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Results for “tumor evolution”

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At least 595 records · Page 33Linked to original sources
PubMed2005

[Molecular genetic methods for the prognostic criteria in multiple myeloma].

Routine cytogenetic and molecular genetic analysis of plasma cell malignancies, such as multiple myeloma, became widespread only recently. As the result of these investigations, it became clear that tumor cell karyotype is fundamental from the viewpoint of therapy selection and prognosis. It is worthwhile to distinguish hyperdiploid and nonhyperdiploid myeloma, while five separate prognostic groups (TCI-5) may be identified on the basis of immunoglobulin gene translocations and cyclin expression. Deletion of the q arm of chromosome 13 or amplification of region 1q21 (and the CKS1B gene) can identify further subgroups of poor prognosis and few therapeutic options. Meanwhile, tumors harboring translocation t(11;14) respond favorably to conventional chemotherapy and exhibit exceptionally good and long-lasting response to high-dose chemotherapy. Progression of the disease may coincide with complex translocations of the c-myc gene or deletions involving the p53 tumor-suppressor gene, spreading of ras-mutations. These events represent clonal evolution at great tumor cell mass and advanced disease, therefore, are only of secondary prognostic significance.

CDC2-CDC28 Kinases↗
PubMedDate not supplied

[Prognostic factors in superficial bladder carcinoma. Analysis of 250 cases].

Surface vesical tumors constitute 80% of transitional cell tumors. They are neoplasms of slow evolution, but characterized by their tendency to recur and progress in time. The prognostic factors, as regards recurrence and progression, are going to depend on a series of macroscopic or microscopic anatomic characteristics. We present our observations on some prognostic aspects in surface vesical carcinoma obtained from a study of 250 patients. By way of conclusion, from our observations we may infer that neither age, nor sex nor location, save in the case of patients under the age of 40, have prognostic value in the evolution of the primary tumor, which will be noticeably better (lower percentage of relapses and longer illness-free period) in patients with a single tumor of low grade and state, and in general in patients receiving intravesical prophylactic chemotherapy treatment, and no difference is found between thio-tepa and adriamycin.

Adult↗
PubMed1986

[Endoscopic diagnosis of duodenal and jejunal diseases].

We presented and studied the endoscopic diagnosis of the duodenal ulcer, duodenal tumors and duodenal bleeding. Duodenal Ulcer is classified according as location, form and evolutive stage. Duodenal tumors are divided in polyps, primitive tumors, pancreas anomaly and lymphoma. Duodenal bleeding can be diagnosed according its cause (inflammatory, tumors vascular and traumatic). It is emphasized the importance of the indications and methods of the enteroscopy. We show our experience in 313 duodenal ulcers cases and 98 enteroscopic diagnosis.

Duodenal Diseases↗
PubMed1997

The effect of time delays on the dynamics of avascular tumor growth.

During avascular tumor growth, the balance between cell proliferation and cell loss determines whether the colony expands or regresses. Mathematical models describing avascular tumor growth distinguish between necrosis and apoptosis as distinct cell loss mechanisms: necrosis occurs when the nutrient level is insufficient to sustain the cell population, whereas apoptosis can occur in a nutrient-rich environment and usually occurs when the cell exceeds its natural lifespan. Experiments suggest that changes in the proliferation rate can trigger changes in apoptotic cell loss and that these changes do not occur instantaneously: they are mediated by growth factors expressed by the tumor cells. In this paper, we consider two ways of modifying the standard model of avascular tumor growth by incorporating into the net proliferation rate a time-delayed factor. In the first case, the delay represents the time taken for cells to undergo mitosis. In the second case, the delay represents the time for changes in the proliferation to stimulate compensatory changes in apoptotic cell loss. Numerical and asymptotic techniques are used to show how a tumor's growth dynamics are affected by including such delay terms. In the first case, the size of the delay does not affect the limiting behavior of the tumor: it simply modifies the details of its evolution. In the second case, the delay can alter the tumor's evolution dramatically. In certain cases, if the delay exceeds a critical value, defined in terms of the system parameters, then the underlying radially symmetric steady state is unstable with respect to time-dependent perturbations. (For smaller delays, this steady state is stable). Using the delay as a measure of the speed with which a tumor adapts to changes in its structure, we infer that, for the second case, a highly responsive tumor (small delay) has a better chance of surviving than does a less-responsive tumor (large delay). We also conclude that the tumor's evolution depends crucially on the manner and speed with which it adapts to changes in its surroundings and composition.

Apoptosis↗
PubMed1999

Influence of laminin substratum on cell proliferation and CALC I gene expression in medullary thyroid carcinoma C cell lines.

Medullary thyroid carcinoma (MTC) originates from C cells, which secrete calcitonin (CT) and CT gene-related peptide (CGRP), the two splice peptide products of the CALC I gene. Normal and hyperplastic C cells are intrafollicular, in contact with the basement membrane (BM) that is maintained around the differentiated tumors. To investigate the relationships between MTC evolution and BM constituents, we examined the modifications induced by laminin-1 and -2 (merosin), two isoforms colocalized in the follicular BM, on three MTC cell lines: murine rMTC 6-23 and CA-77 cells, and human TT cells. Laminin exerted a mitogenic activity on rMTC 6-23 and on TT cells, causing a concurrent decrease in both CT and CGRP mRNA levels and production of the peptides. Conversely, laminin reduced the proliferation rate and enhanced CGRP synthesis and secretion in CA-77 cells. This antiproliferative response, which coincides with an increase in differentiation markers, is comparable to that reported in normal cells and also in the neoplastic Caco-2 cell line. This suggests that laminin could exert opposite effects depending on the stage of tumor evolution.

Animals↗
PubMed1994

Two subclones in a case of uveal melanoma. Relevance of monosomy 3 and multiplication of chromosome 8q.

Monosomy 3 and multiplication of 8q are nonrandom findings in uveal melanoma. We present a case in which two subclones could be detected. Both had monosomy 3 in common. Furthermore, a multiplication of chromosome 8 material was also seen in both subclones. However, it was based on different kinds of aberrations and was accompanied by further anomalies, such as loss of a Y-chromosome, an additional chromosome 7, and an additional marker chromosome, in only one clone. This finding allows some insight into the relevance of the most frequently found anomalies of chromosome 3 and 8 in uveal melanoma. As monosomy 3 occurred before any subclone differentiation, it must be an early, if not primary, event in the genesis of this tumor. Multiplication of chromosome 8, specifically of 8q, however, may contribute to the clonal evolution of this tumor.

Aged↗
PubMed2006

The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1beta.

Although induction of blood vessel growth is acknowledged as a pivotal requirement for the evolution of macroscopic tumors, the events that trigger onset of tumor angiogenesis remain largely obscure. The pervasive Myc oncoprotein is itself a potent inducer of angiogenesis in a wide range of tissues. We have used a reversibly switchable mouse transgenic model of Myc-dependent beta-cell carcinogenesis to delineate the kinetics and causal sequence of angiogenic processes following acute Myc activation. We show that onset of endothelial cell proliferation is induced shortly after Myc-induced cell cycle entry of beta cells. Endothelial cell proliferation is not indirectly induced by local tissue hypoxia but instead via a diffusible angiogenic signal produced by Myc-expressing beta cells. This signal triggers the release of pre-existing, sequestered VEGF from the islet extracellular matrix, that then homes to the endothelial compartment where it induces endothelial cell proliferation. Myc activation in beta cells rapidly induces expression and release of the proinflammatory cytokine interleukin 1beta (IL-1beta). We show that IL-1beta is the principal effector downstream of Myc responsible for triggering rapid onset of islet angiogenesis. Together, our data delineate a complete pathway in vivo by which the highly pleiotropic Myc oncoproteins elicits coexpansion of the vascular compartment during tumorigenic progression.

Animals↗
PubMed1994

NM23 protein in neoplastic and nonneoplastic thyroid tissues.

The expression of nm23 gene products has been associated with a lower metastatic potential and better outcome in malignant tumors. We have used immunohistochemistry to study the expression of nm23 protein in thyroid tissues from 101 patients consisting of 78 malignant neoplasms, 13 adenomas, and 10 other benign conditions. Cytoplasmic staining for nm23 protein was identified in normal tissues and in most benign and malignant lesions and did not correlate with either histological type of clinical outcome. Nuclear staining was seen in 93% of normal tissues and in 29% of primary carcinomas of the thyroid and was associated with a longer disease-free survival (P = 0.03). Membranous staining was present in some tumors but absent in normal thyroid. In conclusion, nm23 protein has a combined pattern of distribution among subcellular compartments in thyroid tissues. Although there was no significant association between cytoplasmic or membranous expression and histological type of tumor or survival nm23 nuclear expression may be a useful marker in assessing the evolution of thyroid tumors.

Adolescent↗
PubMed1995

Abnormalities in the PRAD1 (CYCLIN D1/BCL-1) oncogene are frequent in cervical and vulvar squamous cell carcinoma cell lines.

BACKGROUND: CYCLIN D1, a cell-cycle control gene, recently has been shown to be identical to an oncogene alternatively known as BCL-1 and PRAD1 and implicated in centrocytic lymphomas and parathyroid adenomas, respectively. PRAD1 complexes to the product of the retinoblastoma (Rb) tumor suppressor gene, an event followed by Rb inactivation. Squamous cell carcinomas of the cervix and vulva are gynecologic tumors in which human papillomaviruses have been implicated as an initiating event, and proteins derived from these viruses also complex with an inactivate Rb. Because of the overlap in some of the molecular processes mediated by human papillomaviruses and by the PRAD1 oncogene, the authors analyzed the PRAD1 (CYCLIN D1/BCL-1) genomic structure and expression in vulvar and cervical squamous cell carcinoma cell lines. METHODS: PRAD1 DNA and PRAD1 mRNA expression were assessed by Southern and Northern blotting, respectively, in 13 squamous cell carcinoma cell lines of gynecologic origin (10, cervical cancer; 3, vulvar cancer). RESULTS: We found low baseline levels of a 4.5-kb PRAD1 transcript in a series of control cell lines, which were derived from normal fibroblasts, various hematologic malignancies, and a choriocarcinoma. PRAD1 mRNA overexpression (> or = 10-fold greater than that in control lines) was seen in all three vulvar carcinoma cell lines, two of which also showed amplification (5-fold and > 10-fold) of PRAD1 genomic sequences. Abnormalities of PRAD1 also were seen in 4 of the 10 cervical cancer cell lines and included overexpression of PRAD1 transcripts (3-9-fold) in 3 lines and rearrangement of PRAD1 DNA in an additional line that, however, did not shown any aberration in PRAD1 mRNA as discernible by Northern blotting. PRAD1 abnormalities were observed in three of the four cervical cell lines derived from metastatic sites and in one of the six cervical lines derived from primary tissue. CONCLUSIONS: Seven of 13 squamous cell lines of gynecologic origin showed abnormalities of PRAD1. These abnormalities included amplification and rearrangement of DNA and overexpression of mRNA. The role of PRAD1 as a cell-cycle regulatory gene and its interactions with the Rb tumor suppressor gene suggests that PRAD1 deregulation may be a significant molecular event in the evolution of these tumors.

Blotting, Northern↗