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

The cytologic diagnosis of lymphoid cells in pleural effusion is not readily apparent. The atypical lymphocytes in reactive process or viral infection may mimic immature lymphoblasts in lymphoblastic lymphoma. Therefore, an objective and reliable method to identify malignant lymphoid cells is important. Here we reported the application of T cell receptor (TCR) gene analysis, together with cytomorphology and immunophenotypic studies, to establish the diagnosis of T-lymphoblastic lymphoma in a 20-year-old female who presented with a mediastinal tumor and pleural effusion. The diagnosis of malignant lymphoma was suspected by cytology and then confirmed by TCR beta chain (TCR beta) gene rearrangement. The rearrangement of TCR beta gene revealed by Southern blot technique implied a T-monoclonal lymphoid population which is most likely malignant. Immunophenotypic studies revealed expression of TdT and T cell antigens indicating a T lymphoblastic lymphoma. As shown in this case, antigen receptor gene analysis can be conducted with a much smaller number of cells to identify a malignant clone among a heterogeneous cell population.
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PMID:Application of rearrangements of T cell receptor gene in the diagnosis of mediastinal T-lymphoblastic lymphoma: a case report. 917 4

Thus far, there are no immunohistochemical markers that are specific for thymic epithelial neoplasms, although demonstration of immature T cells in an epithelial tumor can indirectly support a diagnosis of thymoma. In this study, the usefulness of a paraffin section-reactive CD5 antibody (clone CD5/54/B4) for supporting the thymic origin of an epithelial neoplasm was evaluated. Antigen retrieval was effected by microwaving in citrate buffer. Sixteen of 24 thymic carcinomas (67%) were immunoreactive for CD5, including nine of nine squamous cell, two of two undifferentiated, two of four lymphoepithelioma-like, and one case each of basolid carcinoma, clear cell carcinoma, and unclassified thymic carcinoma, but none of four thymic small cell carcinomas. None of 17 cases of benign thymoma and 21 cases of invasive thymoma (including six cases classifiable as well-differentiated thymic carcinoma using the Muller-Hermelink criteria) was immunoreactive for CD5, in the presence of CD5-positive lymphocytes as an internal positive control. Two of three thymic neoplasms with features borderline between thymic carcinoma and invasive thymoma were immunoreactive for CD5. In contrast, none of 61 cases of other malignant neoplasms with a tendency to involve the mediastinum was immunoreactive for CD5, including 40 nonthymic carcinomas and 13 malignant germ cell neoplasma. CD5 staining of thymic epithelial tumors correlated with the absence of tumor-associated CD99-positive thymocytes, as demonstrated in our previous studies. We conclude that CD5 is a useful marker of primary thymic carcinomas. Taken together, CD5 and CD99 (or other immature T-cell markers such as TdT and Cd1a) should be particularly useful in evaluating mediastinal and other biopsy samples of possible thymic epithelial neoplasms and in the subtyping of these tumors.
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PMID:Thymic carcinomas, but not thymomas and carcinomas of other sites, show CD5 immunoreactivity. 925 57

We have studied apoptosis in a subset of thirty hepatocellular carcinomas (HCCs) exhibiting neuroendocrine differentiation (ND). Apoptosis was assessed by use of in situ DNA end labelling, and was quantified employing a TdT labelling index. It turned out that apoptosis occurred in HCCs with ND, albeit at different rates. Apoptosis was visualized as a clearly detectable reaction product mostly localized in tumor cell nuclei and in apoptotic bodies. Almost no staining was observed in nuclei of multinuclear tumor giant cells. In HCCs with ND, apoptosis was not related to type or grade, but tumors mainly consisting of hepatocyte-like cells and/or clear cells showed a significantly higher apoptotic rate. This was also the cell type most frequently disclosing neuroendocrine features. The apoptotic rate was significantly higher in HCCs with ND than in a control group of HCCs not showing ND. The findings suggest that neuroendocrine differentiation in liver cell tumors is associated with an altered pattern of programmed cell death, and that this phenomenon may therefore have an influence on clinical behavior.
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PMID:Apoptosis in hepatocellular carcinomas with neuroendocrine differentiation. 930 58

Flavopiridol is a novel, potent inhibitor of cyclin-dependent kinases (CDK). This synthetic flavone has been reported to exhibit antitumor activity in murine and human tumor cell lines in vitro and in vivo and is currently undergoing clinical phase I evaluation. In the present study, 1 Epstein-Barr virus (EBV)-transformed B-prolymphocytic cell line (JVM-2), 1 EBV-transformed B-CLL cell line (I83CLL), and 1 non-EBV transformed B-CLL cell line (WSU-CLL) were used as targets. Treatment of the cells with flavopiridol (100 nmol/L to 400 nmol/L) led to a marked dose- and time-dependent inhibition of cell growth and survival as determined using trypan blue exclusion. Morphologic analysis showed characteristic apoptotic changes such as chromatin condensation and fragmentation, membrane blebbing, and formation of apoptotic bodies. Furthermore, quantitative assessment of apoptosis-associated DNA strand breaks by in situ TdT labeling showed that a significant number of flavopiridol-treated cells underwent apoptosis. These cellular effects were associated with a significant decrease in bcl-2 expression as observed by Northern and Western blotting. The results showed that flavopiridol downregulates bcl-2 mRNA and bcl-2 protein expression within 24 hours. Genistein and quercetin, two flavonoids that do not inhibit CDKs, did not affect bcl-2 expression. These data suggest an additional mechanism of action of this new flavone which might be useful as an agent in the treatment of chronic lymphoid malignancies.
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PMID:The novel cyclin-dependent kinase inhibitor flavopiridol downregulates Bcl-2 and induces growth arrest and apoptosis in chronic B-cell leukemia lines. 937 41

Prostatic adenocarcinoma may manifest with morphologic features that may be mistaken for benign glandular atrophy. The incidence, morphometric extent, and diagnostic attributes of atrophic prostatic adenocarcinoma have not been defined in radical prostatectomy cases. The size, grade, and stage at which prostatic carcinomas manifest atrophic change and whether these atrophic appearing adenocarcinomatous glands are proliferative, quiescent, or dying (apoptotic) also have not been established. To characterize prostatic adenocarcinoma with atrophic features, we studied 202 consecutive completely embedded radical prostatectomy specimens from previously untreated patients. The histomorphologic attributes of atrophic carcinoma were compiled and compared with benign atrophy and usual prostatic adenocarcinoma without atrophic features. The atrophic carcinoma volume was quantitated by image analysis, the proliferation index was determined by Ki-67 immunolabeling, and the apoptosis index was assessed by TdT [terminal deoxynucleotidyl transferase]-mediated dUTP [deoxyuridine triphosphate]-biotin nick end labeling (TUNEL). Of 202 prostatic adenocarcinoma cases, 32 (15.8%) demonstrated atrophic features. The malignant glands resembled benign atrophic glands by showing profound cytoplasmic volume loss, yet these glands almost always (96.4%) exhibited an infiltrative growth pattern, always lacked basal cells (confirmed by 34betaE12 immunostaining), and exhibited nuclear atypia with nucleomegaly and nucleolomegaly. The atrophic carcinoma foci had a mean volume of 0.3 cc (range, 0.01-2 cc), representing a mean of 16% of total carcinoma volume. The mean proliferation index for atrophic prostatic carcinoma was 4% compared with 1.2% for benign atrophy and 5.3% for usual nonatrophic carcinoma. Apoptosis was identified in only 1 of 32 atrophic prostatic carcinomas. Carcinomas with and without atrophic features did not differ in histologic grade, tumor volume, or pathologic stage. Most atrophic carcinomas were moderately differentiated, of Gleason grade 3. We conclude that the atrophic pattern of prostatic carcinoma is a distinctive morphologic presentation of proliferating, intermediate-grade, prostatic adenocarcinoma that has significant diagnostic rather than prognostic implications.
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PMID:Prostatic adenocarcinoma with atrophic features: a study of 202 consecutive completely embedded radical prostatectomy specimens. 962 26

Lymphocytes recovered from human tumors or peripheral circulation of patients with advanced cancer have abnormalities in signaling via the T cell receptor (TcR) or Fc gamma RIII. Here we show that in comparison with normal T lymphocytes, those isolated from tumor-involved lymph nodes (LNLs) or blood (PBLs) of patients with head and neck carcinoma (HNC) have a variety of defects in expression and function of signaling molecules, including significantly decreased expression of TcR-associated zeta and epsilon chains, decreased Ca2+ flux, as well as impaired kinase activity following triggering with anti-CD3 antibodies and altered expression of downstream protein tyrosine kinase p56lck. Some of these alterations were demonstrable not only in isolated LNLs or PBLs but also in situ in patients' biopsies. Expression of mRNA for the zeta chain in LNLs was comparable with that seen in normal T cells. Significantly, LNLs of patients with HNC were shown to contain numerous apoptotic, TUNEL+ [TdT-mediated dUTP nick-enol labelling] cells in situ. Co-expression of CD3-epsilon+ and TUNEL+ in the same cells in situ was observed. Co-incubation of normal activated T cells or Jurkat cells with HNC cell lines induced apoptosis in a substantial proportion of lymphocytes. HNC cell lines and HNC in situ were shown to express FasL, while LNLs in tumor-involved lymph nodes were Fas+. These data suggest that signaling defects, which are commonly found in lymphocytes of HNC patients, might be a part of the process of apoptosis induced by the tumor in lymphocytes found in its milieu.
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PMID:Mechanisms responsible for signaling and functional defects. 967 51

Tumour growth is directly related to the multiplication of tumour cell numbers which can be caused, firstly, by increased proliferation and, secondly, by prolongation of the life span of tumour cells. The aim was the quantification of the increase and decrease (apoptosis) in cell numbers in relation to the cytological grading of oral squamous epithelial cell carcinoma. Proof of apoptosis-specific fragmentation of DNA (double-strand breaks) by the TUNEL method (TdT-mediated dUTP nick end labelling) and of proliferative activity by the monoclonal antibody MIB 1 was found in 41 oral squamous epithelial carcinomas of different grading. With progression of the cytological grading, an increase of proliferative activity and a decrease of apoptotic activity occurs. The apoptosis rates were 13.5% for G1 carcinomas, 8.5% for G2 carcinomas and 6.1% for G3 carcinomas. The results confirm that during progression to higher malignant cellular phenotypes of oral squamous carcinoma, increased proliferative activity as well as reduced apoptosis rates contribute substantially to the multiplication of tumour cell numbers and show that during progression a loss of control of programmed cell death (apoptosis) occurs. However, the high standard deviations of apoptosis rates within the different grades disprove an individual prognostic significance.
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PMID:[Cell kinetics of oral squamous epithelial carcinomas. Determination of the proliferation index and apoptosis rate with the TUNEL method]. 981 23

Caspase3/CPP32 is a member of the interleukin-1 beta-converting enzyme (ICE) or cell death effector (CED)-3 family, which is involved in the induction of apoptosis and has been considered to be correlated with apoptosis because of the most downstream enzyme in their apoptosis inducing pathway. We immunolocalized Caspase3/CPP32 in both normal and neoplastic human gastric mucosa. We then correlated the findings with cell proliferation studied by Ki67 immunostaining and apoptosis, which was tested for by DNA fragmentation in situ using TdT-mediated dUTP biotin nick end labeling (TUNEL) method in order to examine possible biological significance in cell turnover of normal and pathological human gastric tissues. Caspase3/CPP32 immunoreactivity was detected in both the cytoplasm and nuclei of glandular epithelial cells, predominantly in the Ki67 positive proliferative zone and TUNEL positive foveolar epithelium of normal non-neoplastic gastric mucosa (n = 10) and tumor cells of both adenoma (n = 17) and carcinoma (n = 33). We determined the labeling index (LI) of Ki67, Caspase3/CPP32 and TUNEL positive cells by evaluating the number of positive cells in the same areas of serial tissue sections using computer-assisted image analysis. Ki67 LI in adenocarcinoma (78.6 +/- 12.6%) was significantly [p < 0.0001] higher than that of adenoma (43.8 +/- 8.9%) and non-neoplastic gastric mucosa (24.2 +/- 9.0%). Caspase3/CPP32 LI in adenocarcinoma (17.1 +/- 10.3%) was significantly lower [p < 0.0001] than that of gastric adenoma (33.1 +/- 19.8%) and non-neoplastic gastric mucosa (42.4 +/- 15.8%). TUNEL LI in adenocarcinoma (1.9 +/- 2.1%) was significantly [p < 0.0001] lower than that of non-neoplastic gastric mucosa (6.0 +/- 3.5%), but not significantly different from that of adenoma (3.0 +/- 2.9%). These results indicate that gastric adenocarcinoma is associated with an inhibition of apoptosis and the augmentation of proliferative activity of tumor cells compared to non-neoplastic gastric mucosa. There was a tendency to a positive correlation between the Caspase3/CPP32 and TUNEL LI and an inverse correlation between the Caspase3/CPP32 and Ki67 LI, when evaluating all the specimens, although the correlation did not reach statistical significance. These results also suggest that Caspase3/CPP32 is involved in the development or regulation of apoptotic cell death in cell turnover of normal and neoplastic mucosa of the human stomach.
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PMID:Immunohistochemistry of Caspase3/CPP32 in human stomach and its correlation with cell proliferation and apoptosis. 989 91

Lymphomas in 10 cynomolgus monkeys infected with a simian immunodeficiency virus (SIVsm) were studied with regard to proliferative activity and apoptosis-related gene expression. All were diffuse large-cell lymphomas, showed mono or oligoclonality and a 9/10 diploid cellular DNA content. Expression of a simian homologue to Epstein-Barr virus (HVMF-1) was shown in nine cases. The lymphomas showed moderate to high proliferative activity by Ki67 immunostaining and DNA flow cytometry, and a low number of apoptotic cells detected by TdT-mediated dUTP nick-end labeling (TUNEL). Immunohistochemistry showed abundant tumor infiltrating TIA-1(+) cytotoxic lymphocytes (CTL) and macrophages. Bcl-2, Mcl-1, and also Bax and Bak, but not p53 were demonstrable in the tumor cells by immunostaining. Our findings suggest a causal relationship between HVMF-1 infection and a low apoptotic index of the lymphomas due to the expression of Bcl-2. The apparent inefficient function of tumor-infiltrating CTL could be due to inactivation of CTL and/or resistance of the lymphoma cells to CTL effects. The tumors showed immunoreactivity for CD18, CD29, and CD49d, but not for CD11a, mimicking the phenotype of human Epstein-Barr virus (EBV)-related lymphomas. In summary, our observations indicate a high similarity between this simian model of acquired immunodeficiency syndrome (AIDS)-related lymphomas (ARL) and human ARL and other immunosuppression-related lymphomas.
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PMID:Proliferation and apoptosis-related gene expression in experimental acquired immunodeficiency syndrome-related simian lymphoma. 994 80

Patients with squamous cell carcinoma of the head and neck (SCCHN) frequently have impaired immune responses. Alterations in T-cell receptor-associated signaling molecules in tumor-infiltrating as well as circulating lymphocytes have been reported in these patients. Using quantitative flow cytometry analysis, we have demonstrated that expression of the zeta chain is significantly decreased relative to normal controls in both CD8+ and CD4+ T cells as well as CD3- CD56+ CD16+ natural killer cells in the peripheral blood of patients with SCCHN who, as a result of previous therapies, have no evident disease. Patients with a more aggressive type of SCCHN and those who experienced a recurrence or had a second primary cancer within the last 2 years of the study had the lowest zeta chain expression. In addition, SCCHN patients showed a significantly greater spontaneous ex vivo apoptosis, as measured by a terminal deoxynucleotide transferase-mediated dUTP nick end labeling assay, in PBMCs, compared to normal controls. The observed decreased expression of zeta in T and natural killer cells coincided but did not directly correlate with significantly increased spontaneous apoptosis of lymphocytes obtained from treated patients with no evident disease. The results suggest that in patients with SCCHN, zeta chain defects and lymphocyte apoptosis are manifestations of long-lasting negative effects of tumor on the immune system.
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PMID:Clinical significance of decreased zeta chain expression in peripheral blood lymphocytes of patients with head and neck cancer. 1003 82


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