Male. Middle Aged. Respiratory Mucosa / chemistry. Respiratory Mucosa / pathology. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16415791.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins
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95. Muqit MM, Roberts F: In regards to Conill et al.: Brachytherapy with 192Ir as treatment of carcinoma of the tarsal structure of the eyelid (Int J Radiat Oncol Bio Phys 2004;59:1326-1329). Int J Radiat Oncol Biol Phys; 2006 Jul 1;65(3):959
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / radiotherapy. Carcinoma, Basal Cell / pathology. Carcinoma, Basal Cell / radiotherapy. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / radiotherapy. Humans. Iridium Radioisotopes / therapeutic use

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  • [CommentOn] Int J Radiat Oncol Biol Phys. 2004 Aug 1;59(5):1326-9 [15275716.001]
  • (PMID = 16751086.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iridium Radioisotopes
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96. 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.
  • Anti-epithelial membrane antigen strongly labeled tumor cells and highlighted ductal structures.
  • Less than 1% of cells expressed progesterone or estrogen receptors.
  • Her2/neu reactivity was focally present, showing 1+ membranous reactivity in 10% of cells.
  • Anti-p63 labeled basaloid cells surrounding the tumor lobules.
  • This report illustrates an extraordinary case of adnexal neoplasia displaying various lines of differentiation arising in association with nevus sebaceus.
  • [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


97. Gerdes MJ, Yuspa SH: The contribution of epidermal stem cells to skin cancer. Stem Cell Rev; 2005;1(3):225-31
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  • [Title] The contribution of epidermal stem cells to skin cancer.
  • Tumors arising from the skin are of multiple phenotypes, with differing degrees of malignant potential.
  • In mouse models of skin carcinogenesis, tumors of squamous phenotype are the most common; however, human disease indicates that multiple phenotypes may arise from a common pool of stem cells that are then influenced by epigenetic factors.
  • The use of transgenic and knockout gene technologies with mice is unraveling some of the specific genes regulating fate determination in stem cells other than squamous lineage, including basal cell carcinoma and sebaceous adenomas.
  • The following review examines the evidence for the stem cell origin of epidermal tumors and the contribution of some specific gene families toward stem cell fate decisions during epidermal tumor progression.
  • [MeSH-major] Adenocarcinoma, Sebaceous / genetics. Carcinoma, Basal Cell / genetics. Epidermis. Epigenesis, Genetic. Neoplastic Stem Cells. Skin Neoplasms / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Gene Expression Regulation, Neoplastic / genetics. Humans. Mice. Mice, Knockout