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

Early lesions in the colonic mucosa of humans and rodents are characterized by similar proliferative changes within their epithelial cell population. Progressive phases of abnormal cell development appear during the evolution of neoplastic transformation in colonic cells of rodents exposed to chemical carcinogens and in humans highly susceptible to gastrointestinal cancer. Identification and classification by phenotype of cells of these individuals at increased risk for colon cancer are leading to new methods to improve the detection and diagnosis of neoplasia in high risk individuals and families. An analytical system of precise numerical definitions is aiding an approach to modify the evolution of advanced stages of neoplasia.
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PMID:Early proliferative changes in intestinal cells. 127 72

Proliferative activity of the structural components of normal salivary glands (27 cases) and characteristic histological areas in salivary pleomorphic adenoma (51 cases) was examined by visualization of argyrophilic nucleolar organizer regions (AgNORs). In the normal salivary gland, there were clusters of cells, each with two or three AgNOR dots, within the intercalated ducts. The mean number of AgNORs in this portion was 1.80, which was significantly higher than in the other epithelial parts. This indicates vigorous proliferative activity of the intercalated ducts, and thus the ducts may play an important role as reserve cells in neoplastic transformation. In pleomorphic adenoma, solid nests had a high AgNOR count (1.61), showing a significant difference from the tumor cells scattered in the "stroma". Thus the decrease in proliferative ability might occur concurrently with formation of the extracellular matrix.
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PMID:Proliferative activity in normal salivary gland and pleomorphic adenoma. A study by argyrophilic nucleolar organizer region (AgNOR) staining. 128 Mar 96

Hepatocarcinoma (HCC), the most frequent malignant hepatic neoplasia, is sometimes difficult to diagnose at an early stage since the symptoms may be attributed to concomitant hepatic cirrhosis. The assay of alpha-fetoprotein associated with an ultrasound examination of the hepatic parenchyma is an important screening tool for high-risk patients. Ultrasound examination is considered the most sensitive method and alpha-fetoprotein is a supplementary diagnostic tool. Elevated alpha-fetoprotein only occasionally precedes morphological anomalies and even in these cases the neoplastic aspect emerges within a short period of time. The case reported here illustrates the "astronomic" increase of alpha-fetoprotein in a high-risk patient for HCC (positive HBsAg cirrhosis) without the manifest appearance of any instrumental or histological data confirming the presence of the tumour for two years. When the tumour was identified in instrumental tests it had spread throughout the entire hepatic parenchyma in a form which could no longer be treated using any form of therapy. The case reported here emphasizes the diagnostic value of alphafetoprotein in high-risk patients for HCC, even in the prolonged absence of all other data regarding neoplastic transformation.
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PMID:[A case of hepatocarcinoma preceded by several years by "isolated" increase in alphafetoprotein]. 128 76

Several studies have linked abnormal actin cytoskeletal organization and mutant actin genes with neoplastic transformation. Using in situ hybridization techniques we looked at expression of beta actin mRNA at a cellular level in normal, benign and neoplastic human colorectal tissues and correlated the level of expression with the extent of actin cytoskeletal organization in sequential sections. Normal tissues showed light labelling with the actin riboprobe, but non-neoplastic crypts, with evidence of regeneration and repair, showed greater levels. Higher levels of actin mRNA expression were found in adenomas and metaplastic polyps, but the highest levels were found in carcinomas, particularly those that were poorly differentiated. Cytoskeletal actin organization was, however, reduced in colorectal neoplasia. Normal mucosa showed the highest level of cytoskeletal actin organization, as assessed by phalloidin binding, and adenomas and metaplastic polyps also stained strongly. In contrast, phalloidin binding to poorly differentiated carcinomas was absent or very weak. The inverse relationship between actin mRNA expression and actin filament organization was confined to the carcinomas studied and may indicate defects in actin binding proteins or in post-transcriptional or translational events.
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PMID:Beta actin expression and organization of actin filaments in colorectal neoplasia. 130 45

We report a new and apparently unique human lymphoma cell line termed Deglis. The line was established from a polymorphic centroblastic lymphoma. The cell line and its source carry a dual B-cell and T-cell phenotype and Epstein-Barr virus (EBV) genomes. Simultaneous expression of B-cell (CD19+, CD20+, CD23+, CD37+) and T-cell (CD2+, CD3+/-, CD7+, CD43+) antigens, activation antigens (CD30+, CDw70+) as well as CD68+, a macrophage-associated antigen, was observed on the cell line and its source. Genotypic studies of the cell line showed dual gene rearrangements. JH (on both primary tumor and the cell line) and C kappa were rearranged without expression of cytoplasmic or surface immunoglobulins. T-cell receptor-alpha (TCR-alpha) and TCR-beta genes were rearranged, but TCR-delta and TCR-gamma genes were in germline configuration. Apparently, functional transcripts of TCR-alpha and truncated transcripts for TCR-beta and TCR-delta were observed. EBV-encoded proteins (LMP and EBNA2) were expressed by the parent tumor and the cell line. Southern blot analysis showed the same clonal EBV genomes in the primary tumor and the cell line. Karyotypic analysis of the cell line showed several chromosomal abnormalities but normal chromosomal number. The characteristics of this cell line suggest that neoplastic transformation has occurred in a precursor cell broadly committed to lymphoid lineage. Further studies on this cell line may help resolve some issues in the physiopathology of lymphoid tumors.
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PMID:A novel human lymphoma cell line (Deglis) with dual B/T phenotype and gene rearrangements and containing Epstein-Barr virus genomes. 131 35

Histamine-secreting enterochromaffin-like (ECL) cells of the gastric fundus of the Mastomys can develop into solid ECL cell tumors, either spontaneously or after induction by acid inhibition. We used this tumor tissue to perform in vitro receptor autoradiography for somatostatin (SS), gastrin, and substance-P, using, respectively, [125I]Tyr3-octreotide, [125I]gastrin-17, and [125I]Bolton-Hunter-labeled substance-P as radioligands. A high density of SS receptors was found in the nontumor fundic mucosa, where gastrin receptors were only barely detectable. However, in the group of spontaneously developing ECL cell tumors, a high density of SS and gastrin receptors was observed, homogeneously distributed in the tumor tissue. In addition, the loxtidine-induced ECL cell tumors expressed a high density of SS and gastrin receptors. The receptors were specific for the respective peptide and of high affinity, with a dissociation constant (Kd) of 0.90 nM for SS receptor and 0.87 nM for gastrin receptors. No substance-P receptors were detected on the ECL cell tumors, although they were present in the muscle layers of the Mastomys gastric fundus. These results demonstrate that ECL-derived tumors express receptors for both SS and gastrin. This observation is consistent with the proposal that there is substantial regulation of the histamine-producing ECL cell by SS and gastrin. The presence of gastrin receptors is compatible with a role for gastrin as a trophic factor in ECL cell hyperplasia and neoplasia. The expression of SS receptors may be of diagnostic and therapeutic relevance in the regulation of ECL function and neoplastic transformation.
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PMID:Identification of somatostatin and gastrin receptors on enterochromaffin-like cells from Mastomys gastric tumors. 131 17

We have characterized mammary oncogenesis induced after polyomavirus infection of adult female nude mice regarding histopathogenesis, viral replication and viral and cellular oncogene expression. A unique transient generalized epithelial hyperplasia was observed (starting at 2 weeks post infection), preceding the development of dysplasias (onset 6 weeks post infection) and multiple neoplasias (onset 6 weeks post infection) in all glands. The ductal epithelium was the target for neoplastic transformation, and the occurrence of numerous ductal dysplasias coincided with the appearance of frank tumors. Stromal abnormalities were also seen. Tumor growth was not dependent upon ovarian hormones, and new tumors continued to develop in ovariectomized mice. Viral replication, high although variable, preceded but did not correlate with oncogenesis. Most but not all tumors contained high levels of unintegrated viral DNA. Tumors produced very low levels of live virus. Viral gene expression was markedly increased in the tumors compared with the infected but morphologically normal glands. The expression of c-myc was moderately increased (fourfold); changes in c-int-2 and c-Ha-ras expression were slight and inconsistent, while expression of c-neu and c-int-1 was unchanged.
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PMID:Characterization of the mammary hyperplasia, dysplasia and neoplasia induced in athymic female adult mice by polyomavirus. 132 Feb 44

Rapid progress in understanding the biology of colorectal carcinoma has occurred in the last decade. During this time, the importance of tumor suppressor genes has been delineated. Mutations in proto-oncogenes, and some of the genetic and epigenetic defects that occur during neoplastic transformation, have been characterized. The very recent identification of a technology that detects some mutations in genes by analyzing fecal specimens offers the real prospect of effective, low-cost screening of large segments of the population at risk for the development of large bowel cancer. A better understanding of the mechanisms involved in metastasis is slowly leading to better methods of prognostication for patients with carcinoma of the colon or rectum. This is important because a better biologic identification of patients at high risk for subsequent metastasis will help determine which patients should receive adjuvant therapy. Further, the development of new approaches to inhibit various aspects of the cascade of events necessary to produce metastasis, notably the inhibition of neovascularization, suggests the real possibility that established metastases may be treated by relatively nontoxic medical therapies. As a result, further knowledge of the biology of colorectal cancer will translate into strategies that will continue to improve the control of this prevalent carcinoma.
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PMID:The biology of colorectal carcinoma. 133 32

The significance of the enterochromaffin-like (ECL) cell as a critical endocrine regulator of gastric fundic mucosal function has only recently been recognized. Although the percentage of these cells present in the human fundic mucosa is less than that in rodents, the observation that they secrete histamine and are probably important modulators of parietal cell function has resulted in their attaining some considerable biological significance. The further identification of gastrin and somatostatin receptors on the surface of the ECL cells has suggested that other neurohormonal influences may be significant in the regulation of parietal cell function, utilizing the ECL cell as an intermediate modifier. While abnormalities of ECL cells in the human stomach (hyperplasia/neoplasia) have been mostly confined to observations in patients with pernicious anemia and atrophic gastritis, the recent recognition of hyperplasia in pharmacotherapeutically induced achlorhydric or hypochlorhydric states has excited considerable interest. It has been proposed that the generation of luminal hypo- or achlorhydria by powerful acid inhibitory pharmacotherapy may result in hypergastrinemia. This condition is responsible initially for the development of hyperplasia and, subsequently, possibly even neoplasia of the ECL system of the fundic mucosa. This phenomenon seems to be prevalent in rodents but has so far been only rarely observed in humans, e.g., pernicious anemia, atrophic gastritis. In particular, patients with the gastrinoma component of the multiple endocrine neoplasia type I syndrome exhibit ECL-cell hyperplasia and neoplasia after exposure to acid inhibitory pharmacotherapy. It is therefore likely that an underlying genomic phenomenon is necessary prior to the induction of hyperplasia and subsequent neoplastic transformation. The scientific evaluation of the relationship between gastrin, ECL-cell function, and the development of hyperplasia and neoplasia may provide some important information in regard to the molecular evolution of gastrointestinal neuroendocrine disease states. It is possible that the future pharmacotherapy of acid secretory disease may require regulation not only of parietal cell but of ECL-cell function.
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PMID:The pathobiology of the human enterochromaffin-like cell. 134 Oct 78

This review describes the studies that address the role of the MDR1 (P-glycoprotein) gene in multidrug resistance in cell lines selected in vitro and in clinical cancer. Molecular genetic studies have demonstrated that expression of P-glycoprotein, an efflux pump acting at diverse lipophilic compounds, is sufficient to provide resistance to a large number of lipophilic drugs in tissue culture. The MDR1 gene is expressed in several normal human tissues associated with secretory or barrier functions and in some bone marrow and blood cells, including hematopoietic progenitor cells. MDR1 expression in clinical cancer is often found in untreated tumors of different types. Several studies showed a correlation between MDR1 expression and tumor resistance to combination chemotherapy. MDR1 expression in untreated tumors may reflect their origin from MDR1-positive normal cells or cellular changes associated with neoplastic transformation or progression. MDR1 expression in some types of cancer may be a marker of a more aggressive subpopulation of tumor cells, possessing multiple mechanisms for resistance to treatment.
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PMID:The role of the MDR1 (P-glycoprotein) gene in multidrug resistance in vitro and in vivo. 134 97


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