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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The synthesis of specific protein has been investigated in primary cultures of dog thyroid epithelial cells, which can be induced to progress into G1 phase, in the presence of insulin, by different types of mitogens: thyrotropin (TSH) acting through cyclic adenosine monophosphate (cAMP), epidermal growth factor (EGF), 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or 10% serum. EGF, TPA, or serum specifically induce [35S] methionine labeling of protein 1 (Mr approximately 80,000). The effect of EGF on protein 1 labeling and DNA replication is dependent on insulin. The level of protein 1 labeling as well as that of DNA synthesis is higher when TSH or TSH + serum are added together with EGF. It peaks in mid-G1. TSH alone, in the presence of insulin, stimulates DNA replication without inducing protein 1 synthesis, which thus represents a cell-cycle-dependent event that is not obligatory in mitogenic activation through cyclic AMP. Among the eight proteins whose synthesis is stimulated by TSH, only the labeling of protein 7, molecular weight ratio (Mr approximately 38,000), correlates with the DNA synthetic activity of the cells. The present authors identified protein 7 as cyclin/proliferating cell nuclear antigen (PCNA), the auxiliary protein of DNA polymerase-delta. The effect of TSH on cyclin synthesis is already detectable when most of the cells are in late G1, but its stimulation by EGF or EGF + serum is delayed and detected only after extending the labeling period to the S-phase. These data support the view that the cAMP-mediated mitogenic pathway remains partly distinct from the better known pathways induced by growth factors and tumor promoters, even at late stages of the G1-phase.
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PMID:Protein synthesis during induction of DNA replication in thyroid epithelial cells: evidence for late markers of distinct mitogenic pathways. 264 71

A proliferating cell nuclear antigen (PCNA) was identified with autoantibodies from a patient with systemic lupus erythematosus. Specific antibodies were purified by affinity chromatography in which Novikoff hepatoma nucleolar proteins were conjugated to Sepharose-4B. The purified anti-PCNA antibodies produced bright nucleolar fluorescence in tumor cells as shown by indirect immunofluorescence. PCNA was found in nucleoli of human cell lines, HeLa, Hep-2, and Namalwa, and a solid human renal and a prostate carcinoma. Both strong and weak nucleolar fluorescence areas were found in the renal and prostate carcinoma indicating that there are varying degrees of proliferation among tumor cells. Two human colon carcinoma cell lines, omega (an aggressive, fast-growing clone of human colon carcinoma cell line HCT 116) and CBS [a slow-growing human colon carcinoma cell line (group 3)], with different growth rates were compared. The fast-growing colon carcinoma cells, omega, exhibited a higher percentage of nucleolar fluorescence (28.5%) than that of the slow growing colon cells (13.6%). By enzyme-linked immunosorbent assays, the omega cell extract had a higher PCNA antigen content (2.8-fold) than that of the CBS cell extract which, in turn, was higher than that of human liver extract. PCNA was also found in a human fetal lung fibroblast cell line (IMR-90). Very weak or negative nucleolar fluorescence was observed in several normal human tissues including liver, kidney, prostate, and cheek cells. Nucleolar fluorescence was also observed in rat Novikoff hepatoma cells. Although normal rat livers do not have PCNA nucleolar fluorescence, nuclear and nucleolar fluorescence were observed at 18 hr after partial hepatectomy.
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PMID:Indirect immunofluorescence studies of proliferating cell nuclear antigen in nucleoli of human tumor and normal tissues. 613 81

Using anti-PCNA antibody (PC10), an immunohistochemical study of the expression of PCNA in formalin-fixed and paraffin-embedded materials of colorectal cancer patients was performed and correlation of PCNA expression with clinicopathological findings and DNA ploidy pattern was studied. PCNA labeling rate (PCNA LR) was estimated in the advancing margin of the tumor and ranged from 23.8% to 77.9%. There was a significant difference in lymphatic vessel invasion, liver metastasis and Dukes' stage between the groups with high (> 48.7) and low (< 48.7) PCNA LR (P < 0.05). No differences were seen in tumor size, histological type, lymph node metastasis or DNA ploidy pattern. In patients with younger age, infiltration to neighboring organs, a high degree of venous invasion, and peritoneal dissemination, the frequency of high PCNA LR tended to be higher (P < 0.1). The results above suggest that a high proliferative activity as defined by evaluation of the PCNA LR at the advancing margin of the tumor may be one of the parameters of malignant potential and helpful as a predictor of liver metastasis in colorectal cancer.
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PMID:Analysis of proliferative activity using antiproliferating cell nuclear antigen antibody in colorectal cancer. 747 63

BACKGROUND Understanding the tumor growth rate is very important when considering strategies for the treatment of an acoustic neuroma, although the natural course of acoustic neuromas has not been reviewed in detail. METHODS The clinicopathologic features and the postoperative growth of tumors were evaluated in 32 patients with acoustic neuromas. This study was undertaken to assess the variability of the growth potential of cells within an acoustic tumor and to determine the relationships between the growth rate and the clinicopathologic characteristics of the patients with acoustic neuromas, including age at surgery, gender, tumor location and preoperative size, the duration of the symptoms, the presence of cystic regions, the presence of Antoni type A and B cells, the tumor cell density, tumor vascularity, mitotic rate, the presence of hyaline degeneration and hemosiderin deposition, nucleolar organizer regions (NORs), and the level of proliferating cell nuclear antigen (PCNA). RESULTS The growth patterns of the tumors were divided into three groups according to their growth rate: a regression group, a "no-growth" group (growth rates from 0-0.11 cm/year) and a progression group (growth rates from 0.19-1.72 cm/year). An additional operation was required in all patients whose growth rate was more than 0.38 cm/year. A statistical study on the factors associated with an increased growth rate showed that the three histopathologic factors most significantly associated with a postoperative growth rate were hyaline degeneration (p < 0.05), cell density (p < 0.005), and PCNA labeling index (p < 0.005). CONCLUSIONS These results strongly suggest that acoustic tumors can be subdivided into several groups, based upon different biologic activities and tumor growth rates.
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PMID:Clinicopathologic growth factors of acoustic neuromas. 748 32

Thirty seven cases of recurrent gliomas with survival time from 3 month to 13 years were investigated morphologically and immunohistochemically to evaluate progression and transformation of tumors. Using antibodies against PCNA and p53 the proportion of positively marked cells (nuclei) to all tumor cells was assessed at both primary and secondary surgery. This was compared with morphology and survival time between first and second surgery. In 10 cases (27.0%) there were no positively marked cells. In the remaining 27 cases (73.0% of the whole group), the following indices (percents of positive cells) were calculated: for patients with survival below 1 year (mean = 9m) 28.3% PCNA-positive cells and 30.3% p53-positive cells at first operation. For recidiving tumors both indices were lower namely for PCNA 20.9% and for protein p53-26.7%. For patients with survival over 1 year (mean = 4.8y) the index after I operation for PCNA was 25.5% and was higher than found after II operation-22.3%. In contrary, the index for protein p53 was 20.1% after I operation and was lower as compared with the index after II operation-28.2%. Eleven of twelve fibrillary astrocytomas and all five gemistocytic astrocytomas at first operation underwent changes towards malignisation. The immunocytochemical results confirm the high phenotypic differentiation what is reflected in different indices for PCNA and p53 of tumors.
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PMID:PCNA and protein P53 in recurrent supratentorial glial brain tumors: studies on correlation between morphology and tumor progression. 749 34

We describe a vascular tumor classified as SCH by histological criteria that was found in the mandibular-buccal fold of a 12-year-old girl. Microscopically, the lesion consisted of thin-walled cavernous spaces containing thrombi and phleboliths, and cellular areas composed of spindle-shaped, epithelioid and vacuolated cells. Immunohistochemically, the endothelial vascular lining was highly reactive with HAM56 antibody, while variable reactivity was observed for factor VIII-associated antigen. All cell types were positive for vimentin and anti-PCNA stained less than 3% of the tumor cells. This is the first report of SCH in the oral cavity.
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PMID:Spindle-cell hemangioendothelioma of the oral cavity. A case report. 750 Feb 95

Although many histologic criteria have been utilized to help distinguish benign from malignant adrenocortical tumors, it still may be difficult to assess the biologic potential of a given tumor. We evaluated 19 adenomas and 15 primary carcinomas with the avidin-biotin complex peroxidase method utilizing formalin-fixed, paraffin-embedded tissues with monoclonal antibodies for proliferating cell nuclear antigen (PC10) and Ki-67 (MIB 1) to determine if staining for these antigens could be used to help differentiate benign from malignant adrenocortical neoplasms. We also evaluated whether these markers could be used as prognostic indicators. Labeling indices for both PCNA and Ki-67 were determined by enumerating 1000 tumor cells, and expressed as a percentage of cells with nuclear staining. A PCNA and a Ki-67 score was obtained by the product of the staining intensity (0-3+) and the extent of nuclear staining, expressed as an estimate of the percentage of cells staining. Both PCNA and Ki-67 score and labeling index were correlated with mitotic counts, histologic diagnosis, and clinical outcome. Follow-up period for patients ranged from 4 months to 12 years with a mean of 25 months. Mitotic counts correlated with histologic diagnosis and clinical outcome. Both Ki-67 score and labeling index were significantly higher in malignant than in benign tumors, and correlated with mitotic counts and clinical outcome. There was a strong correlation between Ki-67 score and labeling index, indicating that Ki-67 score may be a more rapid and equally accurate method of estimating proliferative index of a tumor. PCNA score and labeling index did not correlate with histologic diagnosis or clinical outcome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunohistochemical assessment of proliferative activity in adrenocortical neoplasms. 750 13

In order to study the possible biological differences between anaplastic and typical seminoma, the following factors were studied in 11 cases of anaplastic seminoma and 15 cases of typical seminoma: mitotic activity, proliferating cell nuclear antigen (PCNA) expression, immunohistochemical analyses for cytokeratin, vimentin, placental alkaline phosphatase (PLAP), beta-human chorionic gonadotropin (beta-hCG), alpha-fetoprotein (AFP) and c-myc oncoprotein. Anaplastic seminoma was classified according to Mostofi's criteria, which is primarily based on the mitotic activity of the tumor. Mitotic activity was evaluated by both mitotic count and rate. Statistically significant correlations were observed between mitotic count and mitotic rate (R = 0.891), and between the mitotic count and PCNA labeling index (R = 0.792), in both typical and anaplastic seminomas. Immunostaining patterns for cytokeratin, vimentin, PLAP, beta-hCG, AFP and c-myc oncoprotein were not significantly different between typical and anaplastic seminoma. The present data indicated that no apparent clinicopathologic and immunohistochemical parameters discerning anaplastic seminoma from typical seminoma were present, when identifying anaplastic seminoma on the basis of high mitotic count. Anaplastic seminoma may therefore simply represent seminoma with high proliferative activity.
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PMID:Immunohistochemical comparison between anaplastic seminoma and typical seminoma. 750 6

Mutations of the p53 gene are important mechanisms in malignant transformation and are associated with dysregulation of normal cell growth. In the present study the expression of mutated p53-protein and proliferating cell nuclear antigen (PCNA) was investigated in a series of 31 human transitional cell carcinomas (TCC) by immunohistochemistry (IHC). The number of PCNA-positive cells and the pattern of expression was distinct in normal urothelium being confined to the basal cell layer. In dysplastic urothelium and in Carcinoma in situ (CIS) PCNA-immunoreactive nuclei were irregularly distributed throughout all layers. In tumor cell complexes the pattern of PCNA-immunoreactivity was different in papillary and primary infiltrating TCCs. Densitometric quantification of the intensity of the PCNA-reactivity using image analysis revealed an increase from normal to dysplastic urothelium and from dysplastic urothelium to invasive tumors. 21/31 (68%) of the tumors and tumor-associated CIS showed overexpression of p53 varying in percentage, pattern and reaction intensity. The percentage of PCNA-positive cells was higher in tumors overexpressing p53. Double IHC showed colocalization of both molecules in a significant proportion of tumor cells suggesting a link of p53 overexpression and the abnormal proliferative activity. The present results show that p53 over-expression is found in a significant percentage of TCCs and indicate a close association with a defective growth regulation resulting in increased PCNA-levels and enhanced cellular proliferation.
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PMID:[Proliferative activity and p53 expression in transitional cell carcinoma of the urinary bladder]. 751 Dec 89

Nine pilocytic astrocytomas of the optic nerve were investigated with the AgNOR method and by immunohistochemistry with anti-PCNA antibodies. Four patients were male, 5 female (mean age 16.5 years, range 1-55 years). Seven pilocytic astrocytomas were low-grade tumors (grade I, WHO [2]), one tumor contained giant cells and prominent nuclei (grade II), the remaining tumor was anaplastic (grade III). In each case, 5 randomly chosen areas were investigated by light microscopy using objective 40. The PCNA staining index was defined as number of positive tumor cell nuclei divided by the total amount of tumor cell nuclei in the microscopic field. Tumors showing only one immunopositive cell nucleus at low magnification were considered to have a staining index below 0.1%. The staining index of the 7 grade I tumors was below 0,1%, the grade II tumor showed a staining index of 1%, and the anaplastic astrocytoma (grade III) demonstrated a 2.5% staining index. Investigations with the AgNOR method confirmed the above results of a low growth fraction in grade I-III grade astrocytomas of the optic nerve. Though low growth fractions have been reported in anaplastic astrocytomas and glioblastomas of the cerebrum, the low staining index in the anaplastic pilocytic astrocytoma of our series is remarkable: Instead of histological parameters like cellular and nuclear polymorphism and cellular density, the growth fraction could be a better parameter for the clinical course, which has in fact been benign in this case of an anaplastic pilocytic astrocytoma of the optic nerve.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:AgNOR- and PCNA-studies in astrocytomas of the optic nerve. 751 78


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