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  • TUMORS  (5)
  • 1
    Keywords: CELLS ; EXPRESSION ; proliferation ; tumor ; carcinoma ; KINASE ; DISEASE ; PROTEIN ; DIFFERENTIATION ; TUMORS ; CONTRAST ; ACTIVATED PROTEIN-KINASE ; PHOSPHORYLATION ; BREAST ; IN-SITU ; LESIONS ; immunohistochemistry ; MALIGNANCIES ; PATTERNS ; EPITHELIAL-CELLS ; CARCINOMAS ; INTERCELLULAR COMMUNICATION ; MALIGNANCY ; MOLECULAR-BASIS ; BASAL LAMINA ; breast carcinoma ; connexin43 ; GAP JUNCTIONAL COMMUNICATION ; gap junctions
    Abstract: We applied an antiserum (SA226P) specifically recognizing the phosphorylated form of connexin43 (P-Cx43) to human breast samples including normal breast samples, with fibrocystic disease (FCD), fibroadenomas (FA), in situ and infiltrating carcinomas of all major types, and miscellaneous extramarnmary tumors. The findings were compared with those obtained with commercial antisera recognizing all Cx43 forms (pan-Cx43). A subset of samples was stained for Her2-neu and p44/42 to mitogen-activated protein kinase. Paraffin step sections were used. Immunoblots were performed on frozen samples of a representative subset of cases. In the normal breast, FCD, and FA, SA226P stained strongly and extensively most myoepithelial cells (MECs); luminal cells remained unstained. In proliferative FCD and some cellular FA, SA226P stained MEC and the capillary endothelium (CE). In ductal and lobular in situ carcinomas, SA226P reacted strongly and diffusely with the remaining MEC, the CE, and the transformed luminal cells. SA226P stained all infiltrating carcinomas except the tubular variant. In all breast carcinomas, the CE within and adjacent to tumors and some myofibroblasts stained with SA226P. By contrast, pan-Cx43 stained weakly and sporadically the MEC and rare samples of invasive carcinomas. Notably, Mab p44/42 reacted in parallel with the samples stained with SA226P, whereas reactions with Her2 were negative. Immunoblot findings paralleled those obtained immunohistochemically. We conclude that P-Cx43, restricted to MEC in the normal breast, is up-regulated in the same cells in hyperplasias and dysplasias and FA and is strongly up-regulated in invasive carcinomas. Notably, in some proliferative FCD and in most in situ and infiltrating carcinomas, P-Cx43 is strongly expressed in CE within and adjacent to the lesions but not away from them. These findings were paralleled by the strong nuclear reactions noted with Mab p44/42. These phenomena, although not exclusive to malignancy, are particularly conspicuous in breast carcinomas and seemingly reflect active proliferation associated with abnormal gap junctional intercellular communication. (c) 2005 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15948121
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  • 2
    Keywords: CANCER ; EXPRESSION ; carcinoma ; PATHWAY ; PATHWAYS ; TUMORS ; mechanisms ; WOMEN ; p53 ; human papillomavirus ; HPV ; intraepithelial neoplasia ; TRENDS ; YOUNG-WOMEN ; p16(INK4A) ; VULVAR CANCER
    Abstract: OBJECTIVE: The incidence of vulvar squamous cell carcinomas located between the clitoris and urethra in young women is rising in distinct geographic regions, but characteristics of the tumors indicating certain carcinogenic mechanisms are unknown. The present study aimed at characterizing these vulvar cancers for their human papillomavirus (HPV), p16, and p53 status, revealing potential pathways of carcinogenesis. MATERIALS AND METHODS: Squamous cell vulvar cancers of the anterior fourchette were retrospectively collected from 8 German hospitals, with additional squamous cell cancers located at other sites of the vulva from 2 of the hospitals. All tumors were analyzed for HPV DNA by polymerase chain reaction and for p16 and p53 expression by immunohistochemistry. RESULTS: Potentially HPV-associated tumors (HPV and p16 positive, 21.4% [27/126] of the anterior fourchette and 27.7% [13/47] from other locations), p53-overexpressing tumors (35.7% [45/126] and 29.8% [14/47]), and a third group (HPV/p16 negative/p53 not overexpressed, 42.9% [54/126] and 42.6% [20/47]) were observed among tumors from the anterior fourchette as well as among vulvar cancers from other locations. Women with vulvar cancers of the anterior fourchette were of young age irrespective of the HPV/p16/p53 status. CONCLUSIONS: Different types of vulvar cancers can be found in squamous cell tumors of the anterior fourchette, similar to the finding in vulvar cancers from other locations and to what has previously been reported for vulvar squamous cell carcinomas in general.
    Type of Publication: Journal article published
    PubMed ID: 23645067
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  • 3
    Keywords: CANCER ; CELLS ; EXPRESSION ; proliferation ; radiotherapy ; tumor ; CELL ; Germany ; human ; TOXICITY ; NEW-YORK ; PROTEIN ; TUMORS ; PATIENT ; RESPONSES ; IFN-GAMMA ; INDUCTION ; DENDRITIC CELLS ; T cell ; T-CELL ; T-CELLS ; E7 ; papillomavirus ; IMMUNE-RESPONSES ; TARGET ; STAGE ; ASSAY ; cervical cancer ; CERVICAL-CANCER ; MARKERS ; human papillomavirus ; TYPE-16 ; GENOTYPES ; HPV ; E6 ; HPV16 ; HUMAN-PAPILLOMAVIRUS ; ONCOPROTEIN ; VACCINE ; CANCER-PATIENTS ; SAFETY ; ELISPOT ; immune response ; IMMUNE-RESPONSE ; IMMUNOTHERAPY ; vaccination ; HUMAN-PAPILLOMAVIRUS TYPE-16 ; SERIES ; CARCINOMA SCC ANTIGEN ; DE-NOVO ; E7 ONCOPROTEIN ; HLA ; IMMUNOGENICITY ; immunotherapy,ELISpot,T lymphocytes,CTL,uterine cancer ; STAGE IB ; TARGETS ; tumor marker
    Abstract: Purpose. Human papillomavirus (HPV) type 16 and 18 are the most prevalent genotypes in cervical cancer. The viral oncoproteins E6 and E7 are considered to be tumor-specific targets for immunotherapy. HPV E7 antigen-loaded autologous dendritic cells (DC) were evaluated as cellular tumor vaccine in a case series of cervical cancer patients. Methods. Autologous monocyte-derived DCs were pulsed with recombinant HPV16 E7 or HPV18 E7 oncoprotein and administered to 15 stage IV cervical cancer patients. Safety, toxicity, and induction of serological and cellular immune responses were monitored. Results. The vaccine was well-tolerated and no local or systemic side effects or toxicity were recorded. A specific serologic response was seen in 3/11 evaluated patients. Specific cellular immune responses (4/11) were detected with 2/10 positive de novo reactions plus one boosted preexistent response in proliferation assays and 3/11 in IFN-gamma ELISpot assays. A transient drop in tumor marker SCC was observed in 5/9 evaluable patients but did not correlate with markers of the immune response. No objective clinical response was observed. Tumor biopsies available from four patients showed severe or complete loss of HLA expression in three of the advanced tumors. Conclusion. Autologous dendritic cells pulsed with HPV E7 protein can induce T cell responses in a portion of late stage cervical cancer patients. Boosting of immune responses by adjuvants and vaccination of tumor HLA-positive patients will be mandatory in future trials
    Type of Publication: Journal article published
    PubMed ID: 12898233
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  • 4
    Keywords: CANCER ; EXPRESSION ; IN-VITRO ; proliferation ; tumor ; carcinoma ; human ; IN-VIVO ; MODEL ; VITRO ; EXPOSURE ; GENE ; GENES ; PROTEIN ; PROTEINS ; TUMORS ; LINES ; MICE ; CARCINOGENESIS ; CONTRAST ; KERATINOCYTES ; SKIN ; cell cycle ; CELL-CYCLE ; CYCLE ; E7 ; papillomavirus ; SUSCEPTIBILITY ; TRANSGENIC MICE ; PROGRESSION ; PROMOTER ; LINE ; human papillomavirus ; LIFE-SPAN ; E6 ; HUMAN KERATINOCYTES ; keratin ; SQUAMOUS-CELL CARCINOMA ; CARCINOMAS ; REPLICATION ; squamous cell carcinoma ; HUMAN-PAPILLOMAVIRUS TYPE-16 ; SQUAMOUS-CELL CARCINOMAS ; epidermis ; immunosuppression ; RE ; immortalization ; keratinocyte ; CARCINOGEN ; ONCOGENESIS ; CHECKPOINT ; EPIDERMODYSPLASIA-VERRUCIFORMIS ; LIFE ; HYPERPLASIA ; LEVEL ; EVENTS ; BOVINE ; chemical carcinogenesis ; CYCLE ARREST ; DYSPLASIA
    Abstract: The oncoproteins E6 and E7 of human papillomavirus type 38 (HPV38) display several transforming activities in vitro, including immortalization of primary human keratinocytes. To evaluate the oncogenic activities of the viral proteins in an in vivo model, we generated transgenic mice expressing HPV38 E6 and E7 under the control of the bovine homologue of the human keratin 10 (K10) promoter. Two distinct lines of HPV38 E6/E7-expressing transgenic mice that express the viral genes at different levels were obtained. In both lines, HPV38 E6 and E7 induced cellular proliferation, hyperplasia, and dysplasia, in the epidermis. The rate of occurrence of these events was proportional to the levels of HPV38 E6 and E7 expression in the two transgenic lines. Exposure of the epidermis of nontransgenic mice to UV led to p21(WAF1) accumulation and cell cycle arrest. In contrast, keratinocytes from transgenic mice continued to proliferate and were not positive for p21(WAF1), indicating that cell cycle checkpoints are altered in keratinocytes expressing the viral genes. Although the HPV38 E6/E7-expressing transgenic mice did not develop spontaneous tumors during their life span, two-stage carcinogen treatment led to a high incidence of papillomas, keratoacanthomas, and squamous-cell carcinomas in HPV38 mice compared with nontransgenic animals. Together, these data show that HPV38 E6 and E7 display transforming properties in vivo, providing further support for the role of HPV38 in carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 16282489
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  • 5
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; tumor ; CELL ; INHIBITION ; COMMON ; DIAGNOSIS ; NEW-YORK ; GENE ; GENES ; GENOME ; HYBRIDIZATION ; microarray ; transcription ; DRUG ; METABOLISM ; cell line ; TUMORS ; validation ; LINES ; COMPLEX ; COMPLEXES ; CELL-LINES ; chromosome ; FORM ; DELETION ; IDENTIFICATION ; IN-SITU ; PROGRESSION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; ARRAYS ; NUMBER ; genetics ; cervical cancer ; CERVICAL-CANCER ; CELL-LINE ; LINE ; DELETIONS ; PATHOGENESIS ; PCR ; REGION ; REGIONS ; ONCOGENE ; RT-PCR ; immune response ; IMMUNE-RESPONSE ; UTERINE CERVIX ; RECURRENT ; FLUORESCENCE ; MICROARRAY ANALYSIS ; fluorescence in situ hybridization ; cell lines ; heredity ; HIGH-LEVEL ; CDNA MICROARRAY ; in situ hybridization ; molecular ; ONCOLOGY ; ARRAY ; LEVEL ; analysis ; PROFILES ; DYSPLASIA ; EXPRESSION PROFILES ; USA ; CANDIDATE ; genomic ; DRUG-METABOLISM ; CDNA-MICROARRAY ; EPHB2 ; 19Q13.3 ; COMPARATIVE-GENOMIC-HYBRIDIZATION ; INVASIVE-CARCINOMA ; MUC4 EXPRESSION
    Abstract: Cervical cancer (CC) cells exhibit complex karyotypic alterations, which is consistent with deregulation of numerous critical genes in its formation and progression. To characterize this karyotypic complexity at the molecular level, we used cDNA array comparative genomic hybridization (aCGH) to analyze 29 CC cases and identified a number of over represented and deleted genes. The aCGH analysis revealed at least 17 recurrent amplicons and six common regions of deletions. These regions contain several known tumor-associated genes, such as those involved in transcription, apoptosis, cytoskeletal remodeling, ion-transport, drug metabolism, and immune response. Using the fluorescence in situ hybridization (FISH) approach we demonstrated the presence of high-level amplifications at the 8q24.3, 11q22.2, and 20q13 regions in CC cell lines. To identify amplification-associated genes that correspond to focal amplicons, we examined one or more genes in each of the 17 amplicons by Affymetrix UI33A expression arrays and serniquantitative reverse-transcription PCR (RT-PCR) in 31 CC tumors. This analysis exhibited frequent and robust upregulated expression in CC relative to normal cervix for genes EPHB2 (1p36), CDCA8 (1p34.3), AIM2 (1q22-23), RFC4, MUC4, and HRASLS (3q27-29), SKP2 (5p12-13), CENTD3 (Sq31.3), PTK2, RECQL4 (8q24), MMP1 and MMP13 (11q22.2), AKT1 (14q32.3), ABCC3 (17q21-22), SMARCA4 (19p13.3) LIG1 (19q13.3), UBE2C (20q13.1), SMCIL1 (Xp11), KIRA (Xq12), TMSN8 (Xq22), and CSAG2 (Xq28). Thus, the gene dosage and expression profiles generated here have enabled the identification of focal amplicons characteristic for the CC genome and facilitated the validation of relevant genes in these amplicons. These data, thus, form an important step toward the identification of biologically relevant genes in CC pathogenesis. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/ 10452257/suppmat. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17243165
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