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

This study was undertaken to determine the extent of apoptosis in lung carcinoma and to evaluate it as a prognostic marker. A series of 75 lung carcinomas (47 squamous cell carcinomas, 24 adenocarcinomas, 3 small cell carcinomas, and 1 large cell carcinoma) was analyzed for the extent of apoptosis by using the 3' end-labeling method of DNA in tissue sections. Apoptosis was correlated with the rate of cell proliferation, the immunohistochemically detectable p53 and bcl-2, the extent of tumor necrosis, and the survival data. The end-labeling method allowed a precise evaluation of the extent of apoptosis. In tumor tissue, the number of apoptotic bodies was roughly 2-fold greater than the number of apoptotic cells, whereas in nonneoplastic control tissues, the ratio was 1:1. The apoptotic indexes (percentages of apoptotic cells and bodies among tumor cells) were slightly higher in adenocarcinoma than in squamous cell carcinoma. There was no association between the extent of apoptosis and the expression of proliferating cell nuclear antigen or p53. On the other hand, tumor necrosis correlated significantly with proliferating cell nuclear antigen and p53 positivity (P = 0.00025 and 0.00087, respectively). Surprisingly, the extent of apoptosis was also found to be independent of the expression of bcl-2. Patients with apoptotic indexes greater than 1.5% had significantly shorter survival time than patients with apoptotic indexes equal to 1.50% or less (P < 0.01 by log rank). Aberrant p53 positivity also predicted a poor prognosis (P < 0.002 by log rank). By multivariate analysis, enhanced apoptosis showed a 1.9-fold risk (P = 0.04), and p53 positivity showed a 2.3-fold risk (P = 0.005) for a shortened survival. We conclude that both enhanced apoptosis and p53 positivity are independent prognostic markers in non-small cell lung carcinoma, predicting shortened survival time of the patients.
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PMID:Enhanced apoptosis predicts shortened survival in non-small cell lung carcinoma. 758 40

It is often difficult to predict the outcome of melanoma in patients with Clark level III-IV disease. We sought to identify markers of cell proliferation which may be useful in predicting prognosis. Patients with Clark's level III-IV malignant melanoma who had no local recurrences or metastases were matched with patients of comparable level and thickness who did experience recurrences of metastases. Cell proliferation markers p53, proliferating cell nuclear antigen (PCNA), and Ki-67 were assessed by immunohistochemistry. DNA ploidy was determined by flow cytometry. There was no difference in the expression of p53, PCNA, and Ki-67 between patients with metastases and patients without metastases. However, patients with metastases were more likely to have an aneuploid tumor cell population than were patients without metastases (p < 0.03). Expression of cell proliferation markers do not appear to help predict prognosis in advanced level melanoma; however, aneuploidy may be associated with a greater probability of metastasis.
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PMID:Cell proliferation markers in predicting metastases in malignant melanoma. 759 19

Meningiomas are principally benign in nature. Some meningiomas, however, grow fast or recur even after total removal. The biological behavior of meningiomas often can not be predicted from conventional histopathological studies. A monoclonal antibody against proliferating cell nuclear antigen (PCNA) was used to investigate the usefulness of the PCNA index as a parameter to estimate the proliferative activity of meningiomas. Fifty-two meningiomas were examined. The mean PCNA index of recurrent meningiomas (3.37 +/- 0.92%) was significantly higher than that of non-recurrent meningiomas (1.12 +/- 0.51%) (p < 0.005). The PCNA indices of recurrent cases were all higher than 2.0%. A semilog linear regression analysis between tumor doubling time and PCNA index showed a significant correlation (r = 0.90, p < 0.05). An inverse linear correlation between PCNA index and interval to recurrence was observed (r = 0.62, p < 0.05). A good linear correlation was also shown between PCNA index and BUdR labeling index (r = 0.88, p < 0.01). The results of this study suggest that, providing the methods of tissue processing, immunostaining and counting of positive nuclei are unified, the PCNA index is a useful parameter for estimating the biological behavior of meningiomas.
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PMID:Proliferative potential of meningiomas evaluated by proliferating cell nuclear antigen expression. 759 51

In the present study the prognostic value of proliferating cell nuclear antigen (PCNA) index and tumor DNA content were evaluated in 100 patients with renal cell carcinoma. The survival rate of patients with aneuploid tumors was not significantly different from that of those with diploid tumors. DNA ploidy could not be a prognostic factor. PCNA expression was determined by immunohistochemical staining using the PC10 clone. PCNA indices ranged from 2.6 to 33.6% with mean indices of 10.2, 15.7 and 27.9% for grades 1 to 3. There was a significant difference between the indices of each grade of tumor. Patients with a PCNA index of less than 13.6% had a longer survival time than the patients having tumors with a PCNA index of more than 13.6% (p < 0.05). Furthermore, within the group of grade 2 tumors, patients with a lower PCNA index had a significantly better prognosis (p < 0.05). Our findings demonstrated that the PCNA index provides significant prognostic information for renal cell carcinoma.
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PMID:[Proliferating cell nuclear antigen expression as a prognostic indicator for renal cell carcinoma: comparison with pathologic features and DNA content]. 759 33

The cure rates for squamous cell carcinoma of the larynx have improved little over the past few decades. Despite the large number of therapeutic and histopathologic studies that have been performed, there are currently no morphologic or cytologic markers available to predict outcome in patients with laryngeal cancer. In an attempt to create such a system, tissues from 40 patients who underwent surgery for carcinoma of the larynx were examined for this pilot study. The examinations included routine histology, morphologic grading at the tumor front, immunohistochemical identification of the proliferation markers proliferating cell nuclear antigen (PCNA) and Ki67, and quantitative DNA analysis. By means of the stepwise multivariate Cox regression analysis with forward selection, factors that were highly correlated to the development of recurrent disease and survival were determined. We found that the results of the DNA analysis (ie, 2c deviation index, DNA malignancy grade), along with the morphologic tumor front grading and Ki67 score, were closely related to prognosis (p < .01). All of these factors reflect tumor biology. No correlation was found for the Broders grading or for any other clinical parameter. With the test battery used in this preliminary study, patients at high risk for developing tumor recurrences could be recognized. The advantages of this technique are that it is an objective assessment of the tumor and that it can be performed on preoperative biopsy specimens. This might influence decisions regarding therapeutic management and could eventually lead to more appropriate and individualized therapy.
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PMID:Predicting recurrence and survival in patients with laryngeal cancer by means of DNA cytometry, tumor front grading, and proliferation markers. 759 60

The positive effect of castration in prostatic cancer patients is considered to be related to the induction of apoptosis in androgen-dependent tumour cells. However, castration apparently does not induce apoptosis in the highly differentiated, androgen-sensitive Dunning R3327PAP rat prostatic adenocarcinoma. To elucidate potential mechanisms of apoptotic induction in this tumour model, rats with subcutaneously implanted tumours were treated with vehicle (I), castration+vehicle (C) or castration + 50 micrograms of oestradiol benzoate per day s.c. (C + E2). The effects on tumours were examined by morphometry, in situ end labelling (ISEL) of apoptotic cells and immunohistochemically with monoclonal antibodies to proliferating cell nuclear antigen (PCNA) at different time points up to 168 h after castration. Castration inhibited tumour growth and decreased the epithelial cell apoptotic rate (from 12 h) and epithelial cell proliferation rate (from 72 h) compared with that in the I group. Tumour volume, volume densities of epithelium and stroma and stroma cell proliferation rate remained constant in the C group during the study period. C + E2 treatment resulted in increases in cell proliferation in the stroma (from 12 h) and in the volume density of stroma (from 24 h) compared with that in the C and I groups. The number of apoptotic epithelial cells was increased (from 24 h), and this was followed by decreases in the volume density of epithelium (from 24 h), the epithelial cell proliferation rate (from 72 h) and the total tumour volume (from 72 h). We conclude that in the Dunning R3327PAP tumour model C + E2 treatment is more effective than castration alone. C+E2 treatment, in contrast to C, is able to induce tumour cell death and to decrease total tumour volume. The mechanism behind this effect is unknown, but it could be related to stimulatory effects of E2 in the tumour stroma.
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PMID:Castration plus oestrogen treatment induces but castration alone suppresses epithelial cell apoptosis in an androgen-sensitive rat prostatic adenocarcinoma. 759 43

Intense research using animal models has indicated that chemically-induced rat liver cancer proceeds through multiple, distinct stages that can be characterised morphologically and biochemically. Primary human liver cancer, with hepatitis B and other environmental factors such as poor nutrition and food contaminating mycotoxins as contributing etiological factors, is one of the major causes of cancer deaths in African, Asian and some Western countries. Recent advances in surgical and diagnostic techniques have also allowed the identification of potential morphological precursors of primary human liver cancer, and suggested a model consistent with the concepts of initiation--promotion--progression as in the rat. The expression of proliferating cell nuclear antigen (PCNA), silver-staining nucleolar organiser regions (AgNOR), oncogenes and the tumor suppressor gene p53 in preneoplastic and neoplastic lesions of rat and human livers is presently reviewed. This undertaking is an attempt to evaluate whether the current knowledge regarding molecular mechanisms of carcinogenesis is sufficient to permit the use of these molecular parameters as 'intermediate' markers in studies of risk assessment and cancer prevention, without having to resort to tumor appearance as an end-point.
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PMID:The potential for the use of cell proliferation and oncogene expression as intermediate markers during liver carcinogenesis. 760 May 46

Scanning laser cytometric analysis of fluorochrome-labeled cells was used to survey and quantitate the distribution of proliferating cells in formalin-fixed, paraffin-embedded tissue sections from hyperplastic and neoplastic rat livers. The technique used fluorescent immunochemical staining of proliferating cell nuclear antigen (PCNA) as a marker for proliferating cells and propidium iodide as a fluorescent nuclear counterstain. Use of an antigen retrieval treatment improved detection of PCNA and treatment of tissue sections with crystal violet improved the sensitivity of the method by quenching background autofluorescence. PCNA evaluation of cell proliferation in regenerating rat liver 0-48 h post-partial hepatectomy showed that 3-43% of cells stained positively for PCNA, a pattern closely correlating with previously reported rates of maximum DNA synthesis. The PCNA staining patterns observed among cells in neoplastic nodules were more focal in distribution and indicated that from 5 to 25% of the cell nuclei per nodular region stained positively for PCNA. This use of image analysis for the rapid identification of proliferating cell areas in fixed, paraffin-embedded tissue active in neoplastic growth will expedite in situ cytochemical and molecular studies attempting to identify key differences between hyperplastic and neoplastic growth.
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PMID:Scanning microfluorometric analysis of proliferating cell nuclear antigen in formalin-fixed sections of hyperplastic and neoplastic rat liver. 760 Sep 3

For a long time, it has been speculated that pregnancy stimulates the growth of acoustic schwannomas. To test this hypothesis, immunohistochemical stains for estrogen receptor, progesterone receptor, and proliferating cell nuclear antigen (PCNA) were performed. Flow cytometric studies for DNA ploidy and S-phase fraction determinations were also performed. The study subjects included 6 female patients with unilateral acoustic tumors; at the time of tumor removal, 1 woman was pregnant and the other 5 women were 2 to 10 months postpartum. The age-sex-matched control group consisted of 6 men and 12 nonpregnant women, all with acoustic schwannomas similar in size to those of the study group. The study found no statistically significant association between the presence or quantity of estrogen or progesterone receptors and pregnancy, DNA ploidy, proliferation indices, or clinical data. Based on PCNA indices, large tumors tended to be less "biologically active" than small lesions (P < .01). The authors concluded that pregnancy does not significantly stimulate the cellular growth of acoustic schwannomas.
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PMID:Acoustic schwannoma and pregnancy: a DNA flow cytometric, steroid hormone receptor, and proliferation marker study. 760 72

The proposal that Kaposi's sarcoma undergoes cellular transformation from early to late stages was studied with argyrophilic nucleolar organizer regions, proliferating cell nuclear antigen/cyclin, and immunoperoxidase staining for factor VIII-related antigen. Staining of argyrophilic nucleolar organizer regions was significantly increased in the plaque/nodular stage compared to the patch stage. The endothelial-selective marker factor VIII-related antigen stained more intensely in patch stage lesions. This was inversely correlated with staining of argyrophilic nucleolar organizer regions. Proliferating cell nuclear antigen/cyclin staining did not correlate with tumor stage or with factor VIII-related antigen. The changes in argyrophilic nucleolar organizer regions and factor VIII-related antigen staining are evidence for cellular transformation in Kaposi's sarcoma.
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PMID:Argyrophilic nucleolar organizer regions and proliferating cell nuclear antigen/cyclin in Kaposi's sarcoma. Comparison with morphology and with immunoperoxidase staining for factor VIII-related antigen. 760 71


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