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1. Akan B, Böhmig G, Sunder-Plassmann G, Borchhardt KA: Prevalence of hypercalcitoninemia in patients on maintenance dialysis referred to kidney transplantation. Clin Nephrol; 2009 May;71(5):538-42
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  • AIMS: Elevated calcitonin concentrations in dialysis patients had led to thyroidectomy for a benign C-cell hyperplasia in dozens of patients in the past decade.
  • All patients with basal calcitonin concentrations above 50 pg/ml were men (highest calcitonin concentration was 290 pg/ml).
  • Two of them underwent thyroidectomy and had C-cell hyperplasia.
  • [MeSH-major] Biomarkers, Tumor / blood. Calcitonin / blood. Carcinoma, Medullary / epidemiology. Kidney Failure, Chronic / therapy. Kidney Transplantation. Renal Dialysis / methods. Thyroid Neoplasms / epidemiology


2. DeVilliers P, Liu H, Suggs C, Simmons D, Daly B, Zhang S, Raubenheimer E, Larsson A, Wright T: Calretinin expression in the differential diagnosis of human ameloblastoma and keratocystic odontogenic tumor. Am J Surg Pathol; 2008 Feb;32(2):256-60
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  • [Title] Calretinin expression in the differential diagnosis of human ameloblastoma and keratocystic odontogenic tumor.
  • Ameloblastoma is a benign, locally aggressive epithelial odontogenic tumor that has the potential to become malignant and produce metastasis to distant sites such as lungs and kidneys.
  • The histologic presentation can be, in some instances, mistaken for keratocystic odontogenic tumor (KCOT) (formerly known as odontogenic keratocyst).
  • Gene expression profiling of ameloblastomas showed CALB2 expressed in the basal cell layer of columnar cells resembling preameloblasts, in all 5 of the ameloblastomas evaluated.
  • [MeSH-major] Ameloblastoma / diagnosis. Biomarkers, Tumor / metabolism. Jaw Neoplasms / diagnosis. Odontogenic Cysts / diagnosis. Odontogenic Tumors / diagnosis. S100 Calcium Binding Protein G / metabolism
  • [MeSH-minor] Calbindin 2. Diagnosis, Differential. Gene Expression. Gene Expression Profiling. Humans. RNA, Messenger / metabolism. RNA, Neoplasm / analysis

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  • (PMID = 18223328.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / DE016079
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / S100 Calcium Binding Protein G
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3. Shimanovich I, Krahl D, Rose C: Trichoadenoma of Nikolowski is a distinct neoplasm within the spectrum of follicular tumors. J Am Acad Dermatol; 2010 Feb;62(2):277-83
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  • [Title] Trichoadenoma of Nikolowski is a distinct neoplasm within the spectrum of follicular tumors.
  • BACKGROUND: Trichoadenoma is a rare benign follicular tumor first described by Nikolowski 50 years ago.
  • In trichoadenoma the cystic component predominates, while desmoplastic trichoepithelioma is a mostly solid neoplasm.
  • OBJECTIVE: The aim of this study was to investigate whether the morphologic overlap between trichoadenoma and desmoplastic trichoepithelioma translates into a similar immunohistochemical profile.
  • Trichoadenoma is a distinct follicular tumor related but not identical to desmoplastic trichoepithelioma.
  • [MeSH-major] Neoplasms, Basal Cell / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / metabolism. Female. Head and Neck Neoplasms / pathology. Humans. Immunohistochemistry. Keratin-20 / metabolism. Male. Merkel Cells / pathology. Middle Aged. Neoplasms, Fibroepithelial / pathology. Receptors, Androgen / metabolism. Skin / chemistry

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  • [Copyright] Copyright (c) 2009 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20115950.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Biomarkers, Tumor; 0 / Keratin-20; 0 / Receptors, Androgen; 0 / human epithelial antigen-125
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4. González-Moles MA, Mosqueda-Taylor A, Delgado-Rodríguez M, Martínez-Mata G, Gil-Montoya JA, Díaz-Franco MA, Bravo-Pérez JJ, M-González N: Analysis of p53 protein by PAb240, Ki-67 expression and human papillomavirus DNA detection in different types of odontogenic keratocyst. Anticancer Res; 2006 Jan-Feb;26(1A):175-81
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  • MATERIALS AND METHODS: Eighty-three OKC samples (29 cases associated with nevoid basal cell carcinoma syndrome, 29 solitary non-recurrent cases 20 solitary recurrent cases, and 5 chondroid keratocysts) were studied by immunohistochemistry to detect p53 protein (PAb 244) and Ki-67 (MIB-1) expression, and by PCR to detect HPV DNA.
  • The suprabasal expression of Ki-67 was significantly more frequent than its basal expression (p < 0.001).
  • OKCs show proliferation and genuine maturation behavior reminiscent of benign neoplasms with local destructive capacity.
  • [MeSH-major] DNA, Viral / analysis. Ki-67 Antigen / biosynthesis. Odontogenic Cysts / metabolism. Odontogenic Cysts / virology. Papillomaviridae / genetics. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Carcinoma, Basal Cell / metabolism. Carcinoma, Basal Cell / pathology. Carcinoma, Basal Cell / virology. Female. Humans. Immunohistochemistry. Male

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  • (PMID = 16475695.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Ki-67 Antigen; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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5. Garnier B, Simon E, Dumont T, Sellal S, Stricker M, Chassagne JF: [Goal cell carcinoma: really a low malignancy tumor?]. Rev Stomatol Chir Maxillofac; 2005 Feb;106(1):16-21
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  • [Title] [Goal cell carcinoma: really a low malignancy tumor?].
  • [Transliterated title] Les carcinomes cutanés basocellulaires méritent-ils leur réputation de tumeurs à faible malignité?
  • Although basal cell carcinoma often presents as a fairly "benign" lesion early in its course, it remains the most frequent malignancy worldwide.
  • We show that advanced basal cell carcinoma can be mutilating or even life threatening depending on location, type of lesion, or pre-existing co-morbidity.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Facial Neoplasms / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Humans. Neoplasm Invasiveness

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  • (PMID = 15798647.001).
  • [ISSN] 0035-1768
  • [Journal-full-title] Revue de stomatologie et de chirurgie maxillo-faciale
  • [ISO-abbreviation] Rev Stomatol Chir Maxillofac
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 22
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6. Ali TZ, Epstein JI: Basal cell carcinoma of the prostate: a clinicopathologic study of 29 cases. Am J Surg Pathol; 2007 May;31(5):697-705
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  • [Title] Basal cell carcinoma of the prostate: a clinicopathologic study of 29 cases.
  • We studied 29 cases of basal cell carcinoma of the prostate including what others call adenoid cystic carcinoma of the prostate.
  • Other patterns included: basal cell hyperplasialike in 9 cases (32%); small tubules occasionally lined by a hyaline rim in 9 cases (32%), with 4 of these cases also demonstrating intermingling cords of cells; and large solid nests in 8 cases (28.5%), 5 of which had central necrosis.
  • Infiltration around benign glands was seen in 10 (36%) cases, with predominantly small nests and AC-P.
  • Perineural and vascular invasion was seen in 2 basal cell carcinomas with large basaloid nests.
  • Basal cell markers (HMWCK, p63) either:.
  • Basal cell carcinomas are rare tumors with a broad morphologic spectrum.
  • The most common morphology among those with an aggressive behavior is large solid nests more often with central necrosis, high Ki67%, and less staining with basal cell markers.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Biopsy, Needle. Combined Modality Therapy. Humans. Male. Middle Aged. Mitosis. Neoplasm Recurrence, Local. Retrospective Studies. Transurethral Resection of Prostate

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  • (PMID = 17460452.001).
  • [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 / Biomarkers, Tumor
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7. Weyers W, Hörster S, Diaz-Cascajo C: Tumor of follicular infundibulum is Basal cell carcinoma. Am J Dermatopathol; 2009 Oct;31(7):634-41
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  • [Title] Tumor of follicular infundibulum is Basal cell carcinoma.
  • Tumor of follicular infundibulum (TFI) is currently thought to be a benign epithelial neoplasm with follicular differentiation.
  • It is encountered commonly in association with basal cell carcinoma (BCC), often as an incidental finding.
  • [MeSH-major] Carcinoma, Basal Cell / classification. Carcinoma, Basal Cell / pathology. Skin Neoplasms / classification. Skin Neoplasms / pathology

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  • (PMID = 19652582.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Segura S, Puig S, Carrera C, Palou J, Malvehy J: Dendritic cells in pigmented basal cell carcinoma: a relevant finding by reflectance-mode confocal microscopy. Arch Dermatol; 2007 Jul;143(7):883-6
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  • [Title] Dendritic cells in pigmented basal cell carcinoma: a relevant finding by reflectance-mode confocal microscopy.
  • A few studies of RCM on basal cell carcinoma (BCC) have provided specific diagnostic criteria, but large studies on pigmented basal cell carcinoma are lacking.
  • Proliferation of large dendritic-shaped cells within a melanocytic tumor has been associated with the diagnosis of melanoma by RCM.
  • Benign melanocytes and Langerhans cells may populate BCC according to previous histological studies.
  • OBSERVATIONS: Reflectance-mode confocal microscopy revealed highly refractive dendritic structures within tumor nests that correlated with the presence of melanocytes within the tumor by immunochemical analysis.
  • [MeSH-major] Carcinoma, Basal Cell / diagnosis. Dendritic Cells / cytology. Skin Neoplasms / diagnosis

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  • (PMID = 17638732.001).
  • [ISSN] 0003-987X
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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9. Hameed O, Sublett J, Humphrey PA: Immunohistochemical stains for p63 and alpha-methylacyl-CoA racemase, versus a cocktail comprising both, in the diagnosis of prostatic carcinoma: a comparison of the immunohistochemical staining of 430 foci in radical prostatectomy and needle biopsy tissues. Am J Surg Pathol; 2005 May;29(5):579-87
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  • Immunostains, such as those directed against the basal cell marker p63 and, more recently, employing antibodies reactive with alpha-methylacyl-CoA racemase (AMACR), can be useful in this situation.
  • A retrospective review of 31 consecutive radical prostatectomy specimens and 150 prostate needle biopsy samples was performed to select histologic sections showing foci of prostatic carcinoma and/or minimal prostatic carcinoma, high-grade prostatic intraepithelial neoplasia (HGPIN), as well as common benign mimickers of prostatic carcinoma, to include atrophy and basal cell hyperplasia, especially with prominent nucleoli.
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biopsy, Needle. Cell Nucleus / chemistry. Cell Nucleus / pathology. Humans. Male. Retrospective Studies

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  • (PMID = 15832080.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Conference; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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10. Ulukaya E, Yilmaztepe A, Akgoz S, Linder S, Karadag M: The levels of caspase-cleaved cytokeratin 18 are elevated in serum from patients with lung cancer and helpful to predict the survival. Lung Cancer; 2007 Jun;56(3):399-404
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  • Caspase-cleaved cytokeratin 18 fragments (M30 antigen) can be detected in the circulation of patients with carcinoma and are believed to reflect cell death of tumors of epithelial origin.
  • We here measured the levels of such fragments in patients with lung cancer (n=60), patients with benign lung disease (n=22) and healthy control subjects (n=32).
  • Basal M30 antigen levels were evaluated with regard to their predictive power of survival.
  • Patients with basal M30 antigen levels higher than 43.8 U/L had significantly shorter median survival than those with lower basal M30 antigen levels (p=0.013; hazard ratio: 3.9) (95% CI=1.3-11.4).
  • [MeSH-major] Biomarkers, Tumor / blood. Keratin-18 / blood. Lung Neoplasms / blood. Lung Neoplasms / mortality

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  • (PMID = 17316892.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Epitopes; 0 / Keratin-18
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11. Ritwik P, Brannon RB: Peripheral odontogenic fibroma: a clinicopathologic study of 151 cases and review of the literature with special emphasis on recurrence. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2010 Sep;110(3):357-63
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  • OBJECTIVE: The peripheral odontogenic fibroma (POdF) is a rare benign neoplasm of odontogenic origin with limited data on recurrence.
  • RESULTS: POdF should be considered a mixed odontogenic tumor because it is composed of active odontogenic epithelial and ectomesenchymal components.
  • Budding of the basal cell layer of the surface squamous epithelium was associated with higher recurrence (P=.0186); 27 cases with recurrence which exhibited this feature.
  • [MeSH-major] Fibroma / pathology. Jaw Neoplasms / pathology. Neoplasm Recurrence, Local / pathology. Odontogenic Tumors / pathology
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Child. Child, Preschool. Follow-Up Studies. Humans. Infant. Infant, Newborn. Logistic Models. Male. Middle Aged. Mixed Tumor, Malignant / pathology. Sex Distribution. Time Factors. Young Adult

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  • [Copyright] Copyright (c) 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20674403.001).
  • [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] Journal Article; Review
  • [Publication-country] United States
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12. Mogensen M, Joergensen TM, Nürnberg BM, Morsy HA, Thomsen JB, Thrane L, Jemec GB: Assessment of optical coherence tomography imaging in the diagnosis of non-melanoma skin cancer and benign lesions versus normal skin: observer-blinded evaluation by dermatologists and pathologists. Dermatol Surg; 2009 Jun;35(6):965-72
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  • [Title] Assessment of optical coherence tomography imaging in the diagnosis of non-melanoma skin cancer and benign lesions versus normal skin: observer-blinded evaluation by dermatologists and pathologists.
  • OBJECTIVES: To describe OCT features in NMSC such as actinic keratosis (AK) and basal cell carcinoma (BCC) and in benign lesions and to assess the diagnostic accuracy of OCT in differentiating NMSC from benign lesions and normal skin.
  • Observer-blinded evaluation of OCT images from 64 BCCs, 1 baso-squamous carcinoma, 39 AKs, two malignant melanomas, nine benign lesions, and 105 OCT images from perilesional skin was performed; 50 OCT images of NMSC and 50 PS-OCT images of normal skin were evaluated twice.
  • OCT diagnosis is less accurate than clinical diagnosis, but high accuracy in distinguishing lesions from normal skin, crucial for delineating tumor borders, was obtained.

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  • (PMID = 19397661.001).
  • [ISSN] 1524-4725
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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13. Nur S, Chuang L, Ramaswamy G: Immunohistochemical characterization of cancer antigen in uterine cancers. Int J Gynecol Cancer; 2006 Sep-Oct;16(5):1903-10
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  • Ninety cases of primary uterine carcinomas (65 endometrioid [EM] carcinoma, 15 serous papillary [SP] carcinoma, 6 carcinosarcomas [malignant mixed müllerian tumors], and 4 clear cell carcinoma [CC]) and adjacent atrophic and/or hyperplastic endometrium were analyzed by IHC for CA-125 expression.
  • The percentage and intensity of luminal, apical, basal, and diffuse cytoplasmic immunostaining of epithelial cells were categorized on a scale of 0-4.
  • In malignant mixed müllerian tumors (MMMT), the epithelial component stained as above according to the type of epithelial cell differentiation of the neoplastic cells.
  • Benign proliferative glands showed moderate apical luminal, basal, and cytoplasmic staining.
  • [MeSH-major] Adenocarcinoma / metabolism. CA-125 Antigen / metabolism. Endometrial Neoplasms / metabolism. Endometrium / metabolism. Mixed Tumor, Mullerian / metabolism

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  • (PMID = 17009990.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CA-125 Antigen
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14. Glen A, Gan CS, Hamdy FC, Eaton CL, Cross SS, Catto JW, Wright PC, Rehman I: iTRAQ-facilitated proteomic analysis of human prostate cancer cells identifies proteins associated with progression. J Proteome Res; 2008 Mar;7(3):897-907
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  • In order to gain an insight into the molecular mechanisms associated with prostate cancer progression, we employed the shot-gun proteomic approach of isobaric tags for relative and absolute quantitation (iTRAQ), followed by 2D-LC-MS/MS, using the poorly metastatic LNCaP cell line and its highly metastatic variant LNCaP-LN3 cell line as a model.
  • Differential expression of brain creatine kinase (CKBB), soluble catechol-O-methyltransferase (S-COMT), tumor rejection antigen (gp96), and glucose regulated protein, 78 kDa (grp78), was confirmed by Western blotting or independent 2D-PAGE analysis.
  • The clinical relevance of gp96 was assessed by immunohistochemistry using prostate tissues from benign ( n = 95), malignant ( n = 66), and metastatic cases ( n = 3).
  • Benign epithelium showed absent/weak gp96 expression in the basal cells, in contrast to the moderate/strong expression seen in malignant epithelium.
  • Furthermore, there was a statistically significant difference in the intensity of gp96 expression between benign and malignant cases ( p < 0.0005, Mann-Whitney U).
  • [MeSH-major] Neoplasm Proteins / metabolism. Prostatic Neoplasms / metabolism. Proteomics
  • [MeSH-minor] Cell Line, Tumor. Chromatography, Liquid. Disease Progression. Electrophoresis, Gel, Two-Dimensional. Humans. Immunohistochemistry. Male. Reproducibility of Results. Spectrometry, Mass, Electrospray Ionization / methods


15. Reszec J, Sulkowski S: The expression of P53 protein and infection of human papilloma virus in conjunctival and eyelid neoplasms. Int J Mol Med; 2005 Oct;16(4):559-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim of this study was to evaluate P53 protein expression and to detect HPV in the tissue samples of 45 benign (papillomas) and 38 malignant conjunctival and eyelid lesions (27 basal cell carcinomas and 11 squamous cell carcinomas).
  • We also looked for eventual relationships between P53 expression and clinicopathological features such as age, histological type of tumor, grading and staging.
  • We revealed P53 protein expression in 30 out of 45 (66.6%) squamous cell papillomas.
  • In the SCC and BCC groups, P53 was present in 31 out of 38 carcinomas and there was a statistically significant correlation between histological type of tumor and P53 protein expression.
  • Malignant type HPV 16 and 18 were detected in three squamous cell papillomas, two BCCs and one SCC.
  • P53 is probably involved in the development of conjunctival and eyelid tumors due to its high rate of presence in both benign and malignant neoplasms of these organs.
  • [MeSH-major] Conjunctival Neoplasms / pathology. Eyelid Neoplasms / pathology. Papillomaviridae. Papillomavirus Infections / pathology. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adult. Carcinoma, Basal Cell / metabolism. Carcinoma, Basal Cell / pathology. Carcinoma, Basal Cell / virology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / virology. Humans. Middle Aged. Papilloma / metabolism. Papilloma / pathology. Papilloma / virology

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  • (PMID = 16142387.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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16. Marchiani S, Bonaccorsi L, Ferruzzi P, Crescioli C, Muratori M, Adorini L, Forti G, Maggi M, Baldi E: The vitamin D analogue BXL-628 inhibits growth factor-stimulated proliferation and invasion of DU145 prostate cancer cells. J Cancer Res Clin Oncol; 2006 Jun;132(6):408-16
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  • In the present study, we have investigated the effect of the nonhypercalcemic vitamin D analogue BXL-628 on proliferation and invasive properties of the human PC cell line DU145.
  • METHODS: Cell proliferation was determined by cell counting.
  • RESULTS: BXL-628 is able to inhibit both proliferation and invasion of DU145 cells in basal conditions and in response to KGF.
  • CONCLUSIONS: Our results demonstrate that the vitamin D analogue BXL-628 is able to suppress KGF-induced proliferation and invasion of AI-PC cells in vitro, prospecting a possible use of the drug, which is currently in phase II clinical studies for benign prostatic hyperplasia, in the treatment of advanced prostate cancer.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Male. Neoplasm Invasiveness. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • [Cites] J Cell Sci. 2004 Mar 1;117(Pt 7):1235-46 [14996943.001]
  • [Cites] J Cancer Res Clin Oncol. 2004 Oct;130(10):604-14 [15258753.001]
  • [Cites] Biochim Biophys Acta. 1998 Dec 8;1436(1-2):127-50 [9838078.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1997 Sep;6(9):727-32 [9298581.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jul;85(7):2576-83 [10902811.001]
  • [Cites] Prostate. 2002 Jan 1;50(1):15-26 [11757032.001]
  • [Cites] Invest New Drugs. 2003 Aug;21(3):341-5 [14578682.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):455-60 [15659491.001]
  • [Cites] Exp Biol Med (Maywood). 2004 Apr;229(4):277-84 [15044710.001]
  • [Cites] Clin Chem. 1998 Apr;44(4):705-23 [9554481.001]
  • [Cites] Biochim Biophys Acta. 1997 Feb 4;1355(2):155-66 [9042336.001]
  • [Cites] Cell Growth Differ. 2000 Apr;11(4):221-9 [10775039.001]
  • [Cites] Int J Cancer. 2004 Oct 20;112(1):78-86 [15305378.001]
  • [Cites] World J Urol. 2005 Feb;23(1):28-32 [15668801.001]
  • [Cites] Science. 2004 Mar 19;303(5665):1800-5 [15031492.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 Nov;92 (4):307-15 [15663994.001]
  • [Cites] J Urol. 1999 Apr;161(4):1329-36 [10081903.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):305-8 [10667581.001]
  • [Cites] J Urol. 2005 Jan;173(1):10-20 [15592017.001]
  • [Cites] Integr Cancer Ther. 2004 Dec;3(4):349-80 [15523106.001]
  • [Cites] Endocr Rev. 2005 Aug;26(5):662-87 [15798098.001]
  • [Cites] World J Urol. 2005 Feb;23(1):1-9 [15770516.001]
  • [Cites] Lancet. 2003 Mar 8;361(9360):859-64 [12642065.001]
  • [Cites] Mol Cell Endocrinol. 2000 Jun;164(1-2):133-43 [11026565.001]
  • [Cites] Prostate. 1999 Dec 1;41(4):233-42 [10544296.001]
  • [Cites] J Lab Clin Med. 1999 Feb;133(2):120-8 [9989763.001]
  • [Cites] Eur J Endocrinol. 2004 Apr;150(4):591-603 [15080791.001]
  • [Cites] Cancer Res. 1987 Jun 15;47(12):3239-45 [2438036.001]
  • [Cites] Bull Cancer. 2005 Feb;92(2):E13-8 [15749638.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):519-26 [15225831.001]
  • [Cites] Cancer Treat Res. 2003;115:145-67 [12613196.001]
  • [Cites] Endocrinology. 2003 Jul;144(7):3046-57 [12810561.001]
  • [Cites] FEBS Lett. 2000 Jul 14;477(1-2):1-7 [10899301.001]
  • [Cites] Endocrinology. 2003 May;144(5):1653-5 [12697667.001]
  • [Cites] Endocrinology. 2000 Sep;141(9):3172-82 [10965888.001]
  • [Cites] J Cancer Res Clin Oncol. 2003 Mar;129(3):165-74 [12712332.001]
  • (PMID = 16485114.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / BXL628; 126469-10-1 / Fibroblast Growth Factor 7; FXC9231JVH / Calcitriol
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17. Yang HM, Cabral E, Dadras SS, Cassarino DS: Immunohistochemical expression of D2-40 in benign and malignant sebaceous tumors and comparison to basal and squamous cell carcinomas. Am J Dermatopathol; 2008 Dec;30(6):549-54
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  • [Title] Immunohistochemical expression of D2-40 in benign and malignant sebaceous tumors and comparison to basal and squamous cell carcinomas.
  • The distinction of sebaceous carcinoma from benign sebaceous proliferations and other tumors is therefore of utmost importance, and immunohistochemistry may be useful in this differential.
  • A total of 36 cases of sebaceous lesions, including 16 sebaceous carcinomas, 7 sebaceous adenomas, 6 sebaceomas, and 7 cases of normal glands and sebaceous hyperplasia, and 17 cases of basal cell carcinoma and 10 cases of squamous cell carcinoma, were also examined.
  • We found no significant increase in tumor lymphangiogenesis by semiquantitative scoring of lymphovascular density per square millimeter of tumoral/peritumoral stroma in sebaceous carcinoma versus benign sebaceous proliferations.
  • However, D2-40 staining showed a different pattern in the benign tumors, which were positive only in the basaloid cells (most pronounced in sebaceoma), versus sebaceous carcinoma, which was either negative or focally positive in a haphazard pattern in most cases, although some cases of basaloid sebaceous carcinomas showed strong positivity.
  • We also found D2-40 to be only weakly and focally positive in basal cell carcinoma and weakly to moderately positive in squamous cell carcinoma, which showed increased staining with decreased differentiation.
  • Therefore, overall, D2-40 is, of limited diagnostic utility in sebaceous lesions but may be useful in distinguishing sebaceoma and basaloid sebaceous carcinoma from basal cell carcinoma.
  • [MeSH-major] Adenocarcinoma, Sebaceous / metabolism. Antibodies, Monoclonal / metabolism. Carcinoma, Basal Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Sebaceous Gland Neoplasms / metabolism. Sebaceous Glands / metabolism. Skin Neoplasms / metabolism
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / metabolism. Adenoma / pathology. Antibodies, Monoclonal, Murine-Derived. Biomarkers, Tumor / metabolism. Case-Control Studies. Cell Proliferation. Diagnosis, Differential. Humans. Hyperplasia / diagnosis. Hyperplasia / metabolism. Hyperplasia / pathology

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  • (PMID = 19033927.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Biomarkers, Tumor; 0 / monoclonal antibody D2-40
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18. Bordbar A, Dias D, Cabral A, Beck S, Boon ME: Assessment of cell proliferation in benign, premalignant and malignant skin lesions. Appl Immunohistochem Mol Morphol; 2007 Jun;15(2):229-35
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  • [Title] Assessment of cell proliferation in benign, premalignant and malignant skin lesions.
  • A deeper understanding of the variance of epidermal cell proliferation may eventually increase the reproducibility of diagnostic classification.
  • A prospective study of 46 consecutive, unselected biopsies from benign (keratoacanthoma n=14), premalignant (actinic keratosis n=15 and Bowen disease n=10) and malignant (squamous cell carcinoma n=7) skin lesions was studied to assess the presence and extent of differences in expression of the proliferation marker Ki-67 using a monoclonal antibody directed against a c-DNA defined subsegment (MIB-1) and a noncross-linking, proprietary fixative BoonFix.
  • MIB-1 was expressed in the adjacent, non-affected skin in a scattered to confluent linear pattern in the basal/suprabasal cell layer.
  • In actinic keratosis, MIB-1 expression, in addition to basal/suprabasal layers, extended to mid-zones of the epidermis.
  • In invasive squamous cell carcinoma, MIB-1 expression was not consistent between and within cases.
  • Keratoacanthoma cases showed highly variable MIB-1 expression, ranging from no expression to expression in both basal/suprabasal and mid-zone layers of the epidermis.
  • These results warrant further study of modulation of cell proliferation in actinic keratosis.

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  • (PMID = 17525640.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / MIB-1 antibody
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19. Rentsch CA, Cecchini MG, Schwaninger R, Germann M, Markwalder R, Heller M, van der Pluijm G, Thalmann GN, Wetterwald A: Differential expression of TGFbeta-stimulated clone 22 in normal prostate and prostate cancer. Int J Cancer; 2006 Feb 15;118(4):899-906
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  • Verification of their mRNA expression by real-time PCR in patient-matched NP and PC bulk tissue, in laser-captured pure epithelial and cancer cells and in NP and PC cell lines confirmed TSC-22 underexpression, but not Id4 overexpression, in PC and in human PC cell lines.
  • Immunohistochemical analysis showed that TSC-22 protein expression in NP is restricted to the basal cells and colocalizes with the basal cell marker cytokeratin 5.
  • Likewise, PC cell lines do not show detectable TSC-22 protein expression as shown by immunoblotting.
  • TSC-22 should be considered as a novel basal cell marker, potentially useful for studying lineage determination within the epithelial compartment of the prostate.
  • Accordingly, TSC-22 immunohistochemistry may prove to be a diagnostic tool for discriminating benign lesions from malignant ones of the prostate.
  • The suggested tumour suppressor function of TSC-22 warrants further investigation on its role in prostate carcinogenesis and on the TSC-22 pathway as a candidate therapeutic target in PC.
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. Tumor Cells, Cultured

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  • (PMID = 16106424.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / TSC22D1 protein, human; 0 / Transforming Growth Factor beta
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20. Veeresh M, Bavle RM, Vinay KN, Nandakumar H: Basal cell adenoma of the submandibular gland. J Maxillofac Oral Surg; 2010 Sep;9(3):289-91
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  • [Title] Basal cell adenoma of the submandibular gland.
  • Basel cell adenoma is a benign epithelial salivary gland tumor that appears to have unique histologic characteristics.
  • Here we report a case of basel cell adenoma of submandibular gland.

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  • (PMID = 22190808.001).
  • [ISSN] 0974-942X
  • [Journal-full-title] Journal of maxillofacial and oral surgery
  • [ISO-abbreviation] J Maxillofac Oral Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3177454
  • [Keywords] NOTNLM ; Adenoma / Basal cells / Submandibular gland
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21. Sotomayor P, Godoy A, Smith GJ, Huss WJ: Oct4A is expressed by a subpopulation of prostate neuroendocrine cells. Prostate; 2009 Mar 1;69(4):401-10
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  • The stem cell properties of self-renewal and pluripotency in embryonic stem cells and germ cells are regulated by Oct4A, a splice variant of the POU5F1 (Oct3/4) gene, while the function of the alternative splice variant, Oct4B, is unknown.
  • RESULTS: Rare Oct4A expressing cells are present in human benign and malignant prostate glands and the number of Oct4A expressing cells increases in prostate cancers with high Gleason scores.
  • Oct4A expressing cells were non-proliferative, and did not co-express markers of basal epithelial cell or luminal epithelial cell differentiation, or AMACR, a marker of prostate cancer epithelial cells.
  • A subpopulation of the Oct4A expressing cells co-expressed Sox2, an embryonic stem cell marker, but did not express other putative stem cell markers, such as ABCG2, NANOG or CD133.
  • CONCLUSION: The increased number of cells that expressed Oct4A in prostate cancer compared to benign prostate, and in cancers of increasing grade, suggests that Oct4A/Chromogranin A co-expressing cells represent neuroendocrine cells in prostate cancer.

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  • [Copyright] 2008 Wiley-Liss, Inc.
  • [Cites] Am J Surg Pathol. 2007 Jun;31(6):836-45 [17527070.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4807-15 [17510410.001]
  • [Cites] J Biol Chem. 2007 Jul 20;282(29):21551-60 [17525163.001]
  • [Cites] Eur Urol. 2007 Nov;52(5):1365-73 [17126478.001]
  • [Cites] Endocr Relat Cancer. 2007 Sep;14(3):531-47 [17914087.001]
  • [Cites] Cell. 2007 Nov 30;131(5):861-72 [18035408.001]
  • [Cites] Exp Cell Res. 2008 Jan 1;314(1):92-102 [17900565.001]
  • [Cites] Science. 2007 Dec 21;318(5858):1917-20 [18029452.001]
  • [Cites] Nature. 2008 Jan 10;451(7175):141-6 [18157115.001]
  • [Cites] Cell Stem Cell. 2007 Oct 11;1(4):364-6 [18371374.001]
  • [Cites] Endocr Relat Cancer. 1999 Dec;6(4):503-19 [10730904.001]
  • [Cites] Pathol Res Pract. 2000;196(5):277-84 [10834383.001]
  • [Cites] Stem Cells. 2001;19(4):271-8 [11463946.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Ann Oncol. 2001;12 Suppl 2:S159-64 [11762345.001]
  • [Cites] Cancer. 2002 Sep 1;95(5):1028-36 [12209687.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] J Histochem Cytochem. 2003 Jun;51(6):697-706 [12754281.001]
  • [Cites] J Biol Chem. 2004 May 28;279(22):23495-503 [15047715.001]
  • [Cites] Prostate. 2004 Jul 1;60(2):91-7 [15162375.001]
  • [Cites] Cell Tissue Res. 2004 Jun;316(3):369-76 [15127288.001]
  • [Cites] Am J Surg Pathol. 2004 Jul;28(7):935-40 [15223965.001]
  • [Cites] J Cell Sci. 2004 Jul 15;117(Pt 16):3539-45 [15226377.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2004;7(3):188-94 [15289813.001]
  • [Cites] Development. 2004 Oct;131(20):4955-64 [15371309.001]
  • [Cites] Cancer Res. 1988 Apr 15;48(8):1996-2004 [2450643.001]
  • [Cites] Nucleic Acids Res. 1992 Sep 11;20(17):4613-20 [1408763.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Mod Pathol. 1995 Aug;8(6):591-8 [8532689.001]
  • [Cites] Mol Cell Biol. 1997 Jan;17(1):154-62 [8972195.001]
  • [Cites] J Urol. 1997 Jul;158(1):171-4 [9186347.001]
  • [Cites] Br J Urol. 1997 Aug;80(2):281-6 [9284203.001]
  • [Cites] Prostate. 1999 May;39(2):135-48 [10221570.001]
  • [Cites] Carcinogenesis. 2005 Feb;26(2):495-502 [15513931.001]
  • [Cites] Am J Pathol. 2005 Feb;166(2):545-55 [15681837.001]
  • [Cites] J Biol Chem. 2005 Feb 25;280(8):6265-8 [15640145.001]
  • [Cites] Cell. 2005 May 6;121(3):465-77 [15882627.001]
  • [Cites] Cancer Res. 2005 Aug 1;65(15):6640-50 [16061644.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Dec 2;337(4):1047-51 [16229821.001]
  • [Cites] Cancer. 2005 Nov 15;104(10):2255-65 [16228988.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10946-51 [16322242.001]
  • [Cites] Endocr Relat Cancer. 2006 Mar;13(1):151-67 [16601285.001]
  • [Cites] Endocr Relat Cancer. 2006 Mar;13(1):181-95 [16601287.001]
  • [Cites] Eur J Cancer. 2006 Jun;42(9):1213-8 [16632344.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8598-607 [16951173.001]
  • [Cites] Prostate. 2006 Sep 15;66(13):1399-406 [16865726.001]
  • [Cites] J Biol Chem. 2006 Nov 3;281(44):33554-65 [16951404.001]
  • [Cites] Biochem Pharmacol. 2006 Nov 30;72(11):1577-88 [16854382.001]
  • [Cites] Stem Cells. 2006 Dec;24(12):2685-91 [16916925.001]
  • [Cites] Mol Carcinog. 2007 Jan;46(1):1-14 [16921491.001]
  • [Cites] Nat Cell Biol. 2007 Jan;9(1):72-9 [17159997.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):111-5 [17122771.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):106-10 [17122772.001]
  • [Cites] Int J Cancer. 2007 Apr 1;120(7):1598-602 [17205510.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2007;10(1):6-14 [17075603.001]
  • [Cites] Mol Vis. 2007;13:823-32 [17615543.001]
  • (PMID = 19058139.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / P01 CA077739-050005; United States / NCI NIH HHS / CA / CA077739-040005; United States / NCI NIH HHS / CA / P01 CA077739; United States / NCI NIH HHS / CA / CA77739; United States / NCI NIH HHS / CA / CA077739-050005; United States / NCI NIH HHS / CA / CA016056; United States / NCI NIH HHS / CA / P01 CA077739-040005
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / RNA, Messenger; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors; 0 / Synaptophysin
  • [Other-IDs] NLM/ NIHMS197155; NLM/ PMC2865184
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22. Trepp R, Padberg BC, Varga Z, Cathomas R, Inauen R, Reinhart WH: Extensive extranodal metastases of basal-like breast cancer with predominant myoepithelial spindle cell differentiation. Pathol Res Pract; 2010 May 15;206(5):334-7
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  • [Title] Extensive extranodal metastases of basal-like breast cancer with predominant myoepithelial spindle cell differentiation.
  • These include multifocal myoepitheliomatosis, the rare mixed tumor or pleomorphic adenoma, adenoid cystic carcinoma, adenomyoepithelioma and myoepithelial carcinoma (malignant myoepithelioma).
  • All these tumors are benign and/or of low-grade malignancy, with the exception of malignant myoepithelioma.
  • The presented case of a breast carcinoma with dominant myoepithelial/spindle cell differentiation in a 58-year-old woman is an excellent example to document the highly aggressive biological behavior of this tumor phenotype.
  • Despite an extensive chemotherapy and radiotherapy, the tumor was rapidly progressive, forming a finally exulcerating local tumor relapse and widespread metastases to the myocardium, lungs, liver, kidneys and skin.
  • Similarities in morphology and biological behavior compared to patients with "triple-negative" (hormone receptor and Her2) monophasic sarcomatoid carcinomas and pure spindle cell sarcomas are discussed.
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic / pathology. Fatal Outcome. Female. Humans. Middle Aged


23. Gu XJ, Lu JL, Lai RS, Zhang YD, Zhang P, Lu ZJ, Zhu QY: [Clinical value of CK34BE12 combining the expression of protein P53 gene and prostate specific antigen for the differential diagnosis of prostate carcinoma]. Zhonghua Nan Ke Xue; 2006 Apr;12(4):340-2
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  • OBJECTIVE: To improve the level of clinical diagnosis and differential diagnosis of benign and malignant prostate lesions.
  • RESULTS: The basal-cells in all of the benign lesions were stained with the CK34BE12 and PSA, while it had not immunoreactivity with P53.
  • CONCLUSION: Based on the routine histological studies with the expression of CK34BE12 and PSA together, they can indicate the existence of basal-cell distinctly and show indirectly whether the basal-cell is integrated.
  • Combining the expression of P53 to determine the existence of cancer gene, it can help to distinguish benign and malignant prostate lesions.
  • [MeSH-major] Keratins / biosynthesis. Prostate-Specific Antigen / biosynthesis. Prostatic Neoplasms / diagnosis. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 16683569.001).
  • [ISSN] 1009-3591
  • [Journal-full-title] Zhonghua nan ke xue = National journal of andrology
  • [ISO-abbreviation] Zhonghua Nan Ke Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CK-34 beta E12; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins; EC 3.4.21.77 / Prostate-Specific Antigen
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24. Laurendeau I, Ferrer M, Garrido D, D'Haene N, Ciavarelli P, Basso A, Vidaud M, Bieche I, Salmon I, Szijan I: Gene expression profiling of the hedgehog signaling pathway in human meningiomas. Mol Med; 2010 Jul-Aug;16(7-8):262-70
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  • The Hedgehog (Hh) signaling pathway has an important role during embryogenesis and in adult life, regulating proliferation, angiogenesis, matrix remodeling and stem-cell renewal.
  • Deregulation of the Hh pathway is involved in tumor development, since mutations in several components of this pathway were found in patients with basal cell carcinoma, medulloblastoma and other tumors; however, the role of Hh in meningiomas has not been studied yet.
  • Meningiomas represent 30% of primary cranial tumors, are mostly benign and prevail in the second half of life.
  • To provide information concerning molecular alterations, by use of real-time RT-PCR, we studied expression at the mRNA level of 32 Hh pathway and target genes in 36 meningioma specimens of different grades. mRNA levels of 16 genes, involved mainly in Hh pathway activation and cell proliferation, increased in meningiomas in comparison with normal tissue, whereas those of 7 genes, mainly related to Hh pathway repression, decreased.
  • The most significant changes occurred in signal transduction (SMO) and GLI-transcription factor genes, and the target FOXM1 mRNA attained the highest values; their over-expression was found in aggressive and in benign tumors.
  • [MeSH-major] Biomarkers, Tumor / genetics. Hedgehog Proteins / genetics. Meningioma / genetics. RNA, Messenger / genetics

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  • [Cites] J Invest Dermatol. 2004 May;122(5):1180-7 [15140221.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12561-6 [15314219.001]
  • [Cites] Cytogenet Cell Genet. 1996;72(4):297-8 [8641133.001]
  • [Cites] Dev Cell. 2005 Feb;8(2):143-51 [15736317.001]
  • [Cites] Development. 2005 Dec;132(23):5249-60 [16284117.001]
  • [Cites] Cancer Biol Ther. 2005 Oct;4(10):1050-4 [16258256.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 3;103(1):33-8 [16371461.001]
  • [Cites] Dev Biol. 2006 Feb 1;290(1):1-12 [16364285.001]
  • [Cites] Carcinogenesis. 2006 Jul;27(7):1334-40 [16501253.001]
  • [Cites] Curr Opin Cell Biol. 2007 Apr;19(2):159-65 [17303409.001]
  • [Cites] Int J Cancer. 2007 Sep 1;121(5):943-54 [17410535.001]
  • [Cites] Trends Cell Biol. 2007 Sep;17(9):438-47 [17845852.001]
  • [Cites] BMC Dev Biol. 2007;7:111 [17925019.001]
  • [Cites] Curr Biol. 2008 Mar 25;18(6):R238-41 [18364223.001]
  • [Cites] Curr Oncol Rep. 2008 Mar;10(2):107-13 [18377823.001]
  • [Cites] Int J Cancer. 2008 Jun 15;122(12):2707-18 [18381746.001]
  • [Cites] J Natl Cancer Inst. 2008 May 21;100(10):692-7 [18477794.001]
  • [Cites] Nat Rev Cancer. 2008 Jun;8(6):438-49 [18500245.001]
  • [Cites] J Biol Chem. 2008 Jul 25;283(30):20770-8 [18524773.001]
  • [Cites] Genes Dev. 2008 Sep 15;22(18):2454-72 [18794343.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8788-95 [18974121.001]
  • [Cites] Development. 2009 Mar;136(6):1029-38 [19234065.001]
  • [Cites] J Biol Chem. 2009 Aug 21;284(34):22888-97 [19556240.001]
  • [Cites] Neurobiol Dis. 2004 Apr;15(3):483-91 [15056455.001]
  • [Cites] Int J Cancer. 2003 Sep 20;106(5):758-65 [12866037.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2002;3:47-65 [12142354.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):30901-13 [12042312.001]
  • [Cites] Nature. 2002 May 16;417(6886):299-304 [12015606.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):10139-49 [11741991.001]
  • [Cites] Dev Biol. 2001 Aug 1;236(1):30-45 [11456442.001]
  • [Cites] Nature. 2000 Aug 31;406(6799):1005-9 [10984056.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12):1173-8 [19726761.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12):1164-72 [19726763.001]
  • [Cites] N Engl J Med. 2009 Nov 19;361(21):2094-6 [19923581.001]
  • (PMID = 20386868.001).
  • [ISSN] 1528-3658
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hedgehog Proteins; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2896461
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25. Gratzinger D, Zhao S, West R, Rouse RV, Vogel H, Gil EC, Levy R, Lossos IS, Natkunam Y: The transcription factor LMO2 is a robust marker of vascular endothelium and vascular neoplasms and selected other entities. Am J Clin Pathol; 2009 Feb;131(2):264-78
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  • LMO2 reactivity is otherwise virtually absent in nonhematolymphoid tissues except in breast myoepithelium, prostatic basal cells, and secretory phase endometrial glands.
  • LMO2 is uniformly expressed in benign vascular and lymphatic neoplasms and in most malignant vascular neoplasms with the exception of epithelioid vascular neoplasms of pleura and bone.
  • Among nonvascular neoplasms, LMO2 reactivity is present in giant cell tumor of tendon sheath, juvenile xanthogranuloma, a subset of gastrointestinal stromal tumors, small round blue cell tumors, and myoepithelial-derived neoplasms.

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  • (PMID = 19141387.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / CA34233; United States / NCI NIH HHS / CA / CA122105; United States / NCI NIH HHS / CA / CA33399; United States / NCI NIH HHS / CA / R37 CA033399; United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / R01 CA122105; United States / NCI NIH HHS / CA / CA109335; United States / NCI NIH HHS / CA / P30 CA124435
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
  • [Other-IDs] NLM/ NIHMS636776; NLM/ PMC4305438
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26. Frew IJ, Minola A, Georgiev S, Hitz M, Moch H, Richard S, Vortmeyer AO, Krek W: Combined VHLH and PTEN mutation causes genital tract cystadenoma and squamous metaplasia. Mol Cell Biol; 2008 Jul;28(14):4536-48
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  • Epididymal cystadenomas arise frequently in VHL patients, but VHL mutation alone is believed to be insufficient for tumor formation, implying a requirement for cooperating mutations in epididymal pathogenesis.
  • Here we show that epididymal cystadenomas from VHL patients frequently also lack expression of the PTEN tumor suppressor and display activation of phosphatidylinositol 3-kinase (PI3K) pathway signaling.
  • Strikingly, while conditional inactivation of either Vhlh or Pten in epithelia of the mouse genital tract fails to produce a tumor phenotype, their combined deletion causes benign genital tract tumors with regions of squamous metaplasia and cystadenoma.
  • Importantly, these lesions are characterized by expansion of basal stem cells, high levels of expression and activity of HIF1alpha and HIF2alpha, and dysregulation of PI3K signaling.
  • Our studies suggest a model for cooperative tumor suppression in which inactivation of PTEN facilitates epididymal cystadenoma genesis initiated by loss of VHL.
  • [MeSH-major] Cystadenoma / genetics. Genetic Predisposition to Disease. PTEN Phosphohydrolase / genetics. Spermatocele / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics


27. Cheah PL, Looi LM: Significance of Bcl-2 and Bax proteins in cervical carcinogenesis: an immunohistochemical study in squamous cell carcinoma and squamous intraepithelial lesions. Malays J Pathol; 2006 Jun;28(1):1-5
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  • [Title] Significance of Bcl-2 and Bax proteins in cervical carcinogenesis: an immunohistochemical study in squamous cell carcinoma and squamous intraepithelial lesions.
  • Sixteen low grade (LSIL), 22 high grade (HSIL) squamous intraepithelial lesions, 28 invasive (13 stage I and 15 stage II-IV) squamous cell carcinoma (SCC) and 15 benign cervices were immunohistochemically studied for involvement of Bcl-2 and Bax proteins in cervical carcinogenesis.
  • Bcl-2 was upregulated (p < 0.05) in HSIL and Bax in SCC when compared with benign cervical squamous epithelium.
  • Bcl-2 expression was confined to the lower third of the epithelium in the benign cervices and LSIL.
  • SCCs showed "diffuse" (evenly distributed) or "basal" (intensified staining around the periphery of the invading tumour nests) expression of Bcl-2.
  • Of the 5 SCCs with upregulated Bcl-2, 1 of 2 (50%) stage I and 3 (100%) stage II-IV tumours exhibited the "basal" pattern.
  • Benign cervical squamous epithelium, LSIL, HSIL and SCC showed a generally diffuse Bax expression.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / metabolism. Cervical Intraepithelial Neoplasia / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Uterine Cervical Neoplasms / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17694953.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein
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28. Pino M, Galleguillos C, Torres M, Sovino H, Fuentes A, Boric MA, Johnson MC: Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis. Reproduction; 2009 Nov;138(5):837-47
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  • [Title] Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis.
  • Endometriosis is a benign gynecological pathology in which immune system deregulation may play a role in its initiation and progression.
  • In endometriotic lesions, intercellular adhesion molecule-1 (ICAM1) is released from the cell membrane by proteolytic cleavage of its extracellular domain, a process that coincides with increased expression and proteolytic activity of metalloproteinases such as MMP1 and MMP9.
  • The objective of our study was to investigate the association between MMP1 and MMP9 activities and ICAM1 cleavage mediated by tumor necrosis factor (TNF) in eutopic endometrial stromal cells from women with and without (control) endometriosis during culture.
  • Under basal conditions, proMMP9 dimer and MMP9 were higher in endometriosis cell cultures.
  • In stromal cultures derived from control women and those with endometriosis, TNF augmented the intracellular proMMP1 (1.2-fold in control stromal cells) and ICAM1 (1.4- and 1.9-fold), greatly increased MMP1 and proMMP9 levels, and the sICAM1 concentration (2.3- and 4.3-fold) in their media compared with basal levels.
  • The combination of TNF and MMP9 increased the sICAM1 concentration 14-fold in the endometriosis cell media, whereas GM6001 inhibited the stimulatory effect of TNF in both cell cultures.
  • [MeSH-major] Endometriosis / pathology. Endometrium / pathology. Intercellular Adhesion Molecule-1 / metabolism. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 9 / metabolism. Stromal Cells / drug effects. Tumor Necrosis Factor-alpha / pharmacology. Uterine Diseases / pathology
  • [MeSH-minor] Adult. Case-Control Studies. Cells, Cultured. Enzyme Activation / drug effects. Enzyme Activation / genetics. Enzyme Activation / physiology. Female. Humans. Primary Cell Culture. Protein Processing, Post-Translational / drug effects

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  • (PMID = 19661147.001).
  • [ISSN] 1741-7899
  • [Journal-full-title] Reproduction (Cambridge, England)
  • [ISO-abbreviation] Reproduction
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
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29. Bowen AR, LeBoit PE: Fibroepithelioma of pinkus is a fenestrated trichoblastoma. Am J Dermatopathol; 2005 Apr;27(2):149-54
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  • Pinkus described "pre-malignant fibroepithelioma" as a proliferation that gave rise to many tiny basal cell carcinomas within each lesion.
  • Later authors have generally considered it to be an unusual variant of basal cell carcinoma (BCC).
  • The delineation of trichoblastoma as the general term for the benign counterpart of BCC raises the possibility that the fibroepithelioma of Pinkus (FEP) would be better classified under that rubric.
  • Next, FEP, BCC, and FEP with BCC-like areas were stained with MIB-1 (to assess proliferation), p53 (an oncogene product), and CK20 (a Merkel cell marker) antisera.
  • FEP also shows retention of Merkel cells, a characteristic of benign neoplasms with follicular germinative differentiation but not in general of BCC.
  • [MeSH-major] Carcinoma, Basal Cell / classification. Hair Diseases / pathology. Neoplasms, Fibroepithelial / classification. Neoplasms, Fibroepithelial / pathology. Skin Neoplasms / classification
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Child. Female. Humans. Immunohistochemistry. Male. Middle Aged. Sex Factors

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  • (PMID = 15798442.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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30. Al-Ayoubi A, Tarcsafalvi A, Zheng H, Sakati W, Eblen ST: ERK activation and nuclear signaling induced by the loss of cell/matrix adhesion stimulates anchorage-independent growth of ovarian cancer cells. J Cell Biochem; 2008 Oct 15;105(3):875-84
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  • [Title] ERK activation and nuclear signaling induced by the loss of cell/matrix adhesion stimulates anchorage-independent growth of ovarian cancer cells.
  • For normal epithelial cells and fibroblasts, cell adhesion to the extracellular matrix is required to prevent apoptosis and for proper activation and nuclear signaling of the ERK MAP kinase.
  • We demonstrate that ERK and its activator MEK are robustly stimulated after cell detachment from a substratum in several ovarian cancer cell lines, but not a benign ovarian cell line, independent of serum and FAK or PAK activity.
  • Re-attachment of suspended ovarian cells to fibronectin restored basal levels of MEK and ERK activity.
  • Inhibition of ERK activation with the MEK inhibitor U0126 had minor effects on adherent cell growth, but greatly decreased growth in soft agar.
  • [MeSH-major] Cell Nucleus / enzymology. Cell-Matrix Junctions / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. MAP Kinase Signaling System. Ovarian Neoplasms / enzymology
  • [MeSH-minor] Cell Line, Tumor. Female. Focal Adhesion Protein-Tyrosine Kinases / genetics. Focal Adhesion Protein-Tyrosine Kinases / metabolism. Humans. Mitogen-Activated Protein Kinase Kinases / metabolism. Up-Regulation

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18726893.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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31. Liao XY, Xue WC, Shen DH, Ngan HY, Siu MK, Cheung AN: p63 expression in ovarian tumours: a marker for Brenner tumours but not transitional cell carcinomas. Histopathology; 2007 Oct;51(4):477-83
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  • [Title] p63 expression in ovarian tumours: a marker for Brenner tumours but not transitional cell carcinomas.
  • Diffuse nuclear immunoreactivity of p63 was demonstrated in the 17 benign and five borderline Brenner tumours.
  • Only one of the six malignant Brenner tumours displayed p63 expression. p63 immunoreactivity was absent in all the ovarian transitional cell carcinomas (TCC), but was demonstrated extensively in TCCs of the urinary bladder.
  • Besides focal p63 expression in epidermal basal cells of immature and mature teratomas, all other ovarian lesions were devoid of p63 expression. p63 expression was also demonstrated in cervical transitional cell metaplasia and Walthard cell nests of fallopian tubes.
  • CONCLUSIONS: Expression of p63 protein is apparently cell lineage specific and in ovarian neoplasms is confined to benign and borderline Brenner tumours.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brenner Tumor / metabolism. Carcinoma, Transitional Cell / metabolism. Membrane Proteins / metabolism. Ovarian Neoplasms / metabolism

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  • [CommentIn] Histopathology. 2008 Aug;53(2):228 [18518899.001]
  • (PMID = 17880529.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins
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32. Maufort JP, Williams SM, Pitot HC, Lambert PF: Human papillomavirus 16 E5 oncogene contributes to two stages of skin carcinogenesis. Cancer Res; 2007 Jul 1;67(13):6106-12
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  • High-risk human papillomaviruses (HPVs), which cause the vast majority of cervical cancer, other anogenital cancers, and a subset of head and neck squamous cell carcinomas, encode three oncogenes: E5, E6, and E7.
  • To determine the oncogenic properties of HPV16 E5 in vivo, we previously generated K14E5 transgenic mice, in which expression of E5 was directed to the basal compartment of stratified squamous epithelia.
  • In the current study, we determined how E5 contributes to tumor formation in the skin using a multistage model for skin carcinogenesis that specifies the role of genes in three stages: initiation, promotion, and malignant progression.
  • The progressive neoplastic disease in K14E5 mice differed from that in nontransgenic mice in that benign tumors converted from exophytic to endophytic papillomas before progressing to carcinomas.

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  • [Cites] Genes Dev. 1991 May;5(5):714-27 [1709129.001]
  • [Cites] Cancer Cells. 1990 Jan;2(1):8-15 [2201338.001]
  • [Cites] Oncogene. 1992 Jan;7(1):27-32 [1311063.001]
  • [Cites] J Virol. 1993 Aug;67(8):4521-32 [8392596.001]
  • [Cites] J Virol. 1993 Oct;67(10):6170-8 [7690419.001]
  • [Cites] Cell Growth Differ. 1993 Dec;4(12):1071-82 [8117621.001]
  • [Cites] Virology. 1994 Aug 15;203(1):73-80 [8030286.001]
  • [Cites] J Virol. 1995 May;69(5):3185-92 [7707548.001]
  • [Cites] J Gen Virol. 1995 May;76 ( Pt 5):1239-45 [7730808.001]
  • [Cites] J Virol. 1995 Jul;69(7):4489-94 [7769709.001]
  • [Cites] J Virol. 1995 Dec;69(12):8051-6 [7494320.001]
  • [Cites] Arch Virol. 1996;141(5):791-800 [8678826.001]
  • [Cites] Virology. 1996 Sep 1;223(1):251-4 [8806560.001]
  • [Cites] Mol Carcinog. 1997 Mar;18(3):160-70 [9115586.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2286-94 [9410906.001]
  • [Cites] Exp Cell Res. 1998 May 25;241(1):76-83 [9633515.001]
  • [Cites] Virology. 1998 Aug 15;248(1):1-5 [9705249.001]
  • [Cites] Oncogene. 2005 Apr 7;24(15):2585-8 [15735736.001]
  • [Cites] Cancer Res. 2005 Aug 1;65(15):6534-42 [16061632.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8266-73 [16166303.001]
  • [Cites] J Virol. 1999 Jul;73(7):5887-93 [10364340.001]
  • [Cites] Proc Assoc Am Physicians. 1999 Nov-Dec;111(6):581-7 [10591087.001]
  • [Cites] J Clin Microbiol. 2000 Feb;38(2):688-95 [10655368.001]
  • [Cites] Virology. 2000 Feb 15;267(2):141-50 [10662610.001]
  • [Cites] Virus Genes. 2000;20(1):65-9 [10766308.001]
  • [Cites] Eur J Cell Biol. 2000 Jun;79(6):407-12 [10928456.001]
  • [Cites] Semin Gastrointest Dis. 2000 Oct;11(4):229-37 [11057950.001]
  • [Cites] Oncogene. 2000 Dec 7;19(52):6023-32 [11146554.001]
  • [Cites] J Biomed Sci. 2001 Mar-Apr;8(2):206-13 [11287752.001]
  • [Cites] J Virol. 2002 Dec;76(24):13039-48 [12438630.001]
  • [Cites] Virology. 2003 Jun 20;311(1):105-14 [12832208.001]
  • [Cites] Cancer Lett. 2003 Jun 30;196(1):17-22 [12860284.001]
  • [Cites] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349.001]
  • [Cites] Prog Clin Biol Res. 1989;298:3-15 [2501799.001]
  • [Cites] J Virol. 1989 Oct;63(10):4417-21 [2476573.001]
  • [Cites] EMBO J. 1989 Dec 1;8(12):3905-10 [2555178.001]
  • [Cites] Oncogene. 1992 Jan;7(1):19-25 [1311062.001]
  • (PMID = 17616666.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA022443; United States / NCI NIH HHS / CA / P01 CA022443-320006; United States / NCI NIH HHS / CA / R01 CA098428-05; United States / NIDCR NIH HHS / DE / R01 DE017315-03; United States / NCI NIH HHS / CA / CA098428; United States / NCI NIH HHS / CA / CA098428-05; United States / NCI NIH HHS / CA / R01 CA098428-04; United States / NIDCR NIH HHS / DE / DE017315; United States / NCI NIH HHS / CA / CA022443-320006; United States / NIDCR NIH HHS / DE / R01 DE017315-02; United States / NIDCR NIH HHS / DE / R01 DE017315; United States / NCI NIH HHS / CA / CA098428-04S1; United States / NIDCR NIH HHS / DE / R01 DE017315-01; United States / NCI NIH HHS / CA / R01 CA098428-04S1; United States / NCI NIH HHS / CA / P01 CA022443-310006; United States / NCI NIH HHS / CA / CA022443-300006; United States / NCI NIH HHS / CA / CA022443-310006; United States / NCI NIH HHS / CA / P01 CA022443-300006; United States / NCI NIH HHS / CA / CA098428-04; United States / NCI NIH HHS / CA / P01 CA022443; United States / NCI NIH HHS / CA / R01 CA098428
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Oncogene Proteins, Viral; 0 / oncogene protein E5, Human papillomavirus type 16; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 8002-74-2 / Paraffin; 9007-49-2 / DNA; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS193051; NLM/ PMC2858287
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33. Hornick JL, Fletcher CD: Intestinal perineuriomas: clinicopathologic definition of a new anatomic subset in a series of 10 cases. Am J Surg Pathol; 2005 Jul;29(7):859-65
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  • Benign peripheral nerve sheath tumors are uncommon in the gastrointestinal tract, and perineuriomas have not previously been reported to occur at this anatomic location.
  • The colonic submucosal tumor was microscopically well circumscribed, whereas the jejunal perineurioma showed focal infiltration through the muscularis propria into the subserosa.
  • The stroma was collagenous in the colonic tumor and predominantly myxoid in the jejunal tumor.
  • Electron microscopy was performed on the tumor lacking EMA expression, revealing typical features of perineurioma, namely, spindle cells with long bipolar cytoplasmic processes and prominent pinocytotic vesicles, surrounded by discontinuous basal lamina.
  • No tumor recurred.
  • Distinguishing perineuriomas from other spindle cell neoplasms of the gastrointestinal tract can be facilitated by immunostaining for EMA and claudin-1.
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. Male. Microscopy, Electron, Transmission. Middle Aged. Treatment Outcome

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  • [CommentIn] Am J Surg Pathol. 2006 Oct;30(10):1337-9 [17001168.001]
  • (PMID = 15958849.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 26
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34. Barron DA, Strand DW, Ressler SJ, Dang TD, Hayward SW, Yang F, Ayala GE, Ittmann M, Rowley DR: TGF-β1 induces an age-dependent inflammation of nerve ganglia and fibroplasia in the prostate gland stroma of a novel transgenic mouse. PLoS One; 2010 Oct 29;5(10):e13751
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  • TGF-β1 is overexpressed in wound repair and in most proliferative disorders including benign prostatic hyperplasia and prostate cancer.
  • Transgenic mice developed age-dependent lesions leading to severe, yet focal attenuation of epithelium, and a discontinuous basal lamina.

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  • [Cites] Nat Cell Biol. 1999 Sep;1(5):E117-9 [10559949.001]
  • [Cites] Endocrinology. 2000 Dec;141(12):4698-710 [11108285.001]
  • [Cites] J Urol. 2001 Dec;166(6):2472-83 [11696814.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3298-307 [12036948.001]
  • [Cites] J Urol. 2002 Jul;168(1):331-5 [12050565.001]
  • [Cites] J Immunol Methods. 2002 Aug 1;266(1-2):7-18 [12133618.001]
  • [Cites] Clin Cancer Res. 2002 Sep;8(9):2912-23 [12231536.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6021-5 [12414622.001]
  • [Cites] J Pathol. 2003 Jul;200(4):500-3 [12845617.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5859-65 [14522910.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4792-801 [14581350.001]
  • [Cites] Mod Pathol. 2004 Mar;17(3):307-15 [14739905.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):2572-6 [7708687.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 9;92(10):4254-8 [7753792.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Dec 26;217(3):1279-86 [8554587.001]
  • [Cites] Lab Invest. 1996 Jun;74(6):991-1003 [8667617.001]
  • [Cites] Prostate. 1997 Nov 1;33(3):151-6 [9365541.001]
  • [Cites] Prostate. 1999 Sep 1;40(4):248-55 [10420153.001]
  • [Cites] Wound Repair Regen. 2005 Jan-Feb;13(1):7-12 [15659031.001]
  • [Cites] Cancer Res. 2005 Oct 1;65(19):8887-95 [16204060.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4244-53 [17483336.001]
  • [Cites] Cancer Cell. 2007 Dec;12(6):559-71 [18068632.001]
  • [Cites] Oncogene. 2008 Jan 17;27(4):450-9 [17637743.001]
  • [Cites] Urology. 2008 Jul;72(1):205-13 [18314176.001]
  • [Cites] Prostate. 2009 Mar 1;69(4):373-84 [19021203.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2859-63 [19196965.001]
  • [Cites] Stem Cells. 2010 Feb;28(2):344-56 [20020426.001]
  • [Cites] Lab Invest. 2010 Apr;90(4):543-55 [20142803.001]
  • (PMID = 21060787.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058093; United States / NIDDK NIH HHS / DK / R01 DK083293; United States / NCI NIH HHS / CA / U54 CA126568; United States / NCI NIH HHS / CA / R01 CA58093
  • [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 / DNA Primers; 0 / Transforming Growth Factor beta1
  • [Other-IDs] NLM/ PMC2966419
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35. Baykal C, Buyukbabani N, Yazganoglu KD, Saglik E: [Tumors associated with nevus sebaceous]. J Dtsch Dermatol Ges; 2006 Jan;4(1):28-31
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  • Various benign and malignant neoplasms can develop in association with NS, the most common being trichoblastoma, syringocystadenoma papilliferum, viral warts and basal cell carcinoma (BCC).
  • PATIENTS AND METHODS: We retrospectively examined the clinical and histopathological records of 15 NS cases with an associated tumor which were diagnosed between 1996 and 2004.
  • RESULTS: All cases were adults and 3 of them had more than one tumor.
  • Six cases had BCC, which is a higher incidence of malignant tumor association with NS, than that reported in last years.
  • Trichoblastoma was observed in 3 cases and was the most common benign tumor in our series.
  • CONCLUSION: Clinical features are not sufficient enough to make an exact diagnosis of benign or malignant secondary tumors.
  • Though prophylactic excision for NS is done less in last years, especially adult patients should closely be followed for any new changes evoking tumor development on this congenital lesion.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Neoplasms, Multiple Primary / diagnosis. Neoplasms, Second Primary / diagnosis. Nevus / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Carcinoma, Basal Cell / diagnosis. Carcinoma, Basal Cell / pathology. Facial Neoplasms / diagnosis. Facial Neoplasms / pathology. Female. Humans. Male. Middle Aged. Scalp / pathology. Skin / pathology


36. Chung SW, Kwon SY, Jung KY, Woo JS: Synchronous double primary cancers of the unilateral parotid gland. Acta Otolaryngol; 2007 Feb;127(2):209-12
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  • A review of the literature revealed that most reported cases were either a combination of two distinct benign neoplasms or a benign neoplasm and another malignant tumor.
  • Here we report a 39-year-old woman who exhibited basal cell adenocarcinoma and mucoepidermoid carcinoma simultaneously in the left parotid gland.

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  • (PMID = 17364354.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Norway
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37. Sugano DM, Lucci LM, Avila MP, Rehder JR, Pettinati J: [Eyelid trichoepithelioma--report of 2 cases]. Arq Bras Oftalmol; 2005 Jan-Feb;68(1):136-9
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  • [Transliterated title] Tricoepitelioma palpebral--relato de 2 casos.
  • Trichoepithelioma is a benign skin tumor and is most commonly found on the face, however, there are few reports about its occurrence on the eyelids.
  • This lesion should be considered when a single solid nodule on the face appears, and can be differentiated from basal-cell carcinoma.
  • [MeSH-major] Eyelid Neoplasms / pathology. Neoplasms, Basal Cell / pathology. Skin Neoplasms / pathology

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  • (PMID = 15824820.001).
  • [ISSN] 0004-2749
  • [Journal-full-title] Arquivos brasileiros de oftalmologia
  • [ISO-abbreviation] Arq Bras Oftalmol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
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38. Wright NA, Thomas CG, Calame A, Cockerell CJ: Granular cell atypical fibroxanthoma: case report and review of the literature. J Cutan Pathol; 2010 Mar;37(3):380-5
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  • [Title] Granular cell atypical fibroxanthoma: case report and review of the literature.
  • We present a case of granular cell atypical fibroxanthoma of the scalp.
  • The neoplasm occurred as a tender nodule on the frontal scalp of an 82-year-old Caucasian man.
  • The granular cell phenotype has been observed in other cutaneous neoplasms including granular cell tumors, dermatofibromas, dermatofibrosarcoma protuberans, fibrous papules, basal cell carcinomas, leiomyosarcomas, angiosarcomas and primitive polypoid granular cell tumors.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Histiocytoma, Benign Fibrous / pathology. Skin Neoplasms / pathology. Xanthomatosis / pathology
  • [MeSH-minor] Aged, 80 and over. Biomarkers, Tumor. Disease-Free Survival. Humans. Immunohistochemistry. Male. Scalp / metabolism. Scalp / pathology. Scalp / surgery. Treatment Outcome

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  • (PMID = 19341433.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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39. Kamat G, Yelikar B, Shettar S, Karigoudar MH: Pigmented trichoblastoma with sebaceous hyperplasia. Indian J Dermatol Venereol Leprol; 2009 Sep-Oct;75(5):506-8
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  • Trichoblastoma is a rare benign trichogenic tumour with epithelial and mesenchymal components recapitulating the germinal hair bulb and associated mesenchyme.
  • Microscopy of tumour revealed nodular tumour spanning the entire dermis with collection of mesenchymal cells resembling follicular papilla.
  • There is a need for differentiation of this tumor which is benign, from other pigmented tumors having basaloid arrangement of cells such as basal cell carcinoma.

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  • (PMID = 19736433.001).
  • [ISSN] 0973-3922
  • [Journal-full-title] Indian journal of dermatology, venereology and leprology
  • [ISO-abbreviation] Indian J Dermatol Venereol Leprol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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40. Rehman I, Cross SS, Catto JW, Leiblich A, Mukherjee A, Azzouzi AR, Leung HY, Hamdy FC: Promoter hyper-methylation of calcium binding proteins S100A6 and S100A2 in human prostate cancer. Prostate; 2005 Dec 1;65(4):322-30
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  • METHODS: The promoter and exon 1 region of the S100A6 and S100A2 genes was sequenced in bisulfite modified DNA from non-malignant, benign prostatic hyperplasia (BPH), malignant and metastatic prostate tissues and in cell lines.
  • Immunostaining, showed absent S100A2 expression all 41 cases of prostatic cancer, whereas staining was seen in the basal cells of non-malignant epithelium.
  • [MeSH-major] Adenocarcinoma / genetics. Cell Cycle Proteins / genetics. Chemotactic Factors / genetics. DNA Methylation. Prostatic Neoplasms / genetics. S100 Proteins / genetics
  • [MeSH-minor] Base Sequence. Blotting, Western. Cell Line, Tumor. Humans. Immunohistochemistry. Male. Promoter Regions, Genetic. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16015609.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Chemotactic Factors; 0 / RNA, Messenger; 0 / S100 Proteins; 0 / S100A2 protein, human; 105504-00-5 / S100A6 protein, human
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41. McHugh JB, Hoschar AP, Dvorakova M, Parwani AV, Barnes EL, Seethala RR: p63 immunohistochemistry differentiates salivary gland oncocytoma and oncocytic carcinoma from metastatic renal cell carcinoma. Head Neck Pathol; 2007 Dec;1(2):123-31
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  • [Title] p63 immunohistochemistry differentiates salivary gland oncocytoma and oncocytic carcinoma from metastatic renal cell carcinoma.
  • Metastatic renal cell carcinoma (RCC) can pose diagnostic challenges in the head and neck often resembling benign and malignant oncocytic lesions.
  • Morphologic features evaluated were cytoplasmic character (clear versus oncocytic), Fuhrman nuclear grade, mitotic rate, growth pattern, presence of lumens/blood lakes and stromal characteristics.
  • Tumors were stained with antibodies to p63, renal cell carcinoma marker (RCCm), CD10, and vimentin.
  • Eight benign oncocytic tumors (29%) had clear cell features while 6 metastatic RCC (37%) had oncocytic features.
  • Mitotic rates were only significantly different between benign oncocytic tumors and metastatic RCC.
  • Seven benign oncocytic tumors (25%) and 5 oncocytic carcinomas (56%) had RCC-like vascular stroma.
  • All primary salivary gland tumors were positive for p63, predominately in basal cell-type distribution.
  • [MeSH-major] Adenocarcinoma, Clear Cell / diagnosis. Adenoma, Oxyphilic / diagnosis. Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis. Membrane Proteins / metabolism. Salivary Gland Neoplasms / diagnosis. Salivary Gland Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Diagnosis, Differential. Humans. Predictive Value of Tests

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  • [Cites] J Invest Dermatol. 1999 Dec;113(6):1099-105 [10594758.001]
  • [Cites] Otolaryngol Head Neck Surg. 2002 Jun;126(6):657-62 [12087334.001]
  • [Cites] Am J Surg Pathol. 2001 Aug;25(8):1054-60 [11474290.001]
  • [Cites] Adv Anat Pathol. 2002 Sep;9(5):280-9 [12195217.001]
  • [Cites] Laryngoscope. 2002 Sep;112(9):1598-602 [12352670.001]
  • [Cites] Virchows Arch. 2002 Nov;441(5):428-36 [12447671.001]
  • [Cites] J Histochem Cytochem. 2003 Feb;51(2):133-9 [12533521.001]
  • [Cites] J Histochem Cytochem. 2003 Aug;51(8):1097-9 [12871991.001]
  • [Cites] Lab Invest. 1970 Dec;23(6):567-80 [5530737.001]
  • [Cites] Mich Med. 1971 Jul;70(16):616-8 [5571989.001]
  • [Cites] Laryngoscope. 1973 Jun;83(6):898-905 [4711327.001]
  • [Cites] Laryngoscope. 1981 Apr;91(4):517-9 [6261053.001]
  • [Cites] South Med J. 1981 Sep;74(9):1050-2 [7280750.001]
  • [Cites] Pathol Res Pract. 1986 Dec;181(6):684-92 [3562340.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1988 Jan;65(1):61-6 [3422397.001]
  • [Cites] Hum Pathol. 1988 Jul;19(7):862-7 [3402976.001]
  • [Cites] Head Neck. 1989 Mar-Apr;11(2):174-8 [2656583.001]
  • [Cites] Histopathology. 1990 May;16(5):487-93 [2361662.001]
  • [Cites] Am J Surg Pathol. 1991 Jun;15(6):514-28 [2031528.001]
  • [Cites] Pathol Annu. 1992;27 Pt 1:263-304 [1736246.001]
  • [Cites] Cancer. 1996 Dec 1;78(11):2281-7 [8940996.001]
  • [Cites] Semin Diagn Pathol. 1997 Aug;14(3):203-12 [9279976.001]
  • [Cites] J Oral Pathol Med. 1998 May;27(5):225-8 [9682986.001]
  • [Cites] Mol Cell. 1998 Sep;2(3):305-16 [9774969.001]
  • [Cites] Am J Surg Pathol. 2007 Jan;31(1):44-57 [17197918.001]
  • [Cites] Nature. 1999 Apr 22;398(6729):714-8 [10227294.001]
  • [Cites] Laryngoscope. 2005 Jun;115(6):1097-100 [15933529.001]
  • [Cites] Head Neck. 2005 Aug;27(8):696-702 [16021638.001]
  • [Cites] Otolaryngol Head Neck Surg. 2000 Mar;122(3):464 [10699832.001]
  • [Cites] Am J Clin Pathol. 2001 Dec;116(6):823-30 [11764070.001]
  • [Cites] Trends Genet. 2002 Feb;18(2):90-5 [11818141.001]
  • [Cites] Clin Cancer Res. 2002 Feb;8(2):494-501 [11839669.001]
  • [Cites] Arch Pathol Lab Med. 2002 Jun;126(6):676-85 [12033955.001]
  • [Cites] Int J Surg Pathol. 2005 Oct;13(4):329-35 [16273188.001]
  • (PMID = 20614263.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins
  • [Other-IDs] NLM/ PMC2807526
  • [Keywords] NOTNLM ; Metastatic renal cell carcinoma / Oncocytic carcinoma / Oncocytoma / p63
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42. Kazakov AA, Grishina EE, Tarantul VZ, Gening LV: Effect of human cell malignancy on activity of DNA polymerase iota. Biochemistry (Mosc); 2010 Jul;75(7):905-11
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  • [Title] Effect of human cell malignancy on activity of DNA polymerase iota.
  • An increased level of mutagenesis, partially caused by imbalanced activities of error prone DNA polymerases, is a key symptom of cell malignancy.
  • To clarify the possible role of incorrect DNA polymerase iota (Pol iota) function in increased frequency of mutations in mammalian cells, the activity of this enzyme in extracts of cells of different mouse organs and human eye (melanoma) and eyelid (basal-cell skin carcinoma) tumor cells was studied.
  • In the presence of Mg2+, the enzyme was active only in cell extracts of mouse testicles and brain, whereas in the presence of Mn2+ the activity of Pol iota was found in all studied normal mouse organs.
  • It was found that in cell extracts of both types of malignant tumors (basal-cell carcinoma and melanoma) Pol iota activity was observed in the presence of either Mn2+ or Mg2+.
  • In the presence of Mn2+ the Pol iota activity in the basal-cell carcinoma exceeded 2.5-fold that in control cells (benign tumors from the same eyelid region).
  • In extracts of melanoma cells in the presence of either cation, the level of the enzyme activity was approximately equal to that in extracts of cells of surrounding tumor-free tissues as well as in eyes removed after traumas.
  • The distinctive feature of tissue malignancy (in basal-cell carcinoma and in melanoma) was the change in DNA synthesis revealed as Mn2+-activated continuation of DNA synthesis after incorrect incorporation of dG opposite dT in the template by Pol iota.
  • Among cell extracts of different normal mouse organs, only those of testicles exhibited a similar feature.
  • This similarity can be explained by cell division blocking that occurs in all normal cells except in testicles and in malignant cells.
  • [MeSH-major] Carcinoma, Basal Cell / enzymology. DNA-Directed DNA Polymerase / metabolism. Eye Neoplasms / enzymology. Lymphoma, B-Cell, Marginal Zone / enzymology. Melanoma / enzymology
  • [MeSH-minor] Animals. Cell Line, Tumor. Enzyme Activation / drug effects. Enzyme Activators / pharmacology. Humans. Magnesium / pharmacology. Manganese / pharmacology. Mice. Mice, Inbred C57BL. Mutation

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  • (PMID = 20673215.001).
  • [ISSN] 1608-3040
  • [Journal-full-title] Biochemistry. Biokhimii︠a︡
  • [ISO-abbreviation] Biochemistry Mosc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Activators; 42Z2K6ZL8P / Manganese; EC 2.7.7.- / DNA polymerase iota; EC 2.7.7.7 / DNA-Directed DNA Polymerase; I38ZP9992A / Magnesium
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43. Anand BS, Verstovsek G, Cole G: Tubulovillous adenoma of anal canal: a case report. World J Gastroenterol; 2006 Mar 21;12(11):1780-1
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  • Tumors arising from the anal canal are usually of epithelial origin and are mostly squamous cell carcinoma or basal cell carcinoma.
  • We present a case of benign anal adenomas arising from the anus, an extremely rare diagnosis.
  • The squamocolumnar junction was visible at the edges of the lesion confirming the anal origin of the tumor.
  • [MeSH-minor] Aged. Anal Canal / pathology. Cell Transformation, Neoplastic. Humans. Male

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  • [Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]
  • [Cites] J Clin Pathol. 2005 Feb;58(2):217-9 [15677547.001]
  • [Cites] Br J Surg. 1995 Dec;82(12):1634 [8548224.001]
  • (PMID = 16586552.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC4124358
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44. Ahokas K, Skoog T, Suomela S, Jeskanen L, Impola U, Isaka K, Saarialho-Kere U: Matrilysin-2 (matrix metalloproteinase-26) is upregulated in keratinocytes during wound repair and early skin carcinogenesis. J Invest Dermatol; 2005 Apr;124(4):849-56
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  • We studied its role in benign skin disorders characterized by epithelial proliferation, in wound repair, skin cancer, and regulation in keratinocyte (KC) cultures.
  • MMP-26 is expressed by laminin-5-positive KC in the migrating area during wound repair, in benign skin disorders characterized by inflammation and microdisruptions of basement membrane, but in intact skin only in hair follicles.
  • It was detected in occasional atypical KC in pre-malignant lesions but not in basal cell cancer islands.
  • Although MMP-26 was expressed in grades I and II squamous cell cancers (SCC), it was not present in dedifferentiated grade III tumors.
  • But in tissue samples it either co-localized or was detected in adjacent cells of same regions with the tumor suppressor p16.
  • In KC and HaCaT cell cultures, 12-phorbol-13-myristate-acetate, epidermal growth factor, tumor necrosis factor-alpha, transforming growth factor-beta1, interleukin-1 (IL-1)beta, IL-6, insulin-like growth factor, gamma-IFN, retinoic acid, dexamethasone, four matrices or ras-transformation were unable to upregulate MMP-26 expression.
  • The expression pattern of MMP-26 suggests that it may be upregulated in basal KC even without tumorigenesis because of altered cell-matrix interactions and inflammation and, unlike most MMP, becomes downregulated during histological dedifferentiation of SCC.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Squamous Cell / physiopathology. Keratinocytes / physiology. Matrix Metalloproteinases / genetics. Skin Neoplasms / physiopathology
  • [MeSH-minor] Cell Line, Transformed. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. Matrix Metalloproteinases, Secreted. Up-Regulation. Wound Healing / physiology

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  • (PMID = 15816845.001).
  • [ISSN] 0022-202X
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.24.- / MMP26 protein, human; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases, Secreted
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45. Kristiansen G, Fritzsche FR, Wassermann K, Jäger C, Tölls A, Lein M, Stephan C, Jung K, Pilarsky C, Dietel M, Moch H: GOLPH2 protein expression as a novel tissue biomarker for prostate cancer: implications for tissue-based diagnostics. Br J Cancer; 2008 Sep 16;99(6):939-48
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  • As GOLPH2 protein expression in prostate tissues is currently unknown, this study aimed at a comprehensive analysis of GOLPH2 protein in benign and malignant prostate lesions.
  • Immunohistochemically detected GOLPH2 protein expression was compared with the basal cell marker p63 and the prostate cancer marker alpha-methylacyl-CoA racemase (AMACR) in 614 radical prostatectomy specimens.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Membrane Proteins / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Fluorescent Antibody Technique. Golgi Apparatus / metabolism. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prostatectomy. RNA, Messenger / genetics. RNA, Messenger / metabolism. Racemases and Epimerases / genetics. Racemases and Epimerases / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Array Analysis. Trans-Activators / genetics. Trans-Activators / metabolism. Transcription Factors. Tumor Cells, Cultured. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism. Up-Regulation

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  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):811-6 [14711987.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):3877-82 [12873976.001]
  • [Cites] Am J Surg Pathol. 2004 Feb;28(2):239-43 [15043314.001]
  • [Cites] Neoplasia. 2004 Jan-Feb;6(1):1-6 [15068665.001]
  • [Cites] Mod Pathol. 2004 Mar;17(3):307-15 [14739905.001]
  • [Cites] Am J Gastroenterol. 2004 Jun;99(6):1087-95 [15180730.001]
  • [Cites] Cancer Res. 1985 Aug;45(8):3663-7 [2410099.001]
  • [Cites] Am J Clin Pathol. 1998 Jun;109(6):695-703 [9620026.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):779-84 [15642945.001]
  • [Cites] FASEB J. 2005 Feb;19(2):243-5 [15548588.001]
  • [Cites] J Pathol. 2005 Feb;205(3):359-76 [15532095.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):393-406 [16286247.001]
  • [Cites] J Hepatol. 2005 Dec;43(6):1007-12 [16137783.001]
  • [Cites] J Urol. 2006 Mar;175(3 Pt 1):820-34 [16469560.001]
  • [Cites] Mol Cancer Res. 2006 Feb;4(2):79-92 [16513839.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4011-9 [16618720.001]
  • [Cites] Prostate. 2006 Jun 1;66(8):847-57 [16491480.001]
  • [Cites] Clin Cancer Res. 2006 May 1;12(9):2745-51 [16675566.001]
  • [Cites] Nat Genet. 2007 Jan;39(1):41-51 [17173048.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D747-50 [17132828.001]
  • [Cites] Histopathology. 2007 Jan;50(2):243-51 [17222253.001]
  • [Cites] Traffic. 2007 Oct;8(10):1415-23 [17662025.001]
  • [Cites] J Natl Cancer Inst. 2007 Oct 17;99(20):1525-33 [17925536.001]
  • [Cites] J Urol. 2007 Dec;178(6):2252-9 [17936845.001]
  • [Cites] Cancer Res. 2008 Feb 1;68(3):645-9 [18245462.001]
  • [Cites] J Cell Biochem. 2008 May 1;104(1):136-49 [18004786.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1677-82 [10749139.001]
  • [Cites] Gene. 2000 May 16;249(1-2):53-65 [10831838.001]
  • [Cites] Am J Pathol. 2000 Dec;157(6):1769-75 [11106548.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4683-8 [11406537.001]
  • [Cites] Cancer Res. 2001 Aug 1;61(15):5692-6 [11479199.001]
  • [Cites] Nature. 2001 Aug 23;412(6849):822-6 [11518967.001]
  • [Cites] Am J Surg Pathol. 2001 Nov;25(11):1397-404 [11684956.001]
  • [Cites] J Urol. 2001 Dec;166(6):2171-7 [11696729.001]
  • [Cites] Mol Carcinog. 2002 Jan;33(1):25-35 [11807955.001]
  • [Cites] JAMA. 2002 Apr 3;287(13):1662-70 [11926890.001]
  • [Cites] Hepatology. 2002 Jun;35(6):1431-40 [12029628.001]
  • [Cites] Virology. 2002 Sep 30;301(2):236-46 [12359426.001]
  • [Cites] Nature. 2002 Oct 10;419(6907):624-9 [12374981.001]
  • [Cites] J Natl Cancer Inst. 2003 May 7;95(9):661-8 [12734317.001]
  • [Cites] Am J Surg Pathol. 2003 Jun;27(6):772-8 [12766580.001]
  • [Cites] Am J Clin Pathol. 2004 Jan;121(1):99-107 [14750247.001]
  • (PMID = 18781151.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GOLM1 protein, human; 0 / Membrane Proteins; 0 / RNA, Messenger; 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/ PMC2538754
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46. Jung YH, Kang MS: Composite follicular variant of papillary carcinoma and mucoepidermoid carcinoma of thyroid gland: a case report. J Korean Med Sci; 2010 Nov;25(11):1683-7
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  • Pathologically, the tumor had two distinct tumor components with intermingled areas: follicular variant of papillary carcinoma and mucoepidermoid carcinoma.
  • Several small cysts lined by benign ciliated columnar epithelia suggesting that this tumor had originated from solid cell nest were seen around the tumor.
  • Positivity of p63 was seen in squamoid cells and basal cells of cysts.
  • Tumor cells of papillary carcinoma are positive for TTF-1, thyroglobulin but negative for CEA, calcitonin and p63.

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  • [Cites] Mod Pathol. 2000 Jul;13(7):802-7 [10912941.001]
  • [Cites] Am Surg. 2001 Oct;67(10):979-83 [11603557.001]
  • [Cites] Mod Pathol. 2003 Jan;16(1):43-8 [12527712.001]
  • [Cites] Dis Esophagus. 2003;16(3):265-7 [14641323.001]
  • [Cites] J Pathol. 2004 Feb;202(2):247-51 [14743508.001]
  • [Cites] Cancer. 1977 Jan;39(1):210-4 [832236.001]
  • [Cites] Histopathology. 1984 Sep;8(5):847-60 [6083973.001]
  • [Cites] J Pathol. 1988 Jul;155(3):191-200 [3045277.001]
  • [Cites] Arch Pathol Lab Med. 1990 Oct;114(10):1049-52 [2222147.001]
  • [Cites] Am J Surg Pathol. 1995 Oct;19(10):1209-15 [7573680.001]
  • [Cites] Hum Pathol. 1995 Oct;26(10):1099-108 [7557943.001]
  • [Cites] Surg Today. 1995;25(9):843-7 [8555707.001]
  • [Cites] Eur J Surg Oncol. 1995 Dec;21(6):692 [8631425.001]
  • [Cites] Pathol Res Pract. 1995 Dec;191(12):1214-21 [8927569.001]
  • [Cites] Am Surg. 1998 Apr;64(4):307-11 [9544139.001]
  • [Cites] Eur J Gynaecol Oncol. 1998;19(3):291-3 [9641234.001]
  • [Cites] Am J Otolaryngol. 2005 Mar-Apr;26(2):138-41 [15742270.001]
  • [Cites] Pathol Int. 2008 Nov;58(11):741-4 [18844942.001]
  • [Cites] Lung Cancer. 2009 Jan;63(1):159-60 [18992960.001]
  • [Cites] Hum Pathol. 2009 Jul;40(7):1029-35 [19269016.001]
  • (PMID = 21060764.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1; 68238-35-7 / Keratins; 9007-12-9 / Calcitonin; 9010-34-8 / Thyroglobulin
  • [Other-IDs] NLM/ PMC2967012
  • [Keywords] NOTNLM ; Carcinoma, Mucoepidermoid / Carcinoma, Papillary / Solid Cell Nests / Thyroid Gland
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47. Serafin AM, Bohm L: Influence of p53 and bcl-2 on chemosensitivity in benign and malignant prostatic cell lines. Urol Oncol; 2005 Mar-Apr;23(2):123-9
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  • [Title] Influence of p53 and bcl-2 on chemosensitivity in benign and malignant prostatic cell lines.
  • The administration of cancer chemotherapeutic agents results in an increase in the apoptotic cells in the tumor: therefore, it has been assumed that anticancer drugs exhibit their cytotoxic effects via apoptotic signaling pathways.
  • The role of p53 and bax/bcl-2 in drug-induced apoptosis was assessed in six prostate cell lines, 1532T, 1535T, 1542T, 1542N, BPH-1 and LNCaP using TD(50) concentrations of etoposide, vinblastine and estramustine.
  • Cell death was monitored morphologically by fluorescent microscopy, and by flow cytometry (Annexin-V assay).
  • The percentage of cells responding to drug-induced apoptosis was, on average, higher in the tumor cell lines than in the normal cell lines, but showed no correlation with p53 status.
  • Immunoblotting demonstrated that bax and bcl-2 proteins were expressed at a basal level in all cell lines, but did not increase after exposure to TD(50) doses of the three drugs.
  • The results suggest that apoptosis is not a major mechanism of drug-induced cell death in prostate cell lines and appears to be independent of p53 status and bax/bcl-2 expression.
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / genetics. DNA Damage. Dose-Response Relationship, Drug. Gene Expression Profiling. Humans. Male. Necrosis. Tumor Cells, Cultured

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  • (PMID = 15869997.001).
  • [ISSN] 1078-1439
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 35LT29625A / Estramustine; 5V9KLZ54CY / Vinblastine
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48. Sabbisetti VS, Chirugupati S, Thomas S, Vaidya KS, Reardon D, Chiriva-Internati M, Iczkowski KA, Shah GV: Calcitonin increases invasiveness of prostate cancer cells: role for cyclic AMP-dependent protein kinase A in calcitonin action. Int J Cancer; 2005 Nov 20;117(4):551-60
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  • Calcitonin (CT) is synthesized and secreted in prostate epithelium, and its secretion from malignant prostates is several-fold higher than from benign prostates.
  • To identify the role of "CT System" in prostate cancer, we tested the expression of CT and CTR mRNAs in invading tumor cells of prostate cancer specimens.
  • The effect of CT on in vitro invasion of PC cell lines and on activation of gelatinases was also examined.
  • Exogenously added CT increased in vitro invasion of PC cell lines and caused a rapid, several-fold but transient increase in protein kinase A activity.
  • Rp.cAMP, a competitive inhibitor of cAMP-dependent protein kinase A, myristoylated protein kinase A inhibitory peptide (PKI) as well as the expression of dominant negative form of PKA all attenuated basal in vitro invasion of PC-3M cells, and CT could not increase in vitro invasiveness in their presence.
  • The action of CT may be mediated by protein kinase A signaling, which subsequently leads to increased cell invasion and secretion of gelatinases.

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15929083.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096534; United States / NCI NIH HHS / CA / CA96534; United States / NIDDK NIH HHS / DK / DK45044
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Calcitonin; 9007-12-9 / Calcitonin; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.4.24.- / Matrix Metalloproteinases
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49. 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.
  • Buschke-Lowenstein tumor, or giant condyloma acuminatum, is not always included because this lesion is technically benign, although it displays aggressive local invasive behavior that makes it difficult to manage.
  • 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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  • [Cites] Dis Colon Rectum. 2008 Dec;51(12):1842-5 [18584248.001]
  • [Cites] J Am Acad Dermatol. 2007 Aug;57(2 Suppl):S36-7 [17637368.001]
  • [Cites] Dermatol Surg. 2007 Apr;33(4):427-31; discussion 431-2 [17430376.001]
  • [Cites] Br J Dermatol. 2007 Jan;156(1):11-21 [17199561.001]
  • [Cites] Dermatol Surg. 2001 Jun;27(6):587-90 [11442599.001]
  • [Cites] Dis Colon Rectum. 1997 Oct;40(10):1187-94 [9336114.001]
  • [Cites] Br J Dermatol. 1995 Jun;132(6):970-2 [7662577.001]
  • [Cites] Dis Colon Rectum. 2003 May;46(5):612-6 [12792436.001]
  • [Cites] Dis Colon Rectum. 2004 Oct;47(10):1655-60; discussion 1660-1 [15540295.001]
  • (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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50. Pham TT, Selim MA, Burchette JL Jr, Madden J, Turner J, Herman C: CD10 expression in trichoepithelioma and basal cell carcinoma. J Cutan Pathol; 2006 Feb;33(2):123-8
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  • [Title] CD10 expression in trichoepithelioma and basal cell carcinoma.
  • BACKGROUND: Trichoepithelioma (TE) is a benign neoplasm that shares both clinical and histologic features with basal cell carcinoma (BCC).
  • Cases were analyzed for pattern of CD10 expression by tumor cells and surrounding stroma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Basal Cell / metabolism. Neoplasms, Basal Cell / metabolism. Neprilysin / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 16420307.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.24.11 / Neprilysin
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51. Chaichamnan K, Satayasoontorn K, Puttanupaab S, Attainsee A: Malignant proliferating trichilemmal tumors with CD34 expression. J Med Assoc Thai; 2010 Nov;93 Suppl 6:S28-34
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  • Malignant proliferating trichilemmal tumors (MPTT) are rare neoplasm arising from outer root sheath of hair follicle, the diagnosis of which is base essentially on histological features resulting in occasionally misdiagnosis of squamous cell carcinoma.
  • In difficult cases, however evaluation of additional parameters may be needed to differentiate benign proliferating trichilemmal tumor from MPTT or differentiate PTT and MPTT from squamous cell carcinoma.
  • For comparison, concurrent proliferating trichilemmal tumors (PTT) and trichilemmal cysts (TC) as well as well-differentiated squamous cell carcinoma (SCC) were studied.
  • The PTTs and TCs stained negative and few basal cells for p53 and Ki-67, respectively.
  • [MeSH-major] Antigens, CD34 / metabolism. Carcinoma, Squamous Cell / metabolism. Epidermal Cyst / pathology. Hair Follicle / pathology. Scalp / pathology. Skin Neoplasms / pathology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Middle Aged. Neoplasm Recurrence, Local. Treatment Outcome

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  • (PMID = 21280514.001).
  • [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
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Tumor Suppressor Protein p53
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52. Hameed O, Humphrey PA: Immunohistochemistry in diagnostic surgical pathology of the prostate. Semin Diagn Pathol; 2005 Feb;22(1):88-104
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  • Basal cell markers, such as the 34betaE12 antibody and antibodies directed against cytokeratin 5 and 6 or p63, are very useful for demonstration of basal cells as their presence argues against a diagnosis of invasive prostatic carcinoma (PC).
  • However, several benign mimickers of PC, including atrophy, atypical adenomatous hyperplasia (AAH), nephrogenic adenoma, and mesonephric hyperplasia, can stain negatively with these markers, and thus, a negative basal cell marker immunostain alone does not exclude a diagnosis of benignancy.
  • Although there are examples in the literature of high grade PC that stain focally with some of the basal cell markers, these cases are usually readily diagnosed based on H&E appearances and are unlikely to be confused with these benign mimickers.
  • AMACR expression can also be identified in high grade prostatic intraepithelial neoplasia (PIN), prostatic atrophy, AAH, and benign prostatic glands, and accordingly, a diagnosis of PC should not be based solely on a positive AMACR immunostain, especially when the luminal staining is weak and/or noncircumferential.
  • The use of AMACR/basal cell antibody cocktails has been found to greatly facilitate the distinction between PC and its benign mimickers, especially when only limited tissue is available for staining.
  • AMACR positivity and negative basal cell marker reactions are useful to confirm the presence of residual PC after hormonal or radiation therapy.
  • [MeSH-minor] Biomarkers, Tumor / analysis. Carcinoma, Small Cell / diagnosis. Carcinoma, Small Cell / pathology. Diagnosis, Differential. Humans. Leukemia / diagnosis. Lymphoma / diagnosis. Male. Neoplasm Metastasis. Sarcoma / diagnosis. Sensitivity and Specificity. Urinary Bladder Neoplasms / diagnosis


53. Punnya AV, Rekha K: "Ameloblastoma with mucous cells": review of literature and presentation of 2 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2008 Dec;106(6):e20-6
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  • Ameloblastoma, a relatively rare benign odontogenic tumor; originates from the odontogenic epithelium and has been studied extensively for its unique clinicopathologic features.
  • It usually exhibits a range of histopathologic features, such as follicular, plexiform, acanthomatous, granular, basal cell, and desmoplastic variants, which are well recognized.
  • Histologically, the mucous cells in most cases were associated with areas of squamous metaplasia, suggesting a close relation between these 2 cell types.
  • [MeSH-minor] Adolescent. Adult. Cell Differentiation. Epithelial Cells / pathology. Humans. Male. Mucins / analysis

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  • (PMID = 19000605.001).
  • [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
  • [Chemical-registry-number] 0 / Mucins
  • [Number-of-references] 28
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54. Obata H, Aoki Y, Kubota S, Kanai N, Tsuru T: [Incidence of benign and malignant lesions of eyelid and conjunctival tumors]. Nippon Ganka Gakkai Zasshi; 2005 Sep;109(9):573-9
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  • [Title] [Incidence of benign and malignant lesions of eyelid and conjunctival tumors].
  • PURPOSE: To examine the incidence of benign and malignant eyelid lesions and conjunctival tumors.
  • The incidence of benign or malignant lesions, the pathological classification, age, sex, and clinical diagnostic accuracy were all investigated.
  • RESULTS: Sixty-four (73%) of the tumors were found to be benign eyelid tumors.
  • The common benign eyelid tumors were 14 nevocellular nevi, 9 seborrheic keratosis, 7 epidermoid cysts, and 6 papillomas.
  • These included 9 basal cell carcinomas, 9 sebaceous gland carcinomas, 4 malignant lymphomas, and 2 metastatic tumors.
  • Thirty-four (79%) conjunctival tumors were benign, and the common benign conjunctival tumors were 9 nevocellular nevi and 7 papillomas.
  • Nine (21%) conjunctival tumors were malignant, comprising 7 malignant lymphomas and 2 squamous cell carcinomas.
  • The mean ages of malignant eyelid and conjunctival tumor patients were significantly older than those of benign tumor patients.
  • Clinical accuracy in predicting basal cell carcinoma and sebaceous gland carcinoma was 11.1% and 44.4%, respectively.
  • CONCLUSIONS: Approximately 70 approximately 80% of all eyelid and conjunctival tumors are benign.
  • [MeSH-minor] Aged. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / pathology. Female. Humans. Incidence. Lymphoma / epidemiology. Lymphoma / pathology. Male. Middle Aged. Retrospective Studies

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  • (PMID = 16218435.001).
  • [ISSN] 0029-0203
  • [Journal-full-title] Nippon Ganka Gakkai zasshi
  • [ISO-abbreviation] Nippon Ganka Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 27
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55. Gil da Costa RM, Rema A, Pires MA, Gärtner F: Two canine Merkel cell tumours: immunoexpression of c-KIT, E-cadherin, beta-catenin and S100 protein. Vet Dermatol; 2010 Apr;21(2):198-201
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  • [Title] Two canine Merkel cell tumours: immunoexpression of c-KIT, E-cadherin, beta-catenin and S100 protein.
  • Canine Merkel cell tumours are rare neuroendocrine neoplasms that show a relatively benign biological behaviour when compared with their human counterparts.
  • In both lesions, tumour cells were positive for cytokeratins, CGA, NSE, S100 and c-KIT.
  • These results suggest that the generally benign behaviour of canine Merkel cell tumours, when compared with their human counterparts, may be partly explained by the conservation of important intercellular adhesion molecules such as E-cadherin and beta-catenin.
  • Additionally, expression of S100 but not of the p63 protein suggests that these canine tumours present a trend towards neural, rather than basal, epithelial differentiation and do not readily compare with human Merkel cell tumours.
  • [MeSH-major] Cadherins / metabolism. Carcinoma, Merkel Cell / metabolism. Dog Diseases / diagnosis. Proto-Oncogene Proteins c-kit / metabolism. S100 Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Dogs. Female. Gene Expression Regulation, Neoplastic / physiology. Male

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  • (PMID = 19706008.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / S100 Proteins; 0 / beta Catenin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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56. Wang Y, Yang J, Gao Y, Zhao XL, Li HZ, Yao Z: [Relationship between raf kinase inhibitor protein and metastasis of ovarian carcinoma]. Zhonghua Fu Chan Ke Za Zhi; 2009 Jul;44(7):522-8
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  • METHODS: Immunohistochemistry, RT-PCR, and western blot analysis were performed to examine the expression of RKIP in clinical samples of ovarian tumors and five human ovarian carcinoma cell lines.
  • Stable cell lines over-expressed or deleted of RKIP were cloned to investigate the function of RKIP in ovarian cancer cells.
  • The recombinant plasmids expressing sense (ss) or antisense (as) RKIP cDNA or empty vector was transfected into ovarian cancer cell line SKOV3 by lipofectamine.
  • Assays of cell proliferation, soft-agar colony formation, cell adhesion, and cell invasion in vitro were used to examine the malignant phenotypes of the transfected cells.
  • Flow cytometric analysis was performed to observe the effect of RKIP on cell cycle distribution before and after transfection. RESULTS:.
  • (1) The expression levels of RKIP protein in ovarian carcinoma tissues from patients were found to be reduced than those in ovarian benign tumor and borderline tumor.
  • SKOV3 clones stably expressing full-length recombinant ssRKIP, asRKIP, and their respective empty vector were obtained. (2) RKIP was able to block basal levels of MEK and ERK in ovarian cancer cells.
  • 48 and 0.46. (3) Abilities of cell proliferation in the ssRKIP vector-transfected cells were decreased compared with that in the non-transfected cells (P < 0.01). (4)Anchorage-independent growth in the ssRKIP#1 and ssRKIP#4 cells (83.7 +/- 5.7, 106.0 +/- 9.2) were decreased compared with that in the empty vector-transfected cells (158.3 +/- 14.6, P < 0.01). (5)Cell adhesion in the ssRKIP#1 and ssRKIP#4 cells [(68.3 +/- 0.8)%, (64.1 +/- 0.9)%] were decreased compared with that in the non-transfected cells [(100.0 +/- 1.1)%, P < 0.01]. (6) Cell invasion in the ssRKIP#1 and ssRKIP#4 cells (24 +/- 5, 25 +/- 4) were decreased compared with that in the non-transfected cells (68 +/- 5, P < 0.01). (7) ssRKIP cells had a significant increase in the G1 phase and decrease in the G2 + S phase.
  • CONCLUSION: RKIP could inhibits the metastasis, but also the growth of ovarian cancer cells. patients were found to be reduced than those in ovarian benign tumor and borderline tumor.
  • SKOV3 clones stably expressing full-length recombinant ssRKIP, asRKIP, and their respective empty vector were obtained. (2) RKIP was able to block basal levels of MEK and ERK in ovarian cancer cells.
  • The expression level of phosphorylation MEK in ssRKIP#1 and ssRKIP#4 cells were 0.35, 0.34; while the expression level of phosphorylation ERK in ssRKIP #1 and ssRKIP #4 cells were 0.48 and 0.46. (3) Abilities of cell proliferation in the ssRKIP vector-transfected cells were decreased compared with that in the non-transfected cells (P < 0.01). (4) Anchorage-independent growth in the ssRKIP#1 and ssRKIP#4 cells (83.7 +/- 5.7, 106.0 +/- 9.2) were decreased compared with that in the empty vector-transfected cells (158.3 +/- 14.6, P < 0.01). (5) Cell adhesion in the ssRKIP#1 and ssRKIP#4 cells [(68.3 +/- 0.8)%, (64.1 +/- 0.9)%] were decreased compared with that in the non-transfected cells [(100.0 +/- 1.1)%, P < 0.01]. (6) Cell invasion in the ssRKIP#1 and ssRKIP#4 cells (24 +/- 5, 25 +/- 4) were decreased compared with that in the nontransfected cells (68 +/- 5, P < 0.01). (7) ssRKIP cells had a significant increase in the G1 phase and decrease in the G2 + S phase.
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line, Tumor. Cell Proliferation. Female. Genes, Tumor Suppressor. Genetic Vectors. Humans. Immunohistochemistry. Middle Aged. Neoplasm Invasiveness. Neoplasm Metastasis. Phosphorylation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Young Adult

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  • (PMID = 19957553.001).
  • [ISSN] 0529-567X
  • [Journal-full-title] Zhonghua fu chan ke za zhi
  • [ISO-abbreviation] Zhonghua Fu Chan Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Phosphatidylethanolamine Binding Protein; 0 / RNA, Messenger; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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57. Ogawa R, Akaishi S, Hyakusoku H: Differential and exclusive diagnosis of diseases that resemble keloids and hypertrophic scars. Ann Plast Surg; 2009 Jun;62(6):660-4
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  • Previous articles suggested the presence of various kinds of malignant tumors that resemble keloid or hypertrophic scar, including dermatofibrosarcoma protuberans, trichilemmal carcinoma, and keloidal basal cell carcinoma.
  • All tumors were benign: apocrine cystadenoma, adult-onset juvenile xanthogranuloma, mixed tumor, and chronic folliculitis.
  • (1) biopsy should be conducted in anomalous cases because malignant disease may be the original or secondary problem, (2) steroid injection should be performed only after careful consideration because malignancy or infections may be present, (3) careful differential diagnosis is particularly challenging in African-Americans because skin and tumor color are often similar, and (4) the presence of bacterial or fungal infection should be investigated.

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  • (PMID = 19461281.001).
  • [ISSN] 1536-3708
  • [Journal-full-title] Annals of plastic surgery
  • [ISO-abbreviation] Ann Plast Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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58. Olejniczak I, Kozłowski Z, Dabrowska K, Lukomski M: [Tumors of the parotid gland--management and results of surgical treatment]. Otolaryngol Pol; 2008;62(4):446-50
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  • Different methods of surgical treatment can be performed depending on the type, localization and size of tumor.
  • Benign tumors were found in 104 patients with the pleomorphic adenoma as the most common (53 cases).
  • The rest histological type were Whartin's tumor, myoepithelial and basal cell adenoma respectively.
  • The most frequent localization of the tumor after dividing the parotid gland into four parts was postero-inferior pole.

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  • (PMID = 18837221.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
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59. Seili-Bekafigo I, Jonjić N, Stemberger C, Rajković-Molek K: Additional cytomorphological criteria in diagnosis of pilomatricoma--benign tumor with bad reputation. Coll Antropol; 2010 Mar;34(1):117-22
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  • [Title] Additional cytomorphological criteria in diagnosis of pilomatricoma--benign tumor with bad reputation.
  • Pilomatricomas (PM) are benign skin appendageal tumors, with differentiation towards hair-forming cells, usually found in children.
  • PM are often mistaken for "small round blue cell" tumors in children, or for Merkel cell carcinoma, basalioma and metastatic small cell carcinoma in adults, with possible over-aggressive therapeutic approach.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biopsy, Fine-Needle. Carcinoma, Basal Cell / pathology. Carcinoma, Merkel Cell / pathology. Child. Diagnosis, Differential. Eosine Yellowish-(YS). Epithelial Cells / pathology. Female. Humans. Male. Methylene Blue. Middle Aged

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  • (PMID = 20432739.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / May-Grunwald Giemsa; T42P99266K / Methylene Blue; TDQ283MPCW / Eosine Yellowish-(YS)
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60. Abdou AG, Aiad HA, Sultan SM: pS2 (TFF1) expression in prostate carcinoma: correlation with steroid receptor status. APMIS; 2008 Nov;116(11):961-71
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  • It is also considered to be one of the major estrogen-regulated proteins and an indicator of estrogen receptor (ER) functionality. pS2 has previously been investigated in benign and malignant prostate lesions with little information about its relationship to steroid receptor status.
  • 15 benign prostate hyperplasia (BPH) and 47 prostate carcinoma cases were investigated by means of immunohistochemistry for pS2, ER and PR expression.
  • 80% of BPH showed pS2 cytoplasmic immunoreactivity in hyperplastic acini and about half of these cases also exhibited nuclear staining decorating basal or both basal and luminal nuclei. pS2 was highly expressed in prostate carcinoma (91.4%) with both cytoplasmic and nuclear patterns of staining.
  • The nuclear pattern of pS2 immunoreactivity either in benign or malignant prostatic lesions is similar to the published data on ER beta distribution and could also identify a subset of carcinoma patients with a favorable prognosis.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Carcinoma / pathology. Estrogen Receptor alpha / metabolism. Presenilin-2 / biosynthesis. Prostate / pathology. Prostatic Neoplasms / pathology. Receptors, Progesterone / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / metabolism. Cytoplasm / metabolism. Estrogens / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Prognosis. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology

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  • (PMID = 19132993.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / PSEN2 protein, human; 0 / Presenilin-2; 0 / Receptors, Progesterone
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61. Andreadis D, Epivatianos A, Poulopoulos A, Nomikos A, Papazoglou G, Antoniades D, Barbatis C: Detection of C-KIT (CD117) molecule in benign and malignant salivary gland tumours. Oral Oncol; 2006 Jan;42(1):57-65
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  • [Title] Detection of C-KIT (CD117) molecule in benign and malignant salivary gland tumours.
  • Archival formalin-fixed, paraffin-embedded sections of 40 benign and 57 malignant salivary gland tumours were retrieved and retrospectively studied immunohistochemically using a polyclonal C-KIT antibody in an Envision/HRP technique.
  • In addition five samples of chronic submandibular sialadenitis, five normal minor salivary glands and parotid or submandibular gland tissue adjacent to benign tumour were also studied.
  • C-KIT expression was observed in cases of adenoid cystic, acinic cell polymorphous low grade, epithelial-myoepithelial, carcinosarcoma and basal cell adenocarcinomas, as in luminal cells of pleomorphic adenomas, in serous acinar and only in intercalated and a small number of striated ductal cells of inflammatory salivary gland tissue, whereas normal salivary lobules were generally negative except a weak positivity of intercalated cells.
  • Contrary to other reports, this study suggests that, C-KIT protein does not appear to be an exclusively specific marker for benign or malignant salivary gland neoplasms, but may be useful in differential diagnosis of adenoid cystic carcinoma from polymorphous low grade adenocarcinoma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Adenoid Cystic / chemistry. Proto-Oncogene Proteins c-kit / analysis. Salivary Gland Neoplasms / chemistry

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  • (PMID = 16140564.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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62. Sengul D, Sengul I, Astarci MH, Ustun H, Mocan G: CD10 for the distinct differential diagnosis of basal cell carcinoma and benign tumours of cutaneous appendages originating from hair follicle. Pol J Pathol; 2010;61(3):140-6
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  • [Title] CD10 for the distinct differential diagnosis of basal cell carcinoma and benign tumours of cutaneous appendages originating from hair follicle.
  • AIMS: Differential diagnosis between the group of trichoadenoma, trichofolliculoma, trichoepithelioma, trichoblastoma and basal cell carcinoma has been creating some difficulties for the pathologist and the clinicians, particularly in the presence of small specimens.
  • MATERIAL AND METHODS: A total of 30 cases of benign tumours of cutaneous appendages originating from the hair follicle and 30 cases of basal cell carcinoma were retrieved from the archives deposited from 2004 to 2008.
  • The stromal CD10 immunopositivity of benign tumours of cutaneous appendages originating from the hair follicle was stronger than the other (p = 0.003) regarding both the numerical and the degree of expression.
  • However, peripheral CD10 of basal cell carcinoma was stronger than the other for [1+] immunopositivity (p = 0.03).
  • [MeSH-major] Carcinoma, Basal Cell / diagnosis. Carcinoma, Skin Appendage / diagnosis. Hair Follicle / pathology. Neprilysin / metabolism. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 21225496.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.24.11 / Neprilysin
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63. Freier K, Pungs S, Flechtenmacher C, Hofele C: [Activation of sonic hedgehog signaling in keratocystic odontogenic tumors]. HNO; 2009 Apr;57(4):345-50
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  • BACKGROUND: Keratocystic odontogenic tumors are benign neoplasms of the viscerocranium that occur sporadically as well as in association with Gorlin-Goltz syndrome.
  • Multiple basal cell carcinomas of the skin are another typical feature of Gorlin-Goltz syndrome.
  • Aberrant activation of sonic hedgehog signaling has been reported for sporadic and hereditary basal cell carcinoma caused by specific genetic mutations, but for keratocystic odontogenic tumors, the role of aberrant sonic hedgehog signaling has not yet been evaluated in detail.
  • [MeSH-minor] Gene Expression Regulation, Neoplastic. Humans. Tumor Cells, Cultured

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  • [Cites] Cell. 1996 Jun 14;85(6):841-51 [8681379.001]
  • [Cites] J Pathol. 2001 Aug;194(4):473-7 [11523056.001]
  • [Cites] Cancer Res. 1997 Jun 15;57(12):2336-40 [9192803.001]
  • [Cites] Br J Oral Maxillofac Surg. 1997 Feb;35(1):46-8 [9043004.001]
  • [Cites] J Can Dent Assoc. 2008 Mar;74(2):165-165h [18353202.001]
  • [Cites] J Mol Med (Berl). 1999 Jun;77(6):459-68 [10475061.001]
  • [Cites] Cancer. 1992 Dec 15;70(12):2988-94 [1451083.001]
  • [Cites] Anticancer Res. 2003 Sep-Oct;23(5A):3971-7 [14666705.001]
  • [Cites] J Oral Maxillofac Surg. 2006 Mar;64(3):379-83 [16487797.001]
  • [Cites] Am J Pathol. 2006 Sep;169(3):806-14 [16936257.001]
  • [Cites] J Clin Pathol. 2001 Dec;54(12):897-910 [11729208.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12 ):7331-6 [12777630.001]
  • [Cites] Int J Oral Maxillofac Surg. 2004 Sep;33(6):584-92 [15308259.001]
  • [Cites] Development. 1998 Aug;125(15):2803-11 [9655803.001]
  • [Cites] Nat Med. 1998 Jul;4(7):844-7 [9662379.001]
  • [Cites] Mund Kiefer Gesichtschir. 2006 Jan;10(1):1-2 [16328532.001]
  • [Cites] J Oral Pathol. 1988 Jan;17(1):39-42 [3131508.001]
  • [Cites] Pathol Int. 1999 Aug;49(8):687-94 [10504535.001]
  • [Cites] Am J Med Genet. 1997 Mar 31;69(3):299-308 [9096761.001]
  • [Cites] Hum Mol Genet. 2001 Apr;10 (7):757-62 [11257109.001]
  • [Cites] Oncol Rep. 2006 May;15(5):1141-5 [16596176.001]
  • [Cites] Mund Kiefer Gesichtschir. 2002 Nov;6(6):394-401 [12447651.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998 Jul;86(1):42-7 [9690244.001]
  • (PMID = 19082818.001).
  • [ISSN] 1433-0458
  • [Journal-full-title] HNO
  • [ISO-abbreviation] HNO
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hedgehog Proteins
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64. Escaff S, Fernández JM, González LO, Suárez A, González-Reyes S, González JM, Vizoso FJ: Study of matrix metalloproteinases and their inhibitors in prostate cancer. Br J Cancer; 2010 Mar 2;102(5):922-9
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  • BACKGROUND: Extracellular matrix metalloproteases (MMPs) have raised an extraordinary interest in cancer research because of their potential role in basal membrane and extracellular matrix degradation, consequently facilitating tumour invasion and metastases development.
  • More than 2600 determinations on cancer specimens from 133 patients with clinically localised prostate carcinoma, 20 patients with prostatic intraepithelial neoplasia and 50 patients with benign prostate hyperplasia and controls, were performed.
  • RESULTS: When compared with benign pathologies, prostate carcinomas had higher expression of all MMPs and TIMPs.
  • CONCLUSION: The expression of MMPs and TIMPs seems to have an important role in the molecular biology of prostate carcinomas, and their expression by tumours may be of clinical interest to used as indicators of tumour aggressiveness.
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Follow-Up Studies. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Prognosis. Survival Rate. Tissue Array Analysis

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  • [Cites] Clin Exp Dermatol. 1999 Mar;24(2):122-6 [10233668.001]
  • [Cites] J Clin Invest. 1999 May;103(9):1237-41 [10225966.001]
  • [Cites] Nat Rev Cancer. 2005 Jan;5(1):21-8 [15630412.001]
  • [Cites] Urol Res. 2005 Feb;33(1):44-50 [15517230.001]
  • [Cites] Am J Pathol. 2005 Apr;166(4):1173-86 [15793297.001]
  • [Cites] Thromb Haemost. 2005 Apr;93(4):770-8 [15841326.001]
  • [Cites] Cancer Cell. 2005 May;7(5):485-96 [15894268.001]
  • [Cites] Endocr Relat Cancer. 2005 Jun;12(2):215-27 [15947098.001]
  • [Cites] Br J Cancer. 2005 Jun 20;92(12):2171-80 [15928670.001]
  • [Cites] J Clin Pathol. 2005 Jul;58(7):673-84 [15976331.001]
  • [Cites] Prog Urol. 2005 Apr;15(2):250-4 [15999602.001]
  • [Cites] Crit Rev Immunol. 2005;25(6):493-523 [16390324.001]
  • [Cites] Anticancer Res. 2006 Mar-Apr;26(2A):973-82 [16619495.001]
  • [Cites] Clin Exp Metastasis. 2006;23(7-8):335-44 [17136575.001]
  • [Cites] Br J Cancer. 2007 Mar 26;96(6):903-11 [17342087.001]
  • [Cites] Neoplasia. 2007 Apr;9(4):349-57 [17460779.001]
  • [Cites] Am J Pathol. 2007 Jun;170(6):2100-11 [17525276.001]
  • [Cites] Br J Cancer. 2007 Oct 8;97(7):957-63 [17848954.001]
  • [Cites] J Biol Chem. 2008 Mar 7;283(10):6232-40 [18174174.001]
  • [Cites] Int J Oncol. 2008 Apr;32(4):757-65 [18360703.001]
  • [Cites] Oncology. 2008;75(3-4):230-6 [18852494.001]
  • [Cites] J Clin Oncol. 2000 Mar;18(5):1135-49 [10694567.001]
  • [Cites] Int J Cancer. 2000 Mar 20;89(2):118-21 [10756061.001]
  • [Cites] Hum Pathol. 2000 Jul;31(7):860-5 [10923925.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4823-30 [11156241.001]
  • [Cites] J Cell Sci. 2001 Jan;114(Pt 1):111-118 [11112695.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):1022-8 [11221828.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2189-93 [11280785.001]
  • [Cites] Br J Cancer. 2001 Apr 20;84(8):1076-83 [11308257.001]
  • [Cites] Neoplasia. 2001 Nov-Dec;3(6):459-68 [11774028.001]
  • [Cites] Oncogene. 2002 Mar 28;21(14):2245-52 [11948407.001]
  • [Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]
  • [Cites] Am J Clin Pathol. 2002 May;117(5):723-8 [12090420.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):657-72 [12209155.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):68-75 [12538453.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2003;6(1):15-26 [12664060.001]
  • [Cites] Int J Cancer. 2003 Nov 1;107(2):309-16 [12949813.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2003;6(3):217-22 [12970724.001]
  • [Cites] Clin Exp Metastasis. 2003;20(6):541-7 [14598888.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8511-5 [14679018.001]
  • [Cites] Breast Cancer Res. 2004;6(1):R24-30 [14680497.001]
  • [Cites] Am J Pathol. 2004 Apr;164(4):1131-9 [15039201.001]
  • [Cites] Oncol Rep. 2004 Jun;11(6):1187-92 [15138554.001]
  • [Cites] Cancer Cell. 2004 May;5(5):409-10 [15144947.001]
  • [Cites] Nature. 1990 Dec 20-27;348(6303):699-704 [1701851.001]
  • [Cites] J Biol Chem. 1994 Jun 17;269(24):16766-73 [8207000.001]
  • [Cites] In Vivo. 1994 May-Jun;8(3):439-43 [7803731.001]
  • [Cites] Int J Cancer. 1996 Dec 20;69(6):448-51 [8980245.001]
  • [Cites] J Biol Chem. 1997 Mar 21;272(12):7608-16 [9065415.001]
  • [Cites] Crit Rev Oncol Hematol. 1997 May;26(1):43-53 [9246540.001]
  • [Cites] Int J Cancer. 1998 Feb 20;79(1):96-101 [9495366.001]
  • [Cites] Am J Pathol. 1998 Mar;152(3):721-8 [9502414.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] J Immunol. 1998 Dec 15;161(12):6845-52 [9862716.001]
  • [Cites] J Biol Chem. 1999 Mar 12;274(11):6935-45 [10066747.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2004;7(4):327-32 [15356679.001]
  • (PMID = 20160732.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ PMC2833257
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65. Saghafi S, Zare-Mahmoodabadi R, Salehinejad J, Kadeh H, Afzal-Aghaee M: Immunohistochemical analysis of p53 and PCNA expression in calcifying odontogenic cyst. J Oral Sci; 2010 Dec;52(4):609-13
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  • Because of its diverse histopathologic features and biological behavior, there has long been confusion with regard to its nature as a cyst or neoplasm.
  • This study evaluated the proliferative activity of 57 COC samples, including simple cyst (10 cases), cystic neoplasm (34 cases), solid neoplasm (6 cases) and combined lesion (7 cases) by p53 and PCNA immunohistochemical staining.
  • For assessment of p53 and PCNA positivity, the number of positively stained cells with brown-stained nuclei was counted in 1000 cells from each sample. p53 and PCNA expression in the solid neoplasm subtype were significantly higher when compared to cystic neoplasm and simple cyst (P < 0.05).
  • The lowest p53 and PCNA expression was found in the simple cyst subtype. p53 and PCNA expression in the basal and suprabasal layers was significantly higher in the solid subtype when compared to others, and the difference between COC groups was significant.
  • The results demonstrated that within benign types of COC, the amount of p53 and PCNA in proliferative epithelium is significantly higher when compared to non-proliferative epithelium. p53 and PCNA markers are possible parameters for differentiation of COC subtypes.
  • [MeSH-major] Jaw Neoplasms / metabolism. Odontogenic Cyst, Calcifying / metabolism. Proliferating Cell Nuclear Antigen / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 21206164.001).
  • [ISSN] 1880-4926
  • [Journal-full-title] Journal of oral science
  • [ISO-abbreviation] J Oral Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 0 / Tumor Suppressor Protein p53
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66. Barbarino S, McCormick SA, Lauer SA, Milman T: Syringocystadenoma papilliferum of the eyelid. Ophthal Plast Reconstr Surg; 2009 May-Jun;25(3):185-8
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  • PURPOSE: To describe 6 patients with syringocystadenoma papilliferum of the eyelid and to review the literature regarding this rare eyelid tumor.
  • Most cases had a preoperative diagnosis of basal cell carcinoma or cyst.
  • Papillary structures with plasma cell-rich stromal infiltrate protruded in the cystic invaginations.
  • None of the lesions was associated with a malignant neoplasm.
  • This lesion is frequently clinically misdiagnosed as basal cell carcinoma or cyst.
  • Although syringocystadenoma papilliferum of the eyelid can be associated with other benign lesions, no malignant transformation or association with malignant neoplasms has been reported.
  • The evidence suggests that this tumor should be managed with conservative complete excision.

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  • (PMID = 19454927.001).
  • [ISSN] 1537-2677
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 12
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67. Garraway IP, Sun W, Tran CP, Perner S, Zhang B, Goldstein AS, Hahm SA, Haider M, Head CS, Reiter RE, Rubin MA, Witte ON: Human prostate sphere-forming cells represent a subset of basal epithelial cells capable of glandular regeneration in vivo. Prostate; 2010 Apr 1;70(5):491-501
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  • [Title] Human prostate sphere-forming cells represent a subset of basal epithelial cells capable of glandular regeneration in vivo.
  • They may be targets for tumor initiation, so characterization of these cells may have therapeutic implications.
  • Subpopulations of prostate epithelial cells were isolated by cell sorting and interrogated for sphere-forming activity.
  • RESULTS: Prostate tissue specimens were heterogeneous, containing both benign and malignant (Gleason 3-5) glands.
  • A basal phenotype (CD44+CD49f+CK5+p63+CK8-AR-PSA-) was observed among sphere-forming cells.
  • Subpopulations of prostate cells expressing tumor-associated calcium signal transducer 2 (Trop2), CD44, and CD49f preferentially formed spheres.
  • In vivo implantation of sphere-forming cells and rUGSM regenerated tubular structures containing discreet basal and luminal layers.
  • The TMPRSS-ERG fusion was absent in prostaspheres derived from fusion-positive tumor tissue, suggesting a survival/growth advantage of benign prostate epithelial cells.
  • CONCLUSION: Human prostate sphere-forming cells self-renew, have tissue regeneration capability, and represent a subpopulation of basal cells.

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • [Cites] Br J Cancer. 2000 Feb;82(4):990-7 [10732776.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20882-7 [19088204.001]
  • [Cites] Br J Cancer. 2001 Aug 17;85(4):590-9 [11506501.001]
  • [Cites] J Cell Sci. 2001 Nov;114(Pt 21):3865-72 [11719553.001]
  • [Cites] J Pathol. 2001 Dec;195(5):563-70 [11745692.001]
  • [Cites] Mol Cancer Res. 2002 Dec;1(2):113-21 [12496358.001]
  • [Cites] Genes Dev. 2003 May 15;17(10):1253-70 [12756227.001]
  • [Cites] Brain Res. 2003 Dec 12;993(1-2):18-29 [14642827.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] J Cell Sci. 2004 Jul 15;117(Pt 16):3539-45 [15226377.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7274-82 [15378087.001]
  • [Cites] Prostate. 2004 Nov 1;61(3):209-14 [15368472.001]
  • [Cites] J Neurosci Res. 2004 Oct 15;78(2):215-23 [15378509.001]
  • [Cites] J Steroid Biochem Mol Biol. 1996 Nov;59(3-4):243-50 [9010316.001]
  • [Cites] Differentiation. 1998 Jul;63(3):131-40 [9697307.001]
  • [Cites] Hum Pathol. 1998 Sep;29(9):1005-12 [9744319.001]
  • [Cites] J Cell Physiol. 1999 Nov;181(2):304-11 [10497309.001]
  • [Cites] Acta Biochim Pol. 2005;52(2):353-8 [15990920.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9269-79 [16230388.001]
  • [Cites] Science. 2005 Oct 28;310(5748):644-8 [16254181.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10946-51 [16322242.001]
  • [Cites] Nat Med. 2006 Mar;12(3):296-300 [16520777.001]
  • [Cites] Science. 2006 Mar 31;311(5769):1880-5 [16574858.001]
  • [Cites] Cancer Cell. 2006 May;9(5):367-78 [16697957.001]
  • [Cites] Eur J Cancer. 2006 Jun;42(9):1213-8 [16632344.001]
  • [Cites] Brain Res. 2006 Aug 30;1107(1):82-96 [16859652.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8598-607 [16951173.001]
  • [Cites] N Engl J Med. 2006 Sep 21;355(12):1253-61 [16990388.001]
  • [Cites] Nat Methods. 2006 Oct;3(10):801-6 [16990812.001]
  • [Cites] Mol Carcinog. 2007 Jan;46(1):1-14 [16921491.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):181-6 [17185413.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4807-15 [17510410.001]
  • [Cites] Prostate. 2007 Sep 15;67(13):1384-96 [17639507.001]
  • [Cites] Dev Biol. 2007 Dec 1;312(1):396-406 [17976567.001]
  • [Cites] Cancer Res. 2008 Dec 1;68(23):9703-11 [19047148.001]
  • [Cites] Prostate. 2001 Feb 1;46(2):142-53 [11170142.001]
  • (PMID = 19938015.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-16042; United States / NIAID NIH HHS / AI / AI-28697; United States / NHGRI NIH HHS / HG / F31 HG000117; United States / NCI NIH HHS / CA / P30 CA016042; United States / NHGRI NIH HHS / HG / HG000117-05; United States / NIAID NIH HHS / AI / P30 AI028697; United States / NHGRI NIH HHS / HG / F31 HG000117-05
  • [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 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / Glycoproteins; 0 / Integrin alpha6; 0 / Oncogene Proteins, Fusion; 0 / Peptides; 0 / TMPRSS2-ERG fusion protein, human
  • [Other-IDs] NLM/ NIHMS187861; NLM/ PMC2885946
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68. Stelkovics E, Korom I, Marczinovits I, Molnar J, Rasky K, Raso E, Ficsor L, Molnar B, Kopper L, Krenacs T: Collagen XVII/BP180 protein expression in squamous cell carcinoma of the skin detected with novel monoclonal antibodies in archived tissues using tissue microarrays and digital microscopy. Appl Immunohistochem Mol Morphol; 2008 Oct;16(5):433-41
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  • [Title] Collagen XVII/BP180 protein expression in squamous cell carcinoma of the skin detected with novel monoclonal antibodies in archived tissues using tissue microarrays and digital microscopy.
  • In this work, highly sensitive monoclonal antibodies 6D1 and 9G2 were produced, characterized, and used for the detection of collagen XVII in a tissue microarray series of archived samples of nonmelanocytic epithelial neoplasias, including 5 verruca vulgaris, 14 seborrheic keratosis, 38 actinic keratosis, 38 basal cell carcinoma (BCC), 15 basosquamous carcinoma, 58 squamous cell carcinoma (SCC), and 9 normal skin.
  • In normal skin and benign epidermal lesions, collagen XVII protein was restricted to basal keratinocytes.
  • However, possibly as a sign of undifferentiated/transformed state, it was widely expressed in SCC showing elevated levels around invasive tumor fronts with some staining in tumor adjacent stroma, endothelium, and histiocytes.

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  • (PMID = 18633319.001).
  • [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 / Antibodies, Monoclonal; 0 / Autoantigens; 0 / Biomarkers, Tumor; 0 / Non-Fibrillar Collagens; 0 / collagen type XVII
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69. Sun HB, Wang H, Taylor RA, Risbridger GP: [Establishment of a xenograft model of human prostate cancer in mouse]. Zhonghua Yi Xue Za Zhi; 2010 Aug 10;90(30):2136-9
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  • OBJECTIVE: To establish the murine xenograft model of human prostate cancer by grafting tumor tissues beneath the renal capsule of intact male athymic mouse.
  • At Week 4 after initial implantation, grafts were harvested and tumor sizes calculated.
  • P63 protein, a basal cell marker, was detected in prostate basal membrane to identify whether it was benign or malignant tissue.
  • RESULTS: Of all 78 implantation cases in 15 mice, the tumor-forming rates were 100% (39/39) and 94.1% (37/39) respectively in the recombination and prostate cancer alone grafting groups.
  • The recombination group was shown to be more efficient in terms of tumor size and weight in comparison with the prostate cancer alone group [(9.7 ± 3.1) vs (6.8 ± 2.0) mm(3), (12.1 ± 3.6) vs (8.2 ± 2.2) µg, P < 0.01].
  • [MeSH-minor] Animals. Humans. Male. Mice. Mice, Inbred BALB C. Mice, SCID. Tumor Cells, Cultured


70. Zheng ZM, Baker CC: Papillomavirus genome structure, expression, and post-transcriptional regulation. Front Biosci; 2006 Sep 01;11:2286-302
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  • Papillomaviruses are a group of small non-enveloped DNA tumor viruses whose infection usually causes benign epithelial lesions (warts).
  • Papillomaviruses infect keratinocytes in the basal layer of stratified squamous epithelia and replicate in the nucleus of infected keratinocytes in a differentiation-dependent manner.
  • Viral gene expression in infected cells depends on cell differentiation and is tightly regulated at the transcriptional and post-transcriptional levels.

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  • [Cites] EMBO J. 1986 Sep;5(9):2285-92 [3023067.001]
  • [Cites] J Virol. 1987 Jan;61(1):134-42 [3023691.001]
  • [Cites] Nature. 1987 Jan 1-7;325(6099):70-3 [3025749.001]
  • [Cites] Cell. 1987 Jul 3;50(1):69-78 [3036366.001]
  • [Cites] EMBO J. 1988 Feb;7(2):525-31 [2835231.001]
  • [Cites] Cancer Res. 1988 Jul 1;48(13):3780-6 [2837324.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5864-8 [2842752.001]
  • [Cites] J Virol. 1989 Mar;63(3):1441-7 [2536845.001]
  • [Cites] J Virol. 1989 Apr;63(4):1743-55 [2538655.001]
  • [Cites] J Virol. 1989 Aug;63(8):3529-34 [2545923.001]
  • [Cites] Virology. 1989 Sep;172(1):331-40 [2549716.001]
  • [Cites] J Virol. 1990 Apr;64(4):1825-9 [2157064.001]
  • [Cites] J Virol. 1990 Jun;64(6):2849-59 [2159546.001]
  • [Cites] Biochim Biophys Acta. 1990 Jun 1;1032(1):19-37 [2163676.001]
  • [Cites] Virology. 1990 Sep;178(1):254-62 [2167553.001]
  • [Cites] J Virol. 1991 Apr;65(4):2093-7 [1848319.001]
  • [Cites] J Virol. 1991 Sep;65(9):4860-6 [1651408.001]
  • [Cites] J Virol. 1991 Nov;65(11):5806-12 [1717710.001]
  • [Cites] Int J Cancer. 1992 Feb 1;50(3):356-64 [1310488.001]
  • [Cites] Int J Cancer. 1992 Jul 9;51(5):831-4 [1319412.001]
  • [Cites] J Virol. 1992 Oct;66(10):6070-80 [1326657.001]
  • [Cites] Virology. 1992 Dec;191(2):953-9 [1333130.001]
  • [Cites] Biochem Mol Biol Int. 1998 Aug;45(5):1005-9 [9739465.001]
  • [Cites] Nucleic Acids Res. 1998 Dec 1;26(23):5237-42 [9826743.001]
  • [Cites] Mol Cell Biol. 2000 Jan;20(1):113-25 [10594014.001]
  • [Cites] J Virol. 2000 Feb;74(3):1178-86 [10627528.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4677-82 [10781073.001]
  • [Cites] J Virol. 2000 Jul;74(13):5902-10 [10846071.001]
  • [Cites] J Virol. 2000 Aug;74(16):7284-97 [10906182.001]
  • [Cites] J Virol. 2000 Nov;74(22):10612-22 [11044105.001]
  • [Cites] J Virol. 2001 May;75(9):4139-49 [11287563.001]
  • [Cites] J Virol. 2001 Sep;75(17):8147-57 [11483760.001]
  • [Cites] J Virol. 2001 Oct;75(19):9201-9 [11533183.001]
  • [Cites] J Virol. 2002 Mar;76(5):2263-73 [11836404.001]
  • [Cites] J Virol. 2002 Mar;76(6):2739-52 [11861841.001]
  • [Cites] Nucleic Acids Res. 2002 Apr 15;30(8):1842-50 [11937639.001]
  • [Cites] J Virol. 2002 Jun;76(12):5993-6003 [12021332.001]
  • [Cites] J Virol. 2002 Jul;76(14):7040-8 [12072504.001]
  • [Cites] J Mol Biol. 2002 May 17;318(5):1189-206 [12083511.001]
  • [Cites] Oncogene. 2002 Sep 5;21(39):6041-8 [12203116.001]
  • [Cites] Virology. 2002 Sep 15;301(1):43-52 [12359445.001]
  • [Cites] J Virol. 2002 Nov;76(22):11291-300 [12388689.001]
  • [Cites] Genome Biol. 2002 Oct 23;3(11):reviews0008 [12429065.001]
  • [Cites] Anticancer Res. 2005 Mar-Apr;25(2A):765-77 [15868908.001]
  • [Cites] Curr Opin Cell Biol. 2005 Jun;17(3):257-61 [15901494.001]
  • [Cites] J Acquir Immune Defic Syndr. 2005 Jun 1;39(2):143-51 [15905729.001]
  • [Cites] Biochem Soc Trans. 2005 Jun;33(Pt 3):443-6 [15916537.001]
  • [Cites] J Virol. 2005 Jul;79(14):9254-69 [15994820.001]
  • [Cites] J Virol. 2005 Sep;79(18):12002-15 [16140776.001]
  • [Cites] Science. 2005 Sep 2;309(5740):1519-24 [16141061.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6544-9 [16166431.001]
  • [Cites] Mol Cell Biol. 2005 Oct;25(19):8643-55 [16166644.001]
  • [Cites] Gene Ther. 2005 Oct;12(20):1477-85 [16121205.001]
  • [Cites] Development. 2005 Nov;132(21):4653-62 [16224045.001]
  • [Cites] Mol Cell Biol. 2005 Nov;25(21):9595-607 [16227608.001]
  • [Cites] Oncogene. 2006 Mar 30;25(14):2094-104 [16369495.001]
  • [Cites] Mol Ther. 2003 Nov;8(5):762-8 [14599809.001]
  • [Cites] Nature. 2004 Sep 16;431(7006):371-8 [15372045.001]
  • [Cites] J Virol. 2004 Oct;78(20):10888-905 [15452209.001]
  • [Cites] J Virol. 2004 Oct;78(20):11172-86 [15452237.001]
  • [Cites] Eur J Biochem. 1980 Aug;109(2):457-61 [6250842.001]
  • [Cites] Nature. 1982 Oct 7;299(5883):529-34 [6289124.001]
  • [Cites] Virology. 1983 Apr 30;126(2):493-504 [6305000.001]
  • [Cites] EMBO J. 1982;1(2):231-6 [6325156.001]
  • [Cites] Nucleic Acids Res. 1984 Dec 11;12(23):8847-60 [6096809.001]
  • [Cites] Virus Res. 2002 Nov;89(2):213-28 [12445661.001]
  • [Cites] J Virol. 2003 Feb;77(3):2021-8 [12525636.001]
  • [Cites] J Virol. 2003 Feb;77(3):2105-15 [12525645.001]
  • [Cites] Antivir Ther. 2002 Dec;7(4):219-37 [12553476.001]
  • [Cites] N Engl J Med. 2003 Feb 6;348(6):518-27 [12571259.001]
  • [Cites] J Virol. 2003 Apr;77(8):4928-37 [12663798.001]
  • [Cites] J Virol. 2003 May;77(9):5167-77 [12692219.001]
  • [Cites] J Virol. 2003 May;77(10):6066-9 [12719599.001]
  • [Cites] J Virol. 2003 Jun;77(11):6227-34 [12743279.001]
  • [Cites] J Natl Cancer Inst Monogr. 2003;(31):111-6 [12807954.001]
  • [Cites] Virology. 2003 Jun 20;311(1):105-14 [12832208.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8264-9 [12826613.001]
  • [Cites] Oncogene. 2003 Sep 4;22(38):5938-45 [12955072.001]
  • [Cites] J Virol. 2003 Oct;77(19):10186-201 [12970404.001]
  • [Cites] J Virol. 2003 Oct;77(19):10213-26 [12970406.001]
  • [Cites] J Virol. 2003 Nov;77(21):11674-84 [14557653.001]
  • [Cites] J Gen Virol. 2003 Nov;84(Pt 11):2909-20 [14573795.001]
  • [Cites] J Virol. 2003 Dec;77(23):12450-9 [14610169.001]
  • [Cites] Virus Res. 2003 Dec;98(2):95-104 [14659556.001]
  • [Cites] J Virol. 2004 Jan;78(2):612-29 [14694093.001]
  • [Cites] EMBO J. 2004 Feb 11;23(3):616-26 [14749727.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4680-4 [3014503.001]
  • [Cites] J Virol. 2004 Mar;78(5):2609-14 [14963167.001]
  • [Cites] Nat Rev Microbiol. 2004 Apr;2(4):343-7 [15031733.001]
  • [Cites] RNA. 2004 Apr;10(4):565-73 [15037765.001]
  • [Cites] J Mol Biol. 2004 Apr 9;337(5):1091-108 [15046980.001]
  • [Cites] J Biomed Sci. 2004 May-Jun;11(3):278-94 [15067211.001]
  • [Cites] J Gen Virol. 2004 Jun;85(Pt 6):1433-44 [15166426.001]
  • [Cites] Virology. 2004 Jun 20;324(1):17-27 [15183049.001]
  • [Cites] Virology. 2004 Jul 1;324(2):483-92 [15207633.001]
  • [Cites] Virology. 2004 Aug 15;326(1):57-66 [15262495.001]
  • [Cites] Gene Ther. 2004 Sep;11(17):1331-41 [15229628.001]
  • [Cites] Nucleic Acids Res. 2004;32(15):4448-61 [15319446.001]
  • [Cites] J Virol. 2004 Oct;78(19):10598-605 [15367627.001]
  • [Cites] FEBS Lett. 1993 May 3;322(1):21-4 [8387026.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Apr 30;192(2):833-9 [8387290.001]
  • [Cites] Cancer Res. 1993 May 15;53(10 Suppl):2330-7 [7683572.001]
  • [Cites] J Gen Virol. 1993 May;74 ( Pt 5):791-801 [8388016.001]
  • [Cites] J Virol. 1993 Sep;67(9):5605-16 [8394463.001]
  • [Cites] J Virol. 1993 Dec;67(12):7705-10 [7901430.001]
  • [Cites] J Biol Chem. 1994 Apr 22;269(16):11902-11 [8163489.001]
  • [Cites] Proc Natl Sci Counc Repub China B. 1993 Oct;17(4):159-63 [8171167.001]
  • [Cites] Mol Cell Biol. 1994 Aug;14(8):5278-89 [8035806.001]
  • [Cites] J Virol. 1994 Oct;68(10):6567-77 [8083993.001]
  • [Cites] J Virol. 1995 May;69(5):2932-45 [7707519.001]
  • [Cites] J Virol. 1995 Jun;69(6):3381-8 [7745684.001]
  • [Cites] Cancer Gene Ther. 1994 Dec;1(4):267-77 [7627817.001]
  • [Cites] J Virol. 1995 Sep;69(9):5607-20 [7637007.001]
  • [Cites] Nucleic Acids Res. 1995 Jul 25;23(14):2614-20 [7651822.001]
  • [Cites] J Virol. 1995 Oct;69(10):6553-6 [7666558.001]
  • [Cites] Cancer Res. 1995 Oct 15;55(20):4599-605 [7553636.001]
  • [Cites] Cancer Gene Ther. 1995 Dec;2(4):263-71 [8548580.001]
  • [Cites] J Virol. 1996 Apr;70(4):2339-49 [8642661.001]
  • [Cites] J Virol. 1996 Jun;70(6):3355-62 [8648665.001]
  • [Cites] J Virol. 1996 Jul;70(7):4691-9 [8676495.001]
  • [Cites] J Virol. 1996 Oct;70(10):7233-5 [8794373.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 7;94(1):163-8 [8990179.001]
  • [Cites] J Virol. 1997 Jul;71(7):5161-72 [9188583.001]
  • [Cites] Cancer Res. 1997 Sep 15;57(18):3993-9 [9307284.001]
  • [Cites] J Virol. 1997 Dec;71(12):9096-107 [9371566.001]
  • [Cites] Oncogene. 1997 Nov 6;15(19):2303-19 [9393875.001]
  • [Cites] J Virol. 1998 Feb;72(2):1504-15 [9445054.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1189-94 [9448307.001]
  • [Cites] Mol Cell. 1998 Jan;1(2):255-64 [9659922.001]
  • [Cites] J Biol Chem. 1998 Aug 28;273(35):22648-56 [9712894.001]
  • [Cites] Biochem Soc Trans. 2002 Nov;30(Pt 6):1109-15 [12440984.001]
  • [Cites] N Engl J Med. 2002 Nov 21;347(21):1645-51 [12444178.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Nov 24;95(24):14088-93 [9826658.001]
  • [Cites] Virology. 1998 Nov 25;251(2):253-63 [9837789.001]
  • [Cites] J Virol. 1999 Jan;73(1):29-36 [9847303.001]
  • [Cites] J Virol. 1999 Apr;73(4):3062-70 [10074156.001]
  • [Cites] J Virol. 1999 Apr;73(4):3505-10 [10074210.001]
  • [Cites] J Biol Chem. 1999 Apr 23;274(17):11832-41 [10207001.001]
  • [Cites] J Virol. 1999 Jun;73(6):4972-82 [10233959.001]
  • [Cites] J Virol. 1999 Sep;73(9):7185-92 [10438805.001]
  • [Cites] Gene Ther. 1999 Jun;6(6):1114-9 [10455414.001]
  • [Cites] J Virol. 2004 Dec;78(23):12762-72 [15542628.001]
  • [Cites] J Virol. 2004 Dec;78(23):12901-9 [15542642.001]
  • [Cites] Lancet. 2004 Nov 13-19;364(9447):1757-65 [15541448.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 16;97(4):273-82 [15713962.001]
  • [Cites] J Virol. 2005 Mar;79(6):3309-21 [15731225.001]
  • [Cites] J Clin Virol. 2005 Mar;32 Suppl 1:S34-42 [15753010.001]
  • [Cites] J Clin Virol. 2005 Mar;32 Suppl 1:S43-51 [15753011.001]
  • [Cites] J Virol. 2005 Apr;79(7):4270-88 [15767428.001]
  • [Cites] J Virol. 2005 Apr;79(8):4918-26 [15795277.001]
  • [Cites] Lancet Oncol. 2005 May;6(5):271-8 [15863374.001]
  • (PMID = 16720315.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / SC / Z01 SC010357-06; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Number-of-references] 152
  • [Other-IDs] NLM/ NIHMS8367; NLM/ PMC1472295
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71. Yang S, Chen X, Wang L, Zhang J: Non-sebaceous lymphadenoma of the salivary gland: case report with immunohistochemical investigation. Virchows Arch; 2007 May;450(5):595-9
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  • Non-sebaceous lymphadenoma (NSL) is a rare, recently described, benign salivary gland tumor characterized by a dense lymphoid infiltrate and absence of sebaceous differentiation.
  • The tumor was encapsulated and measured 3 x 2 x 2 cm.
  • Microscopically, the tumor comprised islands of epithelial cells with centrally located duct-like structures within a dense lymphoid stroma.
  • Immunohistochemically, the tumor regularly expressed CKs 7, 8/18, and 19, which are typical for columnar differentiation and CKs 17 and 5/6, which are most typically expressed in basal cells of complex epithelia.
  • The immunohistochemical findings in the neoplastic epithelial component of our case suggest a differentiation of "intercalated duct phenotype" without myoepithelial cell participation.
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Humans. Keratins / analysis. Middle Aged. Treatment Outcome

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  • [Cites] Adv Anat Pathol. 2004 Mar;11(2):69-85 [15090843.001]
  • [Cites] J Formos Med Assoc. 2004 Jun;103(6):459-62 [15278191.001]
  • [Cites] Eur Arch Otorhinolaryngol. 1990;247(4):252-5 [2165413.001]
  • [Cites] J Pathol. 1993 Nov;171(3):173-81 [7506306.001]
  • [Cites] Eur J Oral Sci. 2002 Aug;110(4):316-21 [12206594.001]
  • [Cites] Pathologe. 2004 Feb;25(1):73-8 [14767615.001]
  • [Cites] Yonsei Med J. 2002 Aug;43(4):536-8 [12205744.001]
  • [Cites] Arch Pathol Lab Med. 2005 Jul;129(7):e171-2 [15974831.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2000 Sep;8(3):195-202 [10981871.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1994 Apr;77(4):387-91 [8015803.001]
  • [Cites] Oral Oncol. 1998 Mar;34(2):112-8 [9682773.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1994 Jan;77(1):19-26 [8108090.001]
  • [Cites] J Clin Pathol. 2004 Sep;57(9):1007 [15333672.001]
  • [Cites] Anat Embryol (Berl). 1988;178(3):243-51 [3046434.001]
  • [Cites] Virchows Arch. 2002 May;440(5):536-42 [12021929.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1986 Jul;62(1):57-62 [3523364.001]
  • [Cites] Histopathology. 2002 May;40(5):403-39 [12010363.001]
  • [Cites] Histopathology. 2001 Oct;39(4):347-52 [11683933.001]
  • [Cites] Arch Pathol Lab Med. 1999 Sep;123(9):801-6 [10458827.001]
  • [Cites] Hum Pathol. 1987 Dec;18(12):1218-26 [2824327.001]
  • [Cites] Oral Oncol. 1997 May;33(3):204-8 [9307730.001]
  • [Cites] Histopathology. 2002 Oct;41(4):342-50 [12383217.001]
  • [Cites] Oral Oncol. 2002 Jul;38(5):437-40 [12110337.001]
  • [Cites] Eur J Cancer B Oral Oncol. 1996 Jan;32B(1):14-8 [8729613.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1990 Nov;70(5):619-26 [2234882.001]
  • [Cites] Int J Oral Maxillofac Surg. 1989 Jun;18(3):133-7 [2474618.001]
  • (PMID = 17431672.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 68238-35-7 / Keratins
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72. Celis JE, Gromov P, Cabezón T, Moreira JM, Friis E, Jirström K, Llombart-Bosch A, Timmermans-Wielenga V, Rank F, Gromova I: 15-prostaglandin dehydrogenase expression alone or in combination with ACSM1 defines a subgroup of the apocrine molecular subtype of breast carcinoma. Mol Cell Proteomics; 2008 Oct;7(10):1795-809
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  • Molecular profiling technologies, on the other hand, subdivide breast tumors into five subtypes, basal-like, luminal A, luminal B, normal breast tissue-like, and ERBB2-positive, that have different prognostic characteristics.
  • By comparing the protein expression profiles of apocrine macrocysts and non-malignant breast epithelial tissue we have previously reported the identification of a few proteins that are specifically expressed by benign apocrine lesions as well as by the few IACs that were available to us at the time.
  • Here we reiterate our strategy to reveal apocrine cell markers and present novel data, based on the analysis of a considerably larger number of samples, establishing that IACs correspond to a distinct molecular subtype of breast carcinomas characterized by the expression of 15-prostaglandin dehydrogenase alone or in combination with a novel form of acyl-CoA synthetase medium-chain family member 1 (ACSM1).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Cohort Studies. Disease Progression. Electrophoresis, Gel, Two-Dimensional. Female. Humans. Immunohistochemistry. Immunophenotyping. Middle Aged. Neoplasm Invasiveness. Paraffin Embedding. Phenotype. Silver Staining. Tissue Array Analysis

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  • (PMID = 18632593.001).
  • [ISSN] 1535-9484
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.1.1.141 / 15-hydroxyprostaglandin dehydrogenase; EC 6.2.1.- / ACSM1 protein, human; EC 6.2.1.- / Coenzyme A Ligases
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73. Chen WL, Yang ZH, Huang ZQ, Chai Q, Zhang DM: Facial contour reconstruction after benign tumor ablation using reverse facial-submental artery deepithelialized submental island flaps. J Craniofac Surg; 2010 Jan;21(1):83-6
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  • [Title] Facial contour reconstruction after benign tumor ablation using reverse facial-submental artery deepithelialized submental island flaps.
  • Reverse facial-submental artery deepithelialized submental island flaps were used for reconstructing facial contour deformities in 5 patients after benign tumor ablation.
  • Recurrent pleomorphic adenoma in the cheek and inferior temple was present in 3 patients, and recurrent basal cell adenoma was present in 1.
  • The flap can be used reliably for facial contour reconstruction of middle and upper facial contour deformities after benign tumor ablation in the cheek and inferior temple.
  • [MeSH-major] Carcinoma, Basal Cell / surgery. Facial Neoplasms / surgery. Reconstructive Surgical Procedures / methods. Surgical Flaps / blood supply
  • [MeSH-minor] Adult. Cheek. Female. Forehead. Humans. Male. Neoplasm Recurrence, Local / surgery. Postoperative Complications. Retrospective Studies. Treatment Outcome

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  • (PMID = 20061969.001).
  • [ISSN] 1536-3732
  • [Journal-full-title] The Journal of craniofacial surgery
  • [ISO-abbreviation] J Craniofac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Kunju LP, Chinnaiyan AM, Shah RB: Comparison of monoclonal antibody (P504S) and polyclonal antibody to alpha methylacyl-CoA racemase (AMACR) in the work-up of prostate cancer. Histopathology; 2005 Dec;47(6):587-96
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  • METHODS AND RESULTS: A tissue microarray (TMA) with 248 samples of benign prostate, high-grade prostatic intraepithelial neoplasia (HGPIN) and PCa samples, 20 NBXs with minute PCa and 32 NBXs with 'atypical' foci were stained with P504S and p-AMACR.
  • In the 'atypical' NBXs group, 53% were classified as PCa, 12% benign and 35% atypical, suspicious for PCa, after review of the basal marker.
  • Of atypical, suspicious for PCa, P504S/p-AMACR helped convert the diagnosis to PCa in 5/11 (45%) cases, where, despite negative basal cell markers, morphology was less than optimal.
  • However, when utilized in proper context, AMACR may offer significant advantage in converting an 'atypical' diagnosis to PCa where morphology and basal markers are less than optimal in resolving the diagnosis.
  • [MeSH-major] Antibodies / metabolism. Antibodies, Monoclonal / metabolism. Biomarkers, Tumor / metabolism. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology. Racemases and Epimerases / metabolism

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  • (PMID = 16324196.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA69568
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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75. 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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  • 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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76. Cheng L, Bostwick DG: Atypical sclerosing adenosis of the prostate: a rare mimic of adenocarcinoma. Histopathology; 2010 Apr;56(5):627-31
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  • AIMS: Sclerosing adenosis of the prostate is a benign, small, acinar proliferation in dense spindle cell stroma, with a distinct immunohistochemical profiles.
  • All cases of typical and atypical sclerosing adenosis displayed an intact basal cell layer, which was immunoreactive for high-molecular-weight keratin, S100 protein, smooth muscle actin, and prostate-specific antigen, with no differences between ASA and the control group.
  • ASA is a benign lesion and aggressive treatment is unwarranted.
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Biopsy, Needle. Diagnosis, Differential. Humans. Male. Middle Aged. Sclerosis

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  • (PMID = 20459573.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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77. Paner GP, Luthringer DJ, Amin MB: Best practice in diagnostic immunohistochemistry: prostate carcinoma and its mimics in needle core biopsies. Arch Pathol Lab Med; 2008 Sep;132(9):1388-96
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  • CONTEXT: The unrelenting challenge encountered when differentiating limited-volume prostate carcinoma and sometimes subtle variants from its many morphologic mimics has increased the use of ancillary immunohistochemistry in routine prostate needle biopsies.
  • The availability of prostate cancer-associated and basal cell-associated markers has been an invaluable addition to diagnostic surgical pathology.
  • OBJECTIVE: To review commonly used immunohistochemical stains, including innovative combinations, for confirmation or differential diagnosis of prostate carcinoma, and to propose appropriately constructed panels using morphologic patterns in prostate needle biopsies.
  • CONCLUSIONS: Basal cell-associated markers p63, high-molecular-weight cytokeratin 34 beta E12, cytokeratin 5/6 or a cocktail containing p63 and high-molecular-weight cytokeratin 34 beta E12 or cytokeratin 5/6 and prostate carcinoma-specific marker alpha-methylacyl coenzyme A (coA) racemase alone or in combination are useful adjuncts in confirming prostatic carcinoma that either lacks diagnostic, qualitative or quantitative features or that has an unusual morphologic pattern (eg, atrophic, pseudohyperplastic) or is in the setting of prior treatment.
  • The combination of alpha-methylacyl coA racemase positivity with negative staining for basal cell-associated markers supports a malignant diagnosis in the appropriate morphologic context.
  • Dual chromogen basal cell- associated markers (p63 [nuclear] and high-molecular-weight cytokeratin 34 beta E12/cytokeratin 5/6 [cytoplasmic]) and alpha-methylacyl coA racemase in an antibody cocktail provide greater sensitivity for the basal cell layer, easing evaluation and minimizing loss of representation of the focal area interest because the staining is performed on one slide.
  • Prostate-specific antigen and prostatic acid phosphatase markers are helpful in excluding secondary malignancies involving the prostate, such as urothelial carcinoma, and occasionally in excluding nonprostatic benign mimickers, such as nephrogenic adenoma, mesonephric gland hyperplasia, and Cowper glands.
  • [MeSH-major] Biomarkers, Tumor / analysis. Biopsy, Needle. Immunohistochemistry / methods. Prostatic Neoplasms / diagnosis

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  • (PMID = 18788849.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 47
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78. 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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  • 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.
  • Benign glands were positive for ANXII in 286/292 cores (98%) and negative for AMACR in all 292 cores.
  • [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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  • [Cites] J Urol. 2004 Feb;171(2 Pt 1):916-20 [14713853.001]
  • [Cites] Am J Surg Pathol. 2006 Jan;30(1):13-9 [16330937.001]
  • [Cites] J Cell Biochem. 2004 Mar 1;91(4):852-63 [14991775.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3450-5 [14985510.001]
  • [Cites] Mod Pathol. 2004 Mar;17(3):328-48 [14976539.001]
  • [Cites] J Cell Sci. 2004 Jul 15;117(Pt 16):3539-45 [15226377.001]
  • [Cites] Mol Cancer. 2003 Oct 8;2:34 [14613585.001]
  • [Cites] Hum Pathol. 2004 Aug;35(8):1008-13 [15297968.001]
  • [Cites] Histopathology. 2004 Sep;45(3):218-25 [15330799.001]
  • [Cites] Virchows Arch. 2004 Oct;445(4):368-74 [15338305.001]
  • [Cites] J Biol Chem. 1986 Jun 5;261(16):7247-52 [2940239.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4258-62 [3012561.001]
  • [Cites] Mol Cell Biol. 1990 Jun;10(6):3216-23 [2160596.001]
  • [Cites] Differentiation. 1993 Mar;52(3):229-37 [8387039.001]
  • [Cites] Carcinogenesis. 1993 Dec;14(12):2575-9 [8269629.001]
  • [Cites] Eur J Biochem. 1994 Jun 1;222(2):313-23 [8020470.001]
  • [Cites] J Biol Chem. 1995 Jun 16;270(24):14399-404 [7782301.001]
  • [Cites] Oncol Res. 1994;6(12):561-7 [7787249.001]
  • [Cites] Prostate. 1997 Sep 15;33(1):32-7 [9294624.001]
  • [Cites] Nat Med. 1998 Jul;4(7):844-7 [9662379.001]
  • [Cites] Mol Cell. 1998 Sep;2(3):305-16 [9774969.001]
  • [Cites] Biochim Biophys Acta. 2000 Mar 7;1477(1-2):215-30 [10708859.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1677-82 [10749139.001]
  • [Cites] Am J Pathol. 2000 Dec;157(6):1769-75 [11106548.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6331-4 [11522620.001]
  • [Cites] Am J Surg Pathol. 2001 Nov;25(11):1397-404 [11684956.001]
  • [Cites] Cancer. 2001 Sep 15;92(6):1419-26 [11745218.001]
  • [Cites] Cancer Res. 2002 Apr 15;62(8):2220-6 [11956072.001]
  • [Cites] Am J Surg Pathol. 2002 Jul;26(7):926-31 [12131161.001]
  • [Cites] Am J Surg Pathol. 2002 Dec;26(12):1588-96 [12459625.001]
  • [Cites] Oncogene. 2003 Mar 13;22(10):1475-85 [12629510.001]
  • [Cites] Am J Surg Pathol. 2003 Jun;27(6):772-8 [12766580.001]
  • [Cites] Am J Surg Pathol. 2003 Aug;27(8):1128-33 [12883245.001]
  • [Cites] Am J Surg Pathol. 2005 May;29(5):579-87 [15832080.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jun;6(6):449-61 [15928709.001]
  • [Cites] Histol Histopathol. 2005 Jul;20(3):673-80 [15944914.001]
  • [Cites] Histopathology. 2005 Jul;47(1):1-16 [15982318.001]
  • [Cites] BJU Int. 2005 Dec;96(9):1219-23 [16287434.001]
  • [Cites] Cell Prolif. 2005 Dec;38(6):363-74 [16300650.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10946-51 [16322242.001]
  • [Cites] Biochem J. 2004 Mar 1;378(Pt 2):307-15 [14599294.001]
  • (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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79. Paulino AC, Fowler BZ: Secondary neoplasms after radiotherapy for a childhood solid tumor. Pediatr Hematol Oncol; 2005 Mar;22(2):89-101
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  • [Title] Secondary neoplasms after radiotherapy for a childhood solid tumor.
  • This study was conducted to determine the outcome of patients who develop a second neoplasm after radiotherapy (RT) for a childhood solid tumor.
  • From 1956 to 1998, 429 children with a malignant solid tumor were treated at a single radiation oncology facility.
  • The medical records and radiotherapy charts were reviewed to determine if the patient developed a secondary neoplasm after treatment for malignancy.
  • Twenty-three (5.4%) patients developed a secondary neoplasm.
  • There were 14 malignant neoplasms in 13 (3.0%) and 14 benign neoplasms in 11 patients (2.6%).
  • The types of initial solid tumors treated with RT were Ewing sarcoma in 6, Wilms tumor in 6, medulloblastoma in 5, neuroblastoma in 3, and other in 3.
  • For the 14 malignant neoplasms, the median time interval from initial tumor to second malignancy was 10.1 years.
  • The 14 second malignant neoplasms (SMN) were osteosarcoma in 3, breast carcinoma in 2, melanoma in 2, malignant fibrous histiocytoma in 1, dermatofibrosarcoma in 1, leiomyosarcoma in 1, mucoepidermoid carcinoma in 1, colon cancer in 1, chronic myelogenous leukemia in 1, and basal cell carcinoma in 1.
  • The 14 benign neoplasms appeared at a median time of 16.9 years and included cervical intraepithelial neoplasia in 3, osteochondroma in 3, thyroid adenoma in 1, duodenal adenoma in 1, lipoma in 1, cherry angioma in 1, uterine leiomyoma in 1, ovarian cystadenofibroma in 1, and giant cell tumor in 1.
  • Only 5 (36%) of the 14 benign tumors occurred in the RT field, with osteochondroma being the most common.


80. Garcia MT, Acar BC, Jorda M, Gomez-Fernandez C, Ganjei-Azar P: Use of p63 for distinction of glandular versus squamous lesions in cervicovaginal specimens. Cancer; 2007 Feb 25;111(1):54-7
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  • Squamous and atypical glandular cell lesions may show similar cytomorphologic features.
  • The aim of this study was to evaluate the use of p63 as a marker of basal and/or squamous cell derivation in this differential diagnosis.
  • Nuclei of isolated HSIL cells and basal cells from atrophic smears were also positive for p63.
  • Benign and malignant glandular cells were uniformly negative.
  • This antibody is not expressed in AGUS, adenocarcinoma, or normal glandular cells. p63 stains basal cells and may be a diagnostic pitfall in atrophic cervicovaginal specimens.
  • [MeSH-major] Membrane Proteins / metabolism. Neoplasms, Glandular and Epithelial / diagnosis. Neoplasms, Squamous Cell / diagnosis. Uterine Cervical Neoplasms / diagnosis. Vaginal Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / immunology. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Female. Humans. Immunohistochemistry / methods


81. Izikson L, Bhan A, Zembowicz A: Androgen receptor expression helps to differentiate basal cell carcinoma from benign trichoblastic tumors. Am J Dermatopathol; 2005 Apr;27(2):91-5
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  • [Title] Androgen receptor expression helps to differentiate basal cell carcinoma from benign trichoblastic tumors.
  • Histologic differentiation between basal cell carcinoma and benign trichoblastic neoplasms such as trichoepithelioma and trichoblastoma can be difficult on small biopsies.
  • Recent studies have shown androgen receptor expression in a number of mature epithelial structures in the skin and in epithelial neoplasms including basal cell carcinoma.
  • These findings suggested that androgen receptor expression might be a useful adjunct in the histologic differential diagnosis between basal cell carcinoma and benign trichoblastic neoplasms.
  • Therefore, we performed immunohistochemical analysis of androgen receptor expression in 32 basal cell carcinomas and 10 benign trichoblastic tumors (6 trichoepitheliomas and 4 trichoblastomas).
  • In our study, at least focal expression of androgen receptor was detected in 78% of basal cell carcinomas.
  • These results confirm the lack of expression of androgen receptor in benign trichoblastic neoplasms and indicate that androgen receptor expression by tumor cells points to basal cell carcinoma as the most likely diagnosis.
  • [MeSH-major] Carcinoma, Basal Cell / diagnosis. Hair Follicle / metabolism. Receptors, Androgen / biosynthesis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 15798431.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Androgen
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82. Yaskiv O, Cao D, Humphrey PA: Microcystic adenocarcinoma of the prostate: a variant of pseudohyperplastic and atrophic patterns. Am J Surg Pathol; 2010 Apr;34(4):556-61
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  • Cystic change in adenocarcinoma of the prostate is unusual and may be confused with benign cystic atrophy.
  • This alteration was defined as cystic dilatation and rounded expansion of the malignant gland profile, with a flat luminal cell lining layer.
  • Ninety-six percent of the microcystic cases showed alpha-methylacyl CoA racemase overexpression and all cases showed complete basal cell loss (using 34betaE12 and p63 antibodies) in immunohistochemistry.
  • Microcystic adenocarcinoma of the prostate is a distinctive histomorphologic presentation of prostatic adenocarcinoma that is deceptively benign-looking at low magnifications.
  • Detection of intraluminal crystalloids or wispy blue mucin at low magnification, immunostains for alpha-methylacyl CoA racemase, and basal cells, and a search for adjacent usual small acinar adenocarcinoma are helpful diagnostic aids.
  • [MeSH-minor] Atrophy. Biomarkers, Tumor / metabolism. Cysts / enzymology. Cysts / pathology. Humans. Male. Prostatectomy. Racemases and Epimerases / metabolism

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  • (PMID = 20216381.001).
  • [ISSN] 1532-0979
  • [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 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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83. Kumamoto H, Ohki K, Ooya K: Expression of p63 and p73 in ameloblastomas. J Oral Pathol Med; 2005 Apr;34(4):220-6
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  • METHODS: Tissue specimens of nine tooth germs and 48 benign and five malignant ameloblastomas were examined by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) for the expression of p63 and p73.
  • RESULTS: Immunoreactivity for p63 and p73 was evident in epithelial cells neighboring the basement membrane in developing and neoplastic odontogenic tissues. p63 expression in desmoplastic ameloblastomas was significantly higher than in acanthomatous and granular cell ameloblastomas, and ameloblastic carcinomas showed higher p63 expression than metastasizing ameloblastomas. p73 expression was significantly higher in plexiform ameloblastomas than in follicular ameloblastomas, and basal cell ameloblastomas showed higher p73 expression than granular cell ameloblastomas. mRNA transcripts for Delta Np63 and TAp73 were detected in all developing and neoplastic odontogenic tissues.
  • [MeSH-major] Ameloblastoma / genetics. Apoptosis / genetics. DNA-Binding Proteins / genetics. Genes, Tumor Suppressor. Nuclear Proteins / genetics. Phosphoproteins / genetics. Trans-Activators / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Basement Membrane / metabolism. Cell Differentiation / genetics. Cell Proliferation. Epithelial Cells / metabolism. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry. Protein Isoforms / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tooth Germ / metabolism. Transcription Factors. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 15752257.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / Protein Isoforms; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
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84. He X, Marchionni L, Hansel DE, Yu W, Sood A, Yang J, Parmigiani G, Matsui W, Berman DM: Differentiation of a highly tumorigenic basal cell compartment in urothelial carcinoma. Stem Cells; 2009 Jul;27(7):1487-95
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  • [Title] Differentiation of a highly tumorigenic basal cell compartment in urothelial carcinoma.
  • Highly tumorigenic cancer cell (HTC) populations have been identified for a variety of solid tumors and assigned stem cell properties.
  • We identified a highly tumorigenic UC cell compartment that resembles benign urothelial stem cells (basal cells), co-expresses the 67-kDa laminin receptor and the basal cell-specific cytokeratin CK17, and lacks the carcinoembryonic antigen family member CEACAM6 (CD66c).
  • This multipotent compartment resides at the tumor-stroma interface, is easily identified on histologic sections, and possesses most, if not all, of the engraftable tumor-forming ability in the parental xenograft.
  • We analyzed differential expression of genes and pathways in basal-like cells versus more differentiated cells.
  • The basal/HTC gene expression signature was essentially invisible within the context of nontumorigenic cell gene expression and overlapped significantly with genes driving progression and death in primary human UC.
  • The spatially restricted epithelial differentiation program described here represents a conceptual advance in understanding cellular heterogeneity of carcinomas and identifies basal-like HTCs as attractive targets for cancer therapy.
  • [MeSH-major] Carcinoma, Transitional Cell / pathology. Stem Cells / pathology. Urinary Bladder Neoplasms / pathology. Urothelium / pathology
  • [MeSH-minor] Aged. Animals. Antigens, CD / metabolism. Cell Adhesion Molecules / metabolism. Female. GPI-Linked Proteins. Humans. Immunohistochemistry. Keratin-17 / metabolism. Mice. Mice, Nude. Receptors, Laminin / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Xenograft Model Antitumor Assays

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  • [Cites] Cancer Res. 2007 Oct 1;67(19):8985-8 [17908998.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9199-206 [17909025.001]
  • [Cites] Annu Rev Cell Dev Biol. 2007;23:675-99 [17645413.001]
  • [Cites] Hum Pathol. 2007 Nov;38(11):1703-13 [17707461.001]
  • [Cites] Development. 2007 Dec;134(23):4255-63 [17978005.001]
  • [Cites] Sci Signal. 2008;1(8):pe10 [18314504.001]
  • [Cites] Cell Res. 2008 May;18(5):523-7 [18392048.001]
  • [Cites] Am J Physiol Renal Physiol. 2008 Jun;294(6):F1415-21 [18367656.001]
  • [Cites] Cancer Invest. 2008 Aug;26(7):725-33 [18608209.001]
  • [Cites] Oncogene. 2008 Sep 1;27(38):5124-31 [18758481.001]
  • [Cites] Mol Cancer Ther. 2008 Sep;7(9):2672-80 [18790749.001]
  • [Cites] Nat Rev Cancer. 2008 Oct;8(10):755-68 [18784658.001]
  • [Cites] Cancer Res. 2008 Nov 15;68(22):9551-7 [19010932.001]
  • [Cites] J Natl Cancer Inst. 2008 Dec 3;100(23):1672-94 [19033571.001]
  • [Cites] Oncogene. 2008 Dec 4;27(57):7180-91 [18794802.001]
  • [Cites] Clin Cancer Res. 2008 Dec 15;14(24):8010-8 [19088017.001]
  • [Cites] Nat Chem Biol. 2009 Feb;5(2):100-7 [19125156.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] Am J Physiol Renal Physiol. 2000 Jun;278(6):F867-74 [10836974.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1516-22 [11410485.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Int J Oncol. 2002 May;20(5):905-11 [11956582.001]
  • [Cites] Nat Genet. 2003 Jan;33(1):90-6 [12469123.001]
  • [Cites] Novartis Found Symp. 2002;247:91-101; discussion 101-3, 119-28, 244-52 [12539951.001]
  • [Cites] Nucleic Acids Res. 2003 Feb 15;31(4):e15 [12582260.001]
  • [Cites] Am J Pathol. 2003 Aug;163(2):493-504 [12875970.001]
  • [Cites] Methods. 2003 Dec;31(4):265-73 [14597310.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):4040-8 [15173019.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] J Clin Pathol. 1967 Jan;20(1):7-14 [6016890.001]
  • [Cites] Virchows Arch B Cell Pathol. 1976 Oct 1;21(4):279-98 [824809.001]
  • [Cites] J Invest Dermatol. 1983 Jul;81(1 Suppl):109s-15s [6190956.001]
  • [Cites] Blood. 1990 May 15;75(10):1947-50 [2337669.001]
  • [Cites] Cancer. 1990 Aug 1;66(3):537-42 [2364364.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] Oncogene. 1999 May 6;18(18):2883-91 [10362259.001]
  • [Cites] J Urol. 1999 Sep;162(3 Pt 1):931-5 [10458411.001]
  • [Cites] J Oral Pathol Med. 2005 Feb;34(2):116-9 [15641992.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3790-8 [15897578.001]
  • [Cites] Hum Pathol. 2005 May;36(5):522-30 [15948119.001]
  • [Cites] Methods Mol Med. 2005;103:89-101 [15542899.001]
  • [Cites] Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S183-7 [16113095.001]
  • [Cites] Nat Rev Cancer. 2005 Sep;5(9):744-9 [16148886.001]
  • [Cites] Trends Cell Biol. 2005 Sep;15(9):494-501 [16084092.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):383-91 [16428476.001]
  • [Cites] Oncogene. 2006 Mar 9;25(10):1554-9 [16261162.001]
  • [Cites] Cell Stem Cell. 2009 Mar 6;4(3):203-5 [19265659.001]
  • [Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2109-16 [16609023.001]
  • [Cites] Am J Clin Pathol. 2006 Dec;126(6):849-55 [17074684.001]
  • [Cites] Nat Genet. 2006 Dec;38(12):1386-96 [17099711.001]
  • [Cites] Acta Haematol. 2007;117(1):8-15 [17095854.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):973-8 [17210912.001]
  • [Cites] N Engl J Med. 2007 Jan 18;356(3):217-26 [17229949.001]
  • [Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4407-14 [17671123.001]
  • [Cites] J Med Chem. 2008 Dec 11;51(23):7405-16 [18989950.001]
  • (PMID = 19544456.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA088843; United States / NCI NIH HHS / CA / P50CA088843; United States / NIDDK NIH HHS / DK / R01DK072000; United States / NIDDK NIH HHS / DK / R01 DK072000-04; United States / NIDDK NIH HHS / DK / K08 DK059375; United States / NCI NIH HHS / CA / P01CA077664; United States / NCI NIH HHS / CA / K23 CA107040; United States / NIDDK NIH HHS / DK / R01 DK072000; United States / NCRR NIH HHS / RR / 1U54RR023561-01A1; United States / NIDDK NIH HHS / DK / K08DK059375; United States / NCI NIH HHS / CA / P01 CA077664; United States / NCI NIH HHS / CA / K23 CA107040-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Keratin-17; 0 / Receptors, Laminin
  • [Other-IDs] NLM/ NIHMS236727; NLM/ PMC3060766
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85. Yee DS, Narula N, Ramzy I, Boker J, Ahlering TE, Skarecky DW, Ornstein DK: Reduced annexin II protein expression in high-grade prostatic intraepithelial neoplasia and prostate cancer. Arch Pathol Lab Med; 2007 Jun;131(6):902-8
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  • The protein is strongly expressed in normal prostatic epithelial glands, but its expression in benign prostatic lesions has not been reported.
  • OBJECTIVE: To compare annexin II expression in benign prostatic lesions with expression in high-grade prostatic intraepithelial neoplasia and prostate cancer, as well as to correlate expression levels with pathologic grade and stage.
  • Foci with normal prostatic glands, atrophic glands, basal cell hyperplasia, high-grade prostatic intraepithelial neoplasia, and prostatic adenocarcinoma were evaluated.
  • RESULTS: Annexin II expression was present in more than 50% of glands in most (>85%) samples of benign prostatic epithelium, atrophic glands, and basal cell hyperplasia.
  • In high-grade prostatic intraepithelial neoplasia, annexin II staining was markedly reduced in epithelial cells but not in basal cells.
  • CONCLUSIONS: Reduced annexin II expression may be a useful diagnostic biomarker to help identify small foci of moderately differentiated adenocarcinoma on needle core biopsy specimens since it is consistently expressed in benign prostatic glands.
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor. Humans. Immunoenzyme Techniques / methods. Male. Middle Aged. Prostatectomy

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  • (PMID = 17550317.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A2; 0 / Biomarkers, Tumor
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86. Jokinen CH, Wolgamot GM, Argenyi ZB: Collagen-rich variant of benign epithelioid peripheral nerve sheath tumor of the skin. J Cutan Pathol; 2008 Feb;35(2):215-9
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  • [Title] Collagen-rich variant of benign epithelioid peripheral nerve sheath tumor of the skin.
  • Schwannoma and neurofibroma account for the majority of cutaneous benign peripheral nerve sheath tumors and usually pose little diagnostic difficulty in their classic forms.
  • In rare instances, however, benign peripheral nerve sheath tumors may display epithelioid morphology and lack otherwise usual features of schwannoma or neurofibroma, making classification difficult.
  • These unusual changes may prompt consideration of other benign neoplasms or a malignancy.
  • Benign epithelioid peripheral nerve sheath tumor (BEPNST) is a somewhat non-specific term recently proposed to describe these neoplasms of imprecise histogenesis.
  • Specifically, the neoplastic cells in this tumor were nearly obscured by the collagen, which formed large nodules and compressed the majority of the few remaining tumor cells to the periphery of the lesion.
  • [MeSH-minor] Aged. Carcinoma, Basal Cell / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Microscopy, Electron, Transmission. Neck / pathology

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  • (PMID = 18190449.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 9007-34-5 / Collagen
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87. Nakai N, Takenaka H, Kishimoto S: Atypical fibroxanthoma on a bald scalp. J Dermatol; 2005 Oct;32(10):848-51
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  • The patient had a history of basal cell carcinoma on the nape, and chronic solar radiation seemed to be a predisposing factor in the pathogenesis of this association.
  • The AFX was completely resected, and the patient has not had tumor recurrence or metastasis for over four postoperative years.
  • This case therefore provides further support to the theory that AFX displays a clinically benign course, even though it is essentially a malignant tumor histologically located in the dermis.
  • [MeSH-major] Histiocytoma, Benign Fibrous / pathology. Scalp Dermatoses / pathology

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  • (PMID = 16361741.001).
  • [ISSN] 0385-2407
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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88. Peschos D, Damala C, Stefanou D, Tsanou E, Assimakopoulos D, Vougiouklakis T, Charalabopoulos K, Agnantis NJ: Expression of matrix metalloproteinase-9 (gelatinase B) in benign, premalignant and malignant laryngeal lesions. Histol Histopathol; 2006 06;21(6):603-8
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  • [Title] Expression of matrix metalloproteinase-9 (gelatinase B) in benign, premalignant and malignant laryngeal lesions.
  • They are involved in basement membrane disruption, stroma and blood vessel penetration, metastasis and more recently there is evidence that they participate in tumor growth and angiogenic events.
  • Matrix metalloproteinase 2 and 9 (MMP 2 and 9) belong to the gelatinases, a subgroup of MMPs, and have the capacity to degrade the triple helix type IV collagen of basal lamina of the basement membrane.
  • With the present study, we tried to demonstrate the expression of MMP-9 immunohistochemically, comparatively in benign, premalignant and malignant lesions of the larynx.
  • We studied 154 laryngeal lesions including 55 squamous cell carcinomas, 8 in situ carcinomas, 54 cases of dysplasia (of low and intermediate grade), 13 papillomas and 24 cases of keratosis.
  • Overexpression of MMP 9 was observed in 74.4% and 50% in invasive and in situ squamous cell carcinomas respectively.
  • In dysplastic cases, in papillomas and in keratoses the percentage of overexpression was 62.9%, 61.53% and 54.16% respectively and the expression of MMP-9 was significantly higher in invasive squamous cell carcinomas compared to dysplasias (p=0.000004).
  • The MMP-9 expression was related neither to survival nor to the other available clinicopathological parameters (tumor size, grade, clinical stage, lymph node status and patient age).
  • [MeSH-minor] Carcinoma in Situ / chemistry. Carcinoma in Situ / metabolism. Carcinoma in Situ / pathology. Carcinoma, Squamous Cell / chemistry. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Disease Progression. Female. Humans. Immunohistochemistry. Keratosis / metabolism. Keratosis / pathology. Laryngeal Diseases / metabolism. Laryngeal Diseases / pathology. Male. Middle Aged. Neoplasm Invasiveness / pathology. Papilloma / chemistry. Papilloma / metabolism. Papilloma / pathology. Up-Regulation

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  • (PMID = 16528670.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] EC 3.4.24.35 / Matrix Metalloproteinase 9
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89. Katona TM, Ravis SM, Perkins SM, Moores WB, Billings SD: Expression of androgen receptor by fibroepithelioma of Pinkus: evidence supporting classification as a basal cell carcinoma variant? Am J Dermatopathol; 2007 Feb;29(1):7-12
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  • [Title] Expression of androgen receptor by fibroepithelioma of Pinkus: evidence supporting classification as a basal cell carcinoma variant?
  • The classification of fibroepithelioma of Pinkus as basal cell carcinoma or trichoblastoma remains controversial.
  • Immunohistochemical stains for androgen receptor may be useful in differentiating basal cell carcinoma from trichoepithelioma or trichoblastoma.
  • We studied androgen receptor expression in 13 fibroepitheliomas of Pinkus, 11 basal cell carcinomas, 12 trichoepitheliomas, and 3 trichoblastomas.
  • Androgen receptor expression was present in 77% (10/13) of fibroepitheliomas of Pinkus, 73% (8/11) of basal cell carcinomas, 17% (2/12) of trichoepitheliomas, and 0% (0/3) of trichoblastomas.
  • Androgen receptor expression was significantly higher in fibroepitheliomas of Pinkus compared with trichoepitheliomas and trichoblastomas (P = .0007), but not basal cell carcinoma (P = 1.00).
  • Tumor-associated Merkel cells, a feature of benign follicular tumors, was identified by cytokeratin 20 stains.
  • Merkel cells were identified in 85% (11/13) of fibroepitheliomas of Pinkus, 27% (3/11) of basal cell carcinoma cases, and 73% (11/15) of benign follicular tumors.
  • Cytokeratin 20 expression was significantly higher in fibroepithelioma of Pinkus and benign follicular tumors compared with basal cell carcinomas (P = 0.0111 and P = 0.025, respectively).
  • Similar to basal cell carcinomas, fibroepitheliomas of Pinkus express androgen receptors, potentially supporting classification as a basal cell carcinoma.
  • Conversely, fibroepithelioma of Pinkus demonstrates retention of Merkel cells, a feature of benign follicular tumors.
  • [MeSH-major] Carcinoma, Basal Cell / classification. Carcinoma, Basal Cell / metabolism. Neoplasms, Fibroepithelial / classification. Neoplasms, Fibroepithelial / metabolism. Receptors, Androgen / metabolism. Skin Neoplasms / classification. Skin Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Biopsy. DNA, Neoplasm / genetics. Gene Expression Regulation, Neoplastic. Genetic Variation / genetics. Hair Follicle / metabolism. Hair Follicle / pathology. Humans. Keratin-20 / genetics. Keratin-20 / metabolism. Merkel Cells / metabolism. Merkel Cells / pathology. Skin / metabolism. Skin / pathology


90. Pascual-Castroviejo I, Pascual-Pascual SI, Velazquez-Fragua R, García-Guereta L, López-Gutiérrez JC, Olivares P, Tovar J: Association of cutaneous red-to-purple hemangiomas with leptomeningeal hemangiomas. a clinical study of two patients. Neuropediatrics; 2010 Feb;41(1):7-11
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  • Cutaneous hemangioma is a benign vascular tumor of infancy with an initial proliferating period that appears between 1 to 2 weeks of life, extends during 18 months to 2 years of life, and then slowly regresses during several years until it disappears completely.
  • They are characterized by endothelial cell proliferation followed by diminishing hyperplasia and progressive fibrosis.
  • Vascular malformations are present at birth, grow commensurately with the child, and are characterized histologically by a normal rate of endothelial cell turnover, flat endothelium, thin (normal) basal membrane and normal mast cells.

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  • (PMID = 20571984.001).
  • [ISSN] 1439-1899
  • [Journal-full-title] Neuropediatrics
  • [ISO-abbreviation] Neuropediatrics
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] AU0V1LM3JT / Gadolinium
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91. Kawahara A, Harada H, Akiba J, Yokoyama T, Kage M: Fine-needle aspiration cytology of basal cell adenoma of the parotid gland: characteristic cytological features and diagnostic pitfalls. Diagn Cytopathol; 2007 Feb;35(2):85-90
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  • [Title] Fine-needle aspiration cytology of basal cell adenoma of the parotid gland: characteristic cytological features and diagnostic pitfalls.
  • We retrospectively studied the cytological features of aspiration cytology in 12 cases of basal cell adenoma (BCA) and 5 cases mistakenly diagnosed as BCA.
  • The characteristic cytological features of solid type BCA were three-dimensional clusters in 71%, sharp-angle small clusters in 86%, basement membrane- like material in 71%, and cell crush in 86%.
  • In contrast, 3 of the 5 cystic type BCA cases showed inadequate cellular components or no basaloid tumor cells, and the cytological diagnosis of BCA could not be determined.
  • In the 5 cases misdiagnosed as BCA, there were 2 cases of pleomorphic adenoma, 2 cases of benign lymphoepithelial cyst, and 1 case of basal cell adenocarcinoma.

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  • (PMID = 17230571.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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92. Moriya T, Kasajima A, Ishida K, Kariya Y, Akahira J, Endoh M, Watanabe M, Sasano H: New trends of immunohistochemistry for making differential diagnosis of breast lesions. Med Mol Morphol; 2006 Mar;39(1):8-13
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  • Most ductal carcinoma in situ cases are diffusely positive for luminal cell markers (CK8, CK18, CK19), but negative for basal cell markers (CK5/6 and CK14).
  • However, usual ductal hyperplasia may show the mosaic staining patterns for any of these markers, which may indicate a heterogeneous cell population in benign lesions.
  • Myoepithelial markers (alpha-SMA, myosin, calponin, p63, CD10) are almost consistently positive for benign papillomas but they do not completely distinguish intraductal papillary carcinomas.
  • Preservation of myoepithelial layer is the diagnostic key when looking at benign sclerosing lesions, including carcinoma with pseudoinvasive structures.
  • [MeSH-minor] Biomarkers, Tumor. Carcinoma, Lobular / pathology. Diagnosis, Differential. Humans. Papilloma, Intraductal / pathology


93. Arwert EN, Lal R, Quist S, Rosewell I, van Rooijen N, Watt FM: Tumor formation initiated by nondividing epidermal cells via an inflammatory infiltrate. Proc Natl Acad Sci U S A; 2010 Nov 16;107(46):19903-8
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  • [Title] Tumor formation initiated by nondividing epidermal cells via an inflammatory infiltrate.
  • In mammalian epidermis, integrin expression is normally confined to the basal proliferative layer that contains stem cells.
  • In transgenic mice, expression of activated MAPK kinase 1 (MEK1) in the suprabasal, nondividing, differentiated cell layers (InvEE transgenics) results in epidermal hyperproliferation and skin inflammation.
  • We now demonstrate that wounding induces benign tumors (papillomas and keratoacanthomas) in InvEE mice.
  • By generating chimeras between InvEE mice and mice that lack the MEK1 transgene, we demonstrate that differentiating, nondividing cells that express MEK1 stimulate adjacent transgene-negative cells to divide and become incorporated into the tumor mass.
  • Dexamethasone treatment inhibits tumor formation, suggesting that inflammation is involved.
  • InvEE skin and tumors express high levels of IL1α; treatment with an IL1 receptor antagonist delays tumor onset and reduces incidence.
  • Depletion of γδ T cells and macrophages also reduces tumor incidence.
  • In contrast, our studies show that differentiated epidermal cells can initiate tumor formation without reacquiring the ability to divide and that they do so by triggering an inflammatory infiltrate.

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  • [Cites] J Clin Invest. 2001 Aug;108(4):527-36 [11518726.001]
  • [Cites] Dev Cell. 2010 Jun 15;18(6):884-901 [20627072.001]
  • [Cites] EMBO J. 2002 Aug 1;21(15):3919-26 [12145193.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Nov;43(11):3473-9 [12407158.001]
  • [Cites] Dermatol Surg. 2002 Oct;28(10):954-8 [12410683.001]
  • [Cites] Bone Marrow Transplant. 2002 Dec;30(12):843-9 [12476275.001]
  • [Cites] J Immunol. 2003 Jun 1;170(11):5697-703 [12759452.001]
  • [Cites] J Exp Med. 2003 Sep 1;198(5):747-55 [12953094.001]
  • [Cites] J Invest Dermatol. 2004 Sep;123(3):503-15 [15304090.001]
  • [Cites] J Clin Invest. 1986 Jun;77(6):1857-63 [3486886.001]
  • [Cites] Cancer Res. 1989 Nov 15;49(22):6419-24 [2553256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jan;87(2):538-42 [2105486.001]
  • [Cites] Cell. 1990 Sep 7;62(5):863-74 [1975515.001]
  • [Cites] Immunology. 1992 Feb;75(2):293-8 [1532379.001]
  • [Cites] Cancer Immunol Immunother. 1995 Jun;40(6):358-66 [7627992.001]
  • [Cites] Exp Dermatol. 1997 Feb;6(1):22-8 [9067703.001]
  • [Cites] J Immunol. 1997 Nov 15;159(10):5084-8 [9366437.001]
  • [Cites] Cancer Cell. 2005 Mar;7(3):211-7 [15766659.001]
  • [Cites] Cancer Res. 2005 May 1;65(9):3577-85 [15867351.001]
  • [Cites] Arch Ophthalmol. 2005 Jul;123(7):957-63 [16009838.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):175-83 [16498442.001]
  • [Cites] J Clin Invest. 2006 Aug;116(8):2094-104 [16886058.001]
  • [Cites] J Leukoc Biol. 2007 Jan;81(1):1-5 [17032697.001]
  • [Cites] Cancer Res. 2007 Apr 1;67(7):2916-21 [17409394.001]
  • [Cites] Dev Cell. 2007 Apr;12(4):615-29 [17419998.001]
  • [Cites] Crit Rev Oncol Hematol. 2008 Apr;66(1):1-9 [17913510.001]
  • [Cites] Immunol Rev. 2008 Apr;222:155-61 [18364000.001]
  • [Cites] Nature. 2008 May 15;453(7193):314-21 [18480812.001]
  • [Cites] J Exp Med. 2008 Jun 9;205(6):1261-8 [18490490.001]
  • [Cites] Nature. 2008 Jul 24;454(7203):436-44 [18650914.001]
  • [Cites] Methods Mol Biol. 2009;481:141-54 [19096804.001]
  • [Cites] Burns. 2009 May;35(3):318-26 [18951718.001]
  • [Cites] Semin Immunol. 2009 Jun;21(3):110-20 [19369094.001]
  • [Cites] J Cell Sci. 2009 Jul 15;122(Pt 14):2473-80 [19549682.001]
  • [Cites] Nat Med. 2009 Sep;15(9):1010-2 [19734877.001]
  • [Cites] Cancer Metastasis Rev. 2010 Jun;29(2):317-29 [20422276.001]
  • [Cites] Infect Immun. 2001 Dec;69(12):7213-23 [11705890.001]
  • (PMID = 21041641.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1alpha; 0 / Receptors, Antigen, T-Cell, gamma-delta
  • [Other-IDs] NLM/ PMC2993377
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94. Fukumaru K, Yoshii N, Kanzaki T, Kanekura T: Immunohistochemical comparison of beta-catenin expression by human normal epidermis and epidermal tumors. J Dermatol; 2007 Nov;34(11):746-53
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  • beta-Catenin, a cytoplasmic protein that binds directly to the intracellular domain of cadherin, controls various functions such as cell adhesion.
  • In many human carcinomas, E-cadherin-mediated cell-cell adhesion is lost or disturbed and related to metastasis.
  • The purpose of this study was to compare the expression of beta-catenin in the normal epidermal keratinocytes and samples from cutaneous benign and malignant epidermal tumors in 140 patients.
  • Our study population consisted of 140 patients with benign or malignant epidermal tumors.
  • Using immunohistochemical methods, we compared the expression of beta-catenin in their normal epidermal keratinocytes, and in samples from 61 benign (seborrheic keratosis, n = 33; verruca vulgaris, n = 14; keratoacanthoma, n = 14), and 79 malignant (Bowen's disease, n = 18; basal cell carcinoma, n = 33; squamous cell carcinoma, n = 28) epidermal tumors. beta-Catenin was found to be expressed in the cell membrane of normal keratinocytes.
  • Compared to other cell components of the normal epidermis, basal cells showed the strongest beta-catenin expression in all 140 patients.
  • While absent in three of 61 benign tumors, compared to normal basal cells, the expression of beta-catenin in the other 58 tumors was not significantly different; it was reduced in 71 of 79 malignant tumors (P < 0.0001).
  • In Bowen's disease, the expression of beta-catenin on the tumor cell membrane was reduced, however, strong expression was seen in the nuclei and cytoplasm.
  • Our results suggest that beta-catenin expression on the membrane of keratinocytes is associated with the differentiation of normal keratinocytes but not with their stage of differentiation, nor with the proliferation ability of epidermal tumor cells.
  • [MeSH-minor] Bowen's Disease / metabolism. Carcinoma, Basal Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Humans. Immunohistochemistry. Keratoacanthoma / metabolism. Keratosis, Seborrheic / metabolism. Warts / metabolism. Warts / pathology

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  • (PMID = 17973813.001).
  • [ISSN] 0385-2407
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / beta Catenin
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95. Shaker O, Youssef R: Role of apoptosis stimulus factor and its ligand in the induction of apoptosis in some ultraviolet induced diseases. Dermatol Online J; 2006;12(3):4
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  • BACKGROUND: Fas (factor of apoptosis stimulus) is one of the death receptors belonging to the tumor necrosis factor superfamily of receptors.
  • AIM: The aim of the study was to evaluate the role of Fas and Fas-L in basal cell carcinoma (BCC) as an example of malignant neoplasm and discoid lupus erythematosus (DLE) as a benign skin disease, which are both induced by UV.
  • CONCLUSION: Over-expression of Fas-L and lack of expression of Fas by tumor cells together with other factors act in favor of BCC by helping its survival and progression.
  • [MeSH-major] Antigens, CD95 / metabolism. Carcinoma, Basal Cell / pathology. Lupus Erythematosus, Discoid / metabolism. Lupus Erythematosus, Discoid / pathology. Membrane Glycoproteins / metabolism. Skin Neoplasms / pathology. Tumor Necrosis Factors / metabolism

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  • (PMID = 16638418.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factors
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96. Golod O, Soriano T, Craft N: Palisaded encapsulated neuroma--a classic presentation of a commonly misdiagnosed neural tumor. J Drugs Dermatol; 2005 Jan-Feb;4(1):92-4
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  • [Title] Palisaded encapsulated neuroma--a classic presentation of a commonly misdiagnosed neural tumor.
  • PEN is a previously described, benign cutaneous neural tumour, with a histological appearance between that of a neurofibroma and a schwannoma.
  • Clinically, PEN is most commonly misdiagnosed as a basal cell carcinoma, a nevus, or as a neurofibroma.
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Neoplasm Proteins / metabolism

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  • (PMID = 15696992.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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97. Kazakov DV, Kutzner H, Mukensnabl P, Michal M: Low-grade adnexal carcinoma of the skin with multidirectional (glandular, trichoblastomatous, spiradenocylindromatous) differentiation. Am J Dermatopathol; 2006 Aug;28(4):341-5
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  • The conjoint occurrence of follicular, sebaceous, or apocrine differentiations in a cutaneous adnexal neoplasm is a known event, more often encountered in benign neoplasms, whereas reports of cutaneous malignant adnexal tumors with bilineage or trilineage differentiation are few.
  • A new case of a cutaneous malignant adnexal neoplasm with multidirectional differentiation is reported here.
  • A 57-year-old woman presented with a long-standing, slowly growing, asymptomatic solitary tumor the size of a large nut in the coccygeal area, which was surgically excised.
  • Microscopically, the neoplasm was located in the dermis with focal extension into the subcutis.
  • Rare nodules resembled elements seen in a spiradenoma by containing scattered lymphocytes and globules of hyalinized eosinophilic basal membrane material.
  • Mitotic figures, including abnormal ones, were infrequent, but mild nuclear pleomorphism, nuclear crowding, and individual cell necrosis were easily appreciable in both small basaloid cells and cells with clear cytoplasm.
  • We classified this tumor as a well-differentiated adnexal carcinoma demonstrating combined follicular and apocrine differentiation.
  • [MeSH-major] Adnexal Diseases / pathology. Cell Differentiation. Skin Neoplasms / pathology
  • [MeSH-minor] Cell Shape. Female. Humans. Immunohistochemistry. Middle Aged. Neoplasm Invasiveness / pathology. Neoplasm Staging

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  • (PMID = 16871040.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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98. Morikawa T, Nagata M, Tomita K, Kitamura T, Goto A, Chong JM, Fukayama M: Phyllodes tumor of the prostate with exuberant glandular hyperplasia. Pathol Int; 2006 Mar;56(3):158-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phyllodes tumor of the prostate with exuberant glandular hyperplasia.
  • Reported herein is an unusual case of prostatic phyllodes tumor with exuberant glandular hyperplasia that led to misdiagnosis of adenocarcinoma.
  • The tumor was detected in a 52-year-old man who had a 1 year history of dysuria.
  • Histologically, the tumor had an atypical stromal cell proliferation and elongated slit-like glands characteristic of a phyllodes tumor.
  • The tumor was also accompanied by a florid proliferation of small acini, most of which lacked basal cells, a common manifestation of adenocarcinoma in the overall tumor area.
  • The following features of the resected tumor were helpful for concluding that these acini were benign: lack of cytological anaplasia in spite of structural atypia, presence of scattered basal cells confirmed by immunohistochemistry (high-molecular-weight cytokeratin), and histological transition from these acini to apparently benign slit-like glands.
  • The final diagnosis was then made as 'phyllodes tumor of the prostate with exuberant glandular hyperplasia'.
  • Atypical stromal cells might provide a clue for the recognition of this rare tumor at initial diagnosis by needle biopsy.
  • [MeSH-major] Biopsy, Needle. Diagnostic Errors. Phyllodes Tumor / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 16497250.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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99. Hagemann T, Binder C, Binder L, Pukrop T, Trümper L, Grimshaw MJ: Expression of endothelins and their receptors promotes an invasive phenotype of breast tumor cells but is insufficient to induce invasion in benign cells. DNA Cell Biol; 2005 Nov;24(11):766-76
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  • [Title] Expression of endothelins and their receptors promotes an invasive phenotype of breast tumor cells but is insufficient to induce invasion in benign cells.
  • There is increased staining of endothelins (ET-1, -2, and -3) and receptors (ET-RA and -RB) in invasive breast tumors compared to nonneoplastic tissue, and ETs stimulate MCF-7 cell invasion in vitro.
  • We analyzed ETstimulation of benign and transformed mammary epithelial cells, and whether expression of ETs is sufficient to induce invasiveness.
  • In breast cancer patient serum, ET-1 was increased in those patients with lymph node metastases compared to those with no lymph node involvement; ETs, however, had no mitogenic effect on breast tumor cell lines in vitro.
  • The benign mammary epithelial cell line, hTERT-HME1, and the poorly invasive breast tumor cell line MCF-7 secreted low levels of ET-1, while the invasive cell lines SKBR3 and MDAMB231 secreted high levels.
  • Expression of the ETs and receptors by the cell lines broadly correlated with their in vitro invasiveness; overexpression of ETs in MCF-7 cells increased basal invasion.
  • In contrast to transformed cells, ET stimulation or overexpression did not induce an invasive phenotype in benign cells.
  • Benign cells do not respond to ETs, and ET expression is not sufficient to induce invasion; however, the level of ET production by tumor cells correlates with their invasiveness, and increasing expression of the ET axis promotes breast tumor cell invasion via both receptors, while MMP-14 is induced via ET-RA.
  • [MeSH-minor] Calcium / metabolism. Cell Line. Cell Line, Tumor. Endothelin-1 / blood. Endothelin-1 / metabolism. Enzyme Induction. Female. Humans. Lymphatic Metastasis. Mammary Glands, Human / metabolism. Mammary Glands, Human / pathology. Matrix Metalloproteinases / biosynthesis. Neoplasm Invasiveness. Phenotype. Signal Transduction

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  • (PMID = 16274297.001).
  • [ISSN] 1044-5498
  • [Journal-full-title] DNA and cell biology
  • [ISO-abbreviation] DNA Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / Endothelins; 0 / Receptor, Endothelin A; 0 / Receptor, Endothelin B; EC 3.4.24.- / Matrix Metalloproteinases; SY7Q814VUP / Calcium
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100. Chawla AJ, Tan TY, Tan GJ: Basal cell adenomas of the parotid gland: CT scan features. Eur J Radiol; 2006 May;58(2):260-5
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  • [Title] Basal cell adenomas of the parotid gland: CT scan features.
  • Basal cell adenoma (BCA) is a rare tumor of the parotid gland, and except for a few case reports, the imaging features of this pathological entity are not well described.
  • In all cases, the tumor appeared as a round or oval, sharply marginated mass.
  • The latter two patterns have not been previously described in BCA or other parotid tumors, and may therefore aid in distinguishing BCA from other benign parotid neoplasms on CT.

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  • (PMID = 16414228.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Contrast Media
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