Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated whether monoclonal antibody (PC10) of proliferating cell nuclear antigen (PCNA) could be useful as a marker of proliferating cells within formalin-fixed, paraffin-embedded tissue sections of 140 gynecological tumors and their related lesions. There was a positive correlation (r = 0.76) between the labelling index for PCNA and that for Ki67. Immunohistochemical staining for PC10 was confined to the nucleus and showed a diffuse or granular pattern or a mixture of both. The distribution of PC10 staining in non-neoplastic tissues was localized to proliferating cell compartments. In malignant tissues, the localization of the distribution of PCNA-positive cells came to be lost and the proportion of positive cells varied from case to case as well as from field to field within the same tissue section. The cases in which more than 31% of cells were positive for PCNA were as follows: Cervical squamous dysplasia 2/3, squamous carcinoma in situ 2/5, microinvasive squamous carcinoma 2/2, invasive squamous carcinoma 9/13, adenocarcinoma in situ 4/4, microinvasive adenocarcinoma 3/3, invasive adenocarcinoma 6/7, endometrial adenocarcinoma 6/25, ovarian epithelial malignant tumors 11/17, sex cord stromal tumors 2/14, and germ cell tumors 3/22. It is concluded that immunohistochemical staining for PC10 may be useful as a marker for proliferating activity of the cells both in normal and tumor tissues rather than for malignancy.
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PMID:[Immunohistochemical study of proliferating cell nuclear antigen (PCNA) in gynecological tumors and their related lesions]. 134 57

This study was designed to correlate mucosal proliferation in Barrett's oesophagus with expression of a growth promoting peptide, transforming growth factor alpha (TGF alpha). Oesophageal mucosa was studied from 50 patients with oesophageal disease who had been treated by oesophagectomy. Histological analysis showed a range of oesophageal pathology - 18 patients had gastric type Barrett's mucosa, 18 had intestinal type Barrett's mucosa, and 14 had oesophageal adenocarcinomas. Sections were stained immunohistochemically for proliferating cell nuclear antigen (PCNA) (an index of cellular proliferation) and TGF alpha. PCNA immunostaining was seen mainly in the basal cells of the neck/foveolar epithelial compartment of the glands in Barrett's oesophagus. However, in mucosa with high grade dysplasia, the proliferative compartment extended upwards into the superficial layers of the glands. At least 2000 cells were counted in each patient to determine the proportion with PCNA immunoreactivity (PCNA labelling index). The labelling index was highest in adenocarcinoma (25%) and in Barrett's intestinal type mucosa with high grade dysplasia (26%) compared with intestinal type mucosa with no significant dysplasia (20%) and Barrett's gastric type mucosa (12%). There was a significant positive correlation between PCNA labelling indices and TGF alpha expression in Barrett's mucosa (p less than 0.01). In glands showing high grade dysplasia, TGF alpha immunoreactivity was seen in the same regions of the glands as PCNA immunoreactivity, indicating the possibility of involvement of TGF alpha in (pre) neoplastic proliferation in Barrett's oesophagus.
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PMID:Proliferating cell nuclear antigen in oesophageal diseases; correlation with transforming growth factor alpha expression. 135 61

Flow cytometric techniques have been developed for measurement of proliferating cell nuclear antigen (PCNA), which allows studies on the proliferative capacity of cells and tissues. PCNA-DNA dual staining procedures, for both fixed and unfixed cells, and analytical method by FCM are presented. We recommend performing either the fixed or unfixed method. Our studies using the MCF7 human breast adenocarcinoma cell line and the A549 human lung squamous cell carcinoma cell line, in the exponential growth phase, revealed that both ethanol and acetone were satisfactory fixatives, in contrast to methanol and paraformaldehyde, and PI with a concentration of 25 micrograms/ml was most suitable compared with 50 and 100 micrograms/ml.
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PMID:[Flow cytometric techniques for measurement of proliferating cell nuclear antigen (PCNA)]. 136 29

The proliferative activity of gastric adenomas from 18 patients (42 endoscopic procedures) was compared with follow-up results. These cases were gastric adenomas proven by follow-up with repeated endoscopic procedures for more than 2 years, or were confirmed as gastric adenocarcinoma thereafter by histopathologic examination. Among the eighteen cases, nine showed carcinoma in the subsequent biopsies (group 1) and the remaining nine did not result in carcinoma (group 2). The proliferating cell nuclear antigen (PCNA) positivity rates of the two groups were significantly different (P < 0.01). The average PCNA positivity in group 1 was 33.1%, while it was 10.0% in group 2. The risk of developing carcinoma increased as the PCNA positivity increased: 0% in the low PCNA positivity group, 41% in the mid-positivity group and 89% in the high positivity group. We concluded that growth fraction could be taken into account as one of the most important prognostic factors for gastric adenoma, and accordingly repeated endoscopic biopsies with close follow-up should be carried out especially in the high PCNA positivity group.
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PMID:Prognostic significance of proliferating cell nuclear antigen-positive growth fraction in gastric adenomas. 136 46

Cell renewal in the large intestine mucosa is normally tied to a rigidly compartmentalized model. Immunohistochemical identification of cells in S phase through uptake of bromodeoxyuridine is the method of choice for detailed compartmental mapping of proliferation, while immunohistochemical detection of proliferation-associated antigens (Ki-67, PCNA, DNA polymerase alpha) provides information in advanced tumor cases. Mucosal hyperproliferation due to inflammation may be transient (self-limited colitis, Crohn's disease, acute radiation damage) or lasting (ulcerative colitis). Progressive shifting of the proliferation zone to the crypt surface (Stage II abnormality) is a late feature of irradiated rectal mucosa and subgroups of ulcerative colitis patients at high risk for cancer. Hyperproliferation and Stage II abnormality coexist in the mucosa of patients with colorectal neoplasia, but are mutually independent and correlated to different clinical and pathological features of the disease. These cytokinetic abnormalities are highly predictive markers of the adenoma-carcinoma sequence, but are not associated with de novo adenocarcinoma. Proliferation increases progressively in the subsequent steps of this sequence, except in early cancer.
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PMID:Cell proliferation in colorectal tumor progression: an immunohistochemical approach to intermediate biomarkers. 146 8

Neoadjuvant total androgen ablation therapy leads to involutional changes in prostatic carcinoma and may have the potential to downstage operable prostate cancers. We studied 27 clinically localized prostatic carcinomas after 3 months of combined treatment with a luteinizing hormone-releasing hormone agonist, goserelin acetate, and the antiandrogen flutamide, followed by radical retropubic prostatectomy, for changes in the serum prostate-specific antigen (PSA) level, changes in prostatic volume, therapy-induced histopathologic changes, DNA ploidy, and proliferative activity. Ten hormonally untreated, grade-matched prostatic adenocarcinomas served as controls. The mean pretherapy serum PSA level was 17.5 ng/ml, and posttherapy PSA levels were all < 4.0 ng/ml, with 18 men having undetectable levels. The mean reduction in prostatic volume following hormonal therapy was 37% (range 16-52%). Pathologic staging confirmed 20 pT2N0, six pT3N0, and one pT3N1. All prostates showed residual adenocarcinoma (extremely focal in seven cases [26%] with loss of glandular architecture, cytoplasmic vacuolization, and nuclear pyknosis. High-grade adenocarcinoma was nondiploid in 25% of hormonally treated prostates and 80% of 10 untreated controls. Immunostaining for proliferating cell nuclear antigen showed > 10% nuclear reactivity in 33% of treated carcinomas and 90% of untreated carcinomas. In conclusion, 3 months of neoadjuvant androgen ablation for localized prostatic carcinoma significantly lowers serum PSA and prostatic volume and produces involutional changes in residual carcinomas that mimic high-grade disease. However, pretreated carcinomas have predominantly a diploid DNA content and low proliferative activity as opposed to untreated carcinomas. Thus, grading of pretreated adenocarcinomas by conventional methods may be misleading. Preoperative total androgen ablation has a profound effect on a subset of prostatic carcinoma cells, possibly by facilitating programmed cell death.
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PMID:Clinical and pathobiological effects of neoadjuvant total androgen ablation therapy on clinically localized prostatic adenocarcinoma. 752 15

Clinical and immunohistochemical studies were conducted to evaluate prostatic papillary adenocarcinoma and prostatic papillary hyperplasia. Subjects consisted of 5 cases of papillary adenocarcinoma and 2 cases of papillary hyperplasia. There is no conclusive clinical factor for preoperative diagnosis, but we attach importance to endoscopic findings. PSA, PAP, high molecular weight cytokeratin, and PCNA were evaluated immunohistochemically. PSA became positive in every instance but one--a case of papillary adenocarcinoma which became +/-. PAP was + in all cases, except for 1 case of papillary adenocarcinoma. Basal cells were positive for high molecular weight cytokeratin in 2 cases of papillary hyperplasia but were missing in papillary adenocarcinoma. Although PCNA was free from positive nuclei in papillary hyperplasia, positive nuclei were found in all cases of papillary adenocarcinoma. Considering these immunohistochemical results, papillary adenocarcinoma can be said to originate in the glandular epithelium of the prostate, as does ordinary prostatic carcinoma.
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PMID:A clinical and immunohistochemical study of papillary adenocarcinoma of the prostate. 753 25

The degree of DNA-instability as revealed by the immunohistochemical staining with monoclonal anti-single-stranded DNA antibody after acid hydrolysis (DNA-instability test) was used as the marker of malignancy. This was applied to human gastric regenerative epithelium in chronic peptic ulcer (5 cases), adenoma (35 cases), and well differentiated tubular adenocarcinoma (5 cases). Proliferative activity was evaluated by proliferating cell nuclear antigen (PCNA) immunohistochemistry, and the quantitative analyses of the mean number and mean area of silver-stained nucleolar organizer regions (AgNORs) per one nucleus were performed for all these cases. All cancers and adenomas were positively stained by the DNA-instability test diffusely, indicating the malignant character of the latter from the view point of DNA-instability, in contrast to the negative stainability of all regenerative epithelium. The percent number of PCNA-positive cells and mean number and mean area of AgNORs tended to be larger in adenoma and cancer than in regenerative epithelium, although the differences were not usually statistically significant. Supporting the malignant character of adenoma, single cell necroses and abnormal mitoses were almost always present in the lesion. In conclusion, all adenoma lesions were regarded as malignant in nature, namely, in-situ carcinoma, existing at an early stage of progression of malignancy.
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PMID:Early progression stage of malignancy as revealed by immunohistochemical demonstration of DNA instability; I, Human gastric adenomas. 753 25

Two-dimensional polyacrylamide gel electrophoresis combined with a non-enzymatic sample preparation technique is useful for analysing clinical tumour material. Using these techniques, we analysed the relationship between the histopathological findings in primary lung malignancies and the expression of a number of unidentified polypeptides that were detected in the molecular weight region 20-35 kDa. In this study 45 cases of primary lung cancer (PLC) (21 cases of adenocarcinoma, ten cases of squamous cell carcinoma, five cases of large-cell carcinoma, one case of adenosquamous cell carcinoma, five cases of small-cell carcinoma and three cases of carcinoid tumour) were examined. For reference, a human diploid fibroblast cell line (W138) and normal peripheral lymphocytes were used. Sixteen polypeptides were judged to be associated with histopathological features. These polypeptides seem to be valuable as differentiation markers. The simultaneous evaluation of these polypeptides and some other proliferation markers (e.g. PCNA, PCNA 'satellite', Numatin/protein B23 and lamin B) seems to clarify the characteristics of each case of PLC. Furthermore, it is possible to classify PLC based on the two-dimensional electrophoresis findings, and this classification of PLC is suggested to reflect the biological features of the tumour more precisely than that based only on morphology.
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PMID:Detection of polypeptides associated with the histopathological differentiation of primary lung carcinoma. 754 29

Eicosanoids have been implicated in colon carcinogenesis, but their role remains unclear. The levels of PGE2 are elevated in colon cancer tissues and in blood draining colon tumors. The effect of eicosanoids on the proliferation of colonic cells is unknown. We studied the effect of several prostaglandins (PGs) and leukotriene (LT)B4 on the proliferation rate of the human colon adenocarcinoma cell lines SW1116 and HT-29 and of 16,16-dimethyl PGE2 (dmPGE2) on the colon of BALB/c mice. PGs E2, F2 alpha, I2, the methyl ester of PGE2, dmPGE2, and LTB4 (10(-10), 10(-8), 10(-6) M), administered for up to 72 h, stimulated cell proliferation in SW1116 cells and all but PGF2 alpha and PGI2 stimulated proliferation in HT-29 cells. The proliferative effect was time- and concentration-dependent. However, in SW1116 cells the response to PGs was 'bell-shaped', being maximal at 10(-8) M, with the 10(-10) and 10(-6) M concentrations being less effective. In HT-29 cells, the addition of methyl groups to the PGE2 molecule increased the proliferative effect. None of these eicosanoids affected the distribution of these cells in the cell cycle or their rate of programmed cell death (apoptosis). dmPGE2 stimulated 3.6-fold the proliferation of colonocytes in normal BALB/c mice. This was determined by bivariate flow cytometric analysis of the expression of proliferating cell nuclear antigen (PCNA) in virtually pure populations of mouse colonocytes. dmPGE2 did not alter the cell cycle distribution of these cells. We conclude that several PGs as well as LTB4 stimulate the proliferation of human colon carcinoma cells in vitro, while dmPGE2 has a similar effect on mouse colonocytes in vivo. These findings raise the possibility that eicosanoids may contribute to colonic carcinogenesis by stimulating the proliferation rate of tumor cells in the colon.
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PMID:Selected eicosanoids increase the proliferation rate of human colon carcinoma cell lines and mouse colonocytes in vivo. 754 86


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