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

Location of gastrinomas by means of portal venous sampling is a technique in which venous blood from various sites in the portal system around the pancreas and duodenum is obtained and assayed for gastrin levels. A gradient of 50% or greater compared to systemic gastrin levels from a given location regionally identifies the site of gastrin overproduction, thereby locating the tumor. The only area in which venous sampling may help, in the authors' opinion, is in the small subset of patients who have occult gastrinoma not imaged with any other modality, in the body or tail of the pancreas that cannot be found with intraoperative ultrasound or palpation. It is considered that a secretin angiogram is equally effective and is a simpler procedure. Similarly, in insulinoma regional location of the tumor by means of a calcium angiogram has eliminated the usefulness of portal venous sampling. Controversial areas of surgical treatment of APUDomas often reflect a balance between the risks and benefits of aggressive surgery, as data to support an aggressive surgical approach to obtain improved survival often do not exist. For example, if patients with occult MTC can undergo cervical reexploration with minimal or no morbidity the potential benefit of removing malignant disease, warrants this approach. Similarly, if patients with MEN-1 can be explored safely with resection of pancreatic and duodenal tumors, then this position can be defended. On the other hand, if a subgroup of patients with MEN-2 and pheochromocytomas can be spared bilateral adrenalectomy without compromising their long-term outcome in terms of disease-free survival, then this conservative approach is warranted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Controversies in surgical therapy for APUDomas. 790 10

We characterized three clones of different metastatic capacity (MTC, MTLn2 and MTLn3) derived from the 13762NF rat mammary adenocarcinoma for their production and response to TGF-beta. All three clones expressed comparable amounts of TGF-beta 1 mRNA and secreted 100-300 pg/10(6) cells/24 h in a soluble latent form. TGF-beta was found in extracellular matrices produced by all three tumor clones. Addition of exogenous TGF-beta induced different responses. While the low metastatic clone MTC was highly sensitive to the growth inhibitory effect of TGF-beta (ID50 approximately 50 pg/ml), a 6-fold higher dose was necessary for the high metastatic clone MTLn3 (ID50 approximately 300 pg/ml). The clone with intermediate metastatic potential MTLn2 was unresponsive to TGF-beta (1 pg/ml to 3 ng/ml). Our data suggest that tumor cells can modulate their biological properties in an autocrine and/or paracrine fashion by virtue of expression of TGF-beta.
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PMID:Transforming growth factor-beta production and induction of cellular responses in 13762NF rat mammary adenocarcinoma cell clones. 796 May 77

BCL1/PRAD1 is the gene locus involved in the t(11;14)(q13;q32) translocation, which often occurs in a proposed subtype of non-Hodgkin's lymphoma of B-cell phenotype (B-NHL), named mantle cell lymphoma (MCL). When 67 Japanese patients with B-NHL were examined using two separate probes composed of the BCL1 MTC probe and the PRADI cDNA probe, rearrangement of BCL1/PRAD1 or overexpression of PRAD1 was detected in 11 patients. Among 13 patients with MCL, 8 had the abnormalities (61%) and the MTC probe detected the BCL1 rearrangement in 5 (38%). Five of the 6 MCL patients studied (83%) showed PRAD1 overexpression. These frequencies were compatible with those reported for Western patients. Although the remaining three with BCL1/PRAD1 abnormalities were diagnosed as having other histologies, 11 patients had advanced diseases, with dissemination to the extranodal sites. Except for one with diffuse large cell lymphoma, they had a slowly progressive disease, and none of the patients displayed clinical or pathological transformation. The tumor cells usually expressed CD5 and lacked CD10. The cells were completely uniform in the expression of IgM and/or IgD, and in the absence of C mu gene deletion. It thus appears that B-malignancies involving the BCL1/PRAD1 locus constitute a refined disease entity.
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PMID:Clinical aspects of B-cell malignancy involving the BCL1/PRAD1 locus. 808 22

Organ-specific colonization of metastatic tumor cells is regulated through complex interactions of specific adhesion molecules on the tumor cell surface with organ specific microvascular endothelium. The present paper shows the real time tumor cell trafficking under the actual blood flow, which became able to be determined using a new technology, positron emission tomography. This technology would be useful to evaluate the interaction of characteristic tumor cells with various organs in vivo. High and low metastatic rat mammary adenocarcinoma cell variants, MTLn3 and MTC, respectively, were labeled with [2-18F]2-fluoro-2-deoxy-D-glucose in vitro. The labeled cells preferentially accumulated in the lungs, in which the disposition was more intense for MTLn3 than for MTC cells especially for the first 2-10 min after injection, apparently reflecting the organ specific interaction of metastatic tumor cells which may lead to metastasis. Such a short time change of cell disposition is easily determined in a living animal by this new technique. Furthermore, sialidase treatment of MTLn3 cells suppressed the accumulation of these cells in lungs, suggesting that some sialyl glycoconjugates on the MTLn3 cell surface play an important role in cell adhesion to lung endothelium. Positron emission tomography scanning thus enables the noninvasive study of the interaction of characteristic tumor cells with specific endothelium in a living animal.
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PMID:Positron emission tomography analysis of metastatic tumor cell trafficking. 816 82

This brief review of the pathobiology of C-cells has stressed cellular and molecular aspects of MTC development. In the genetic forms of MTC, an alteration in one or more genes on chromosome 10, through an as yet unknown series of events, results in initial hyperproliferation of C-cells. Subsequent genetic steps, possibly at other chromosome loci, presumably result in selected clonal transformation of the hyperproliferative C-cells at risk for tumor development. Some of these same molecular events are probably operative in the development of sporadic MTC as well. Once MTC has developed, it has the potential to undergo tumor progression events which result in loss of C-cell differentiation. Studies in a culture model of these events have revealed that activation of signal transduction pathways, similar to those active in differentiation of other neural crest-derived cells, can restore differentiation features of normal C-cells to MTC. Continued identification of the molecular factors mediating this restoration should teach us much about the relationships between general neural crest differentiation and that of normal C-cells. It will also reveal much about the pathobiology of C-cells contributing to each step of MTC development.
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PMID:Pathobiology of the C-cells. 850 52

In 1986, familial medullary thyroid carcinoma (FMTC) was recognized clinically as a distinct entity, clearly distinguished from multiple endocrine neoplasia (MEN), being characterized by the development of MTC in the absence of any additional neoplasms. Ret proto-oncogene was first identified in 1985 using transformation assay. The gene was mapped to the chromosome 10, similar to MEN and FMTC, and was expressed at high levels in MTC. In 1993, ret mutations were identified in patients with MEN2A and FMTC, and many other mutations has been clarified up to today. What is the normal function of RET and how ret mutations lead to tumor formation in MEN and FMTC are focus of intensive studies at present.
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PMID:[Familial occurrence of thyroid tumors]. 853 29

The nm23 gene [encoding nucleoside diphosphate kinase (NDPK)] may act as a metastasis suppressor in certain tumor cells. We investigated the role of NDPK isoforms (alpha and beta) in the metastatic processes, using rat mammary-adenocarcinoma cell lines of poor (MTC) and high (MTLn3) spontaneous metastatic potential respectively. In these cell lines, as in most rat tissues, the alpha isoform (nm23-H2 homolog) was more highly expressed than the beta isoform (nm23-H1 homolog) at the mRNA and protein levels. When examined by Northern- and Western-blot analyses, expression of the 2 isoforms was reduced in highly metastatic MTLn3 cells compared with poorly metastatic MTC cells. The reduced expression was also associated with diminished NDPK-enzyme activity in the cell extracts. Southern-blot and RT-PCR-SSCP analyses suggested that the 2 genes were not grossly altered or mutated in their translation regions. MTLn3 cell clones transfected with NDPKalpha or NDPKbeta cDNA were all tumorigenic when implanted into the mammary fat pad of syngeneic rats. Among those, only clones transfected with the NDPKalpha gene exhibited reduced lung metastasis in a spontaneous metastasis assay.
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PMID:Decreased expression of nucleoside diphosphate kinase alpha isoform, an nm23-H2 gene homolog, is associated with metastatic potential of rat mammary-adenocarcinoma cells. 862 Dec 39

Lymph node metastases at presentation are common in PTC and MTC (about one third of patients at presentation), but are rare in other types of thyroid malignancy, though HCC frequently recurs in lymph nodes. Nodal metastases can be detected by a variety of means, but high resolution ultrasonography may be the method of choice. Unlike other epithelial malignancies, in thyroid cancer neither prognostic significance nor optimal treatment of nodal metastasis are known with certainty. For PTC lymph node metastases at presentation do not seem to adversely affect survival, but do increase the risk of locoregional tumor recurrence. By contrast, in FTC nodal metastases at presentation may adversely affect cause-specific mortality, but because of their rarity definite conclusions are impossible. Except for the oxyphilic variant of FTC (HCC) nodal recurrence in FTC is rare. The most firm evidence of prognostic relevance for nodal metastases in thyroid malignancies exists in medullary thyroid cancer, where most studies suggest that survival and recurrence are both adversely affected by node-positive status at presentation. Primary treatment of nodal metastases is removal of macroscopically affected nodes at initial surgery, optionally supplemented with adjuvant radioiodine treatment in an attempt to reduce recurrence risk. The value, however, of postoperative radioiodine in preventing either nodal recurrence or cancer death in patients with papillary and follicular thyroid cancer remains controversial. Extensive lymph node dissection at presentation offers no advantage (and may cause increased morbidity) in papillary carcinoma, but may be useful in medullary thyroid carcinoma, where nodal metastases seem to increase the risk of cause-specific mortality. In all tumor types postoperative nodal recurrences should primarily be treated surgically.
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PMID:Thyroid cancer nodal metastases: biologic significance and therapeutic considerations. 878 93

In medullary carcinoma of the thyroid (MTC), drug resistance remains the major obstacle to effective chemotherapy. In this work, we studied the effect of S9788 on doxorubicin (DOX) efficiency in a MTC cell line (TT cells) injected in nude mice. After two passages, TT cells were injected in 40 nude mice divided into four groups [controls and groups receiving DOX alone (10 mg/kg), S9788 alone (50 mg/kg) or both DOX + S9788]. The weight of the mice, tumoral volume (TV), doubling time (DT) of the tumor and survival time of mice were evaluated in each group. In addition, the efficiency of DOX with or without S9788 was assessed by the inhibition of tumoral growth and specific growth delay. In vitro, glycoprotein P 170 (P-gp) was detected on tissular sections and on tumoral cells by immunocytochemistry or flow cytometry with several monoclonal antibodies: JSB1, MRK 16, C219 and UIC2. In vivo the weight of the mice decreased slightly with DOX and dropped dramatically with DOX + S9788. The DT of the tumors increased with DOX over controls (22.5 +/- 8.5/12.7 +/- 3.9 days) and showed a higher value with DOX + S9788 (29.2 +/- 11.4 days). Inhibition of tumoral growth, 89% with DOX, fell to 47.6% with DOX + S9788. Specific growth delay increased with the double treatment (130 versus 75% with DOX alone). In vitro, P-gp was not detected on tissular sections and cells whatever the method and the antibody used. In conclusion, S9788 potentiates the efficiency of DOX treatment in vivo. The absence of P-gp may result from the absence of translation of the MDR1 gene. The reversal effect of S9788 may involve another resistance mechanism such as the MDR Sister of MRP.
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PMID:Effect of S9788 on the efficiency of doxorubicin in vivo and in vitro in medullary thyroid carcinoma xenograft. 879 7

Medullary thyroid carcinoma in both sporadic and familial forms is a curable disease if detected early and treated by the proper surgery. The advent of genetic screening for the RET protooncogene portends great promise in the earlier diagnosis and treatment of familial forms of MTC. New chemotherapy protocols have produced some tumor regression in patients with metastatic MTC. Improved use of Adriamycin and hyper-fractionated radiotherapy combined with debulking procedures has prolonged survival in anaplastic thyroid cancer. Thyroid gland lymphoma, if diagnosed early and treated by combined chemoradiotherapy, carries a good prognosis for survival. The best treatment for thyroid sarcomas and SCC of the thyroid is early diagnosis and aggressive surgery combined with radiotherapy.
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PMID:Thyroid cancers. II. Medullary, anaplastic, lymphoma, sarcoma, squamous cell. 884 33


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