Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid tumorigenesis proceeds through the progressive accumulation of alterations in genes involved in the regulation of cell proliferation and differentiation accompanying the acquisition of phenotypic, biological and clinical characteristics of increasing malignancy and dedifferentiation. The molecular alterations specific to thyrocyte carcinogenesis are examined. Ras mutations seem to represent an early occurrence in thyroid tumorigenesis being common to both benign and malignant follicular tumors; they would represent the early mutational events able to enhance the cell proliferation. Subsequent alterations in several genes will probably result in the determination of a follicular or papillary phenotype. In particular, mutational events activating ret, met and trk thyrokinase receptors direct the tumor growth and development towards the papillary type. Progression towards a follicular phenotype would instead occur in two stages: first there is the loss of function of genes on chromosome 11q13 which may direct the tumor cell towards the phenotype of follicular adenoma, second, there is the inactivation of the probable suppressor oncogene on chromosome 3p which might be fundamental in the transition from adenoma to follicular carcinoma. Undifferentiated or anaplastic tumors are characterized by the presence of p53 gene mutations.
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PMID:Molecular biology of thyroid neoplasms. 1137 May 34

Galectin-3 belongs to a group of endogenous lectins with an affinity to glycoconjugates containing beta-galactoside residues. It has been detected in numerous tissues and studied in connection with tumor growth, dedifferentiation, and metastasis. Only few studies have dealt with galectin-3 detection in tumors of the thyroid gland and with its possible role for differential diagnosis. We studied 118 cases of thyroid gland tumors with a monoclonal antibody against galectin-3; we compared the preparations by a semiquantitative score to determine differences in expression. Normal thyroid gland tissue, goiter tissue, and tissue with functional enhancement were largely negative for galectin-3. Adenomas with a typical cytological pattern were predominantly negative, but a focal positive reaction in single cells and cell groups or follicles was possible. Almost all papillary carcinomas showed a distinct galectin-3 expression. While findings in follicular carcinomas and oxyphilic adenomas and carcinomas were very uneven, with both positive and negative tumors, the galectin-3 reaction can be helpful in recognizing follicular variants of the papillary carcinoma. Investigation of the biological significance of tumors should always be cautious and consider known histological criteria for malignancy.
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PMID:[Expression of galectin-3 in thyroid gland and follicular cell tumors of the thyroid. A critical study of its possible role in preoperative differential diagnosis]. 1140 51

A 45-year-old man underwent surgery for a silent corticotroph-cell pituitary adenoma which developed in 9 months. The tumor was termed silent because it exhibited increased corticotropic secretion without clinical signs of hypercorticism. This classes it as a non-functional adenoma. The non-functional group includes different types of adenomas such as gonadotroph and other silent thyreotroph and somatotroph adenomas with variable proliferative potential. Silent corticotroph-cell adenoma is considered as an aggressive tumor. In contrast, gonadotroph adenomas usually grow slowly and postoperative tumor remnants can remain stable for years. Because of this variability in tumor growth, the therapeutic decision is difficult if there is a postoperative remnant. No precise guidelines can be established. We suggest that non-functional pituitary adenomas should be considered separately, according to the histological type. This classification is essential for improving knowledge and specifying indications for radiotherapy.
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PMID:[Should silent corticotroph-cell adenoma be classified as a non-functional pituitary adenoma?]. 1140 83

We aimed to assess the relationship of the angiogenic cytokines VEGF-A, VEGF-C, and VEGF-D and their receptors VEGFR-2 and VEGFR-3 in the adenoma-carcinoma sequence and in metastatic spread of colorectal cancer (CRC). mRNA expression levels were measured using semi-quantitative reverse transcription polymerase chain reaction in 70 CRC (35 with paired mucosae) and 20 adenomatous polyps. Immunohistochemistry and ELISA assessed protein expression. VEGF-D mRNA expression was significantly lower in both polyps and CRCs compared with normal mucosa (P=.0002 and.002, respectively), whereas VEGF-A and VEGF-C were significantly raised in CRCs (P=.006 and.004, respectively), but not polyps (P=.22 and P=.5, respectively). Receptor expression was similar in tumor tissue and normal mucosae. Tumors with lymph node metastases had significantly higher levels of VEGF-A compared with non-metastatic tumors (P=.043). There was no association between VEGF-C or VEGF-D and lymphatic spread. The decrease in VEGF-D occurring in polyps and carcinomas may allow the higher levels of VEGF-A and VEGF-C to bind more readily to the VEGF receptors, and produce the angiogenic switch required for tumor growth. Increased expression of VEGF-A within CRCs was associated with lymphatic metastases, and therefore, this member of the VEGF family may be the most important in determining metastatic spread.
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PMID:VEGF-A, VEGF-C, and VEGF-D in colorectal cancer progression. 1168 53

Selective COX-2 inhibitors reduce adenoma formation and cancer progression in rodent models of colorectal cancer. To assess the therapeutic activity of selective COX-2 inhibitors, we tested the effect of SC-58125 treatment on the growth of human colon carcinoma cells in nude mice. Delaying treatment by 2, 4, or 7 weeks following implantation of the carcinoma cells resulted in a significant inhibition of tumor growth. Furthermore, short-term (48 hours) treatment with SC-58125 was sufficient to attenuate tumor growth for up to 15 days. SC-58125 treatment did not alter the rate at which cells underwent apoptosis, but did result in a delayed progression through the cell cycle at the G(2)/M transition. Accordingly, p34(cdc2) protein levels and activity were decreased following SC-58125 treatment. We conclude that SC-58125 primarily exerts a cytostatic effect in vivo, which is likely to be mediated through inhibition of progression through the G(2)/M phase of the cell cycle.
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PMID:A cyclooxygenase-2 inhibitor (SC-58125) blocks growth of established human colon cancer xenografts. 1168 54

A hybrid cellular automaton model is described and used to simulate early tumor growth and examine the roles of host tissue vascular density and tumor metabolism in the ability of a small number of monoclonal transformed cells to develop into an invasive tumor. The model incorporates normal cells, tumor cells, necrotic or empty space, and a random network of native microvessels as components of a cellular automaton state vector. Diffusion of glucose and H(+)ions (the latter largely resulting from the tumor's excessive reliance on anaerobic metabolism) to and from the microvessels, and their utilization or production by cells, is modeled through the solution of differential equations. In this way, the cells and microvessels affect the extracellular concentrations of glucose and H(+)which, in turn, affect the evolution of the automaton. Simulations of the model demonstrate that: (i) high tumor H(+)ion production is favorable for tumor growth and invasion; however for every H(+)ion production rate, there exists a range of optimal microvessel densities (leading to a local pH favorable to tumor but not to normal cells) for which growth and invasion is most effective, (ii) at vascular densities below this range, both tumor and normal cells die due to excessively low pH, (iii) for vascular densities above the optimal range the microvessel network is highly efficient at removing acid and therefore the tumor cells lose their advantage over normal cells gained by high local H(+)concentration. While significant spatial gradients of glucose formed, no regions of detrimentally poor glucose perfusion (for either cell type) were observed, regardless of microvessel density. Depending on metabolic phenotype, a variety of tumor morphologies similar to those clinically observed were realized in the simulations. Lastly, a sharp transition (analogous to that of the adenoma-carcinoma sequence) between states of initial tumor confinement and efficient invasiveness was observed when H(+)production reached a critical value.
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PMID:A cellular automaton model of early tumor growth and invasion. 1173 84

The pivotal role of vascular endothelial growth factor (VEGF-A) in the regulation of angiogenesis, in particular in the onset and maintenance of tumor angiogenesis, has been demonstrated repeatedly in experimental model systems and, more recently, in clinical trials. Experimental evidence has also suggested that up-regulated expression of VEGF-A may cooperate with other genetic or epigenetic changes to induce or accelerate tumor progression to invasive and metastatic cancers. Here we report the generation of transgenic mouse lines that express human VEGF-A165 under the control of the rat insulin promoter in the beta cells of pancreatic islets of Langerhans (Rip1VEGF-A). These mice do not exhibit detectable changes in islet development, vascularization, or physiology. Intercrosses of these mice with a transgenic mouse model of pancreatic beta cell carcinogenesis (Rip1Tag2) result in an earlier onset of tumor angiogenesis and with it accelerated tumor growth and mortality. The transition from benign tumors (adenoma) to malignant tumors (carcinoma) is modestly accelerated; however, tumor metastases are not observed. Our findings indicate that in beta-cell tumorigenesis, overexpression of VEGF-A165 accelerates the onset of tumor angiogenesis and with it tumor progression but is not sufficient to induce tumor metastasis.
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PMID:Overexpression of vascular endothelial growth factor-A165 enhances tumor angiogenesis but not metastasis during beta-cell carcinogenesis. 1180 16

We describe a rare case of macroprolactinoma with subclinically synchronous growth hormone (GH) production. A 59-year-old man with a giant adenoma in his pituitary had elevated serum prolactin (PRL) and insulin-like growth factor (IGF)-I levels, despite normal levels of basal GH. Serum GH levels were paradoxically increased in response to an intravenous administration of thyrotropin-releasing hormone (TRH). Prolonged exposure to glucose as a result of oral glucose tolerance testing (oGTT) failed to decrease GH levels. Two-week treatment with cabergoline, a dopamine D2 receptor agonist, decreased serum PRL and GH levels, and size of the tumor. Immunohistochemistry and in situ hybridization revealed PRL-producing cells capable of synchronous GH production. Acidophilic stem cell adenoma may be responsible for these phenomena. The nature of high proliferation and invasive tumor growth should be kept in mind when managing patients with this cell type of adenoma. IGF-I levels should be followed in PRLoma, even when basal GH levels are within the normal range, because mixed PRL- and GH-producing tumors would lie underneath. Further endocrinological examinations such as TRH test and oGTT are recommended when elevated IGF-I levels are detected.
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PMID:A case of macroprolactinoma with subclinical growth hormone production. 1200 49

The development of transsphenoidal microsurgery and the refinement of endocrinological and radiological diagnostic procedures have afforded therapeutic options appropriate for each individual case in patients with pituitary-dependent hypercortisolism. Compared with other secreting pituitary tumors, the corticotroph adenoma seems to be the most biologically active tumor. Clinical evidence of hypercortisolism mainly occurs at an early stage of tumor growth when the tumor is very small, below the detection threshold of modern imaging techniques. While the treatment of large tumors remains difficult due to the non-discrete boundary lines of the tumor and extension or invasion, surgical removal of very tiny tumors requires reliable preoperative or peroperative identification in order to achieve total tumor resection for clinical remission and pituitary preservation to prevent hypopituitarism. We reviewed all the current surgical techniques or clever surgical procedures used to achieve both goals with the lowest complication rate. We report here the state-of-the-art of surgical management of corticotroph pituitary adenoma focusing on preoperative radiological and biological data required for performing guided intrasellar surgical exploration and reliable tumor identification. Different technical aspects of the nasosphenoidal approaches are reported as well as the modified transdiaphragmatic or transtubercular transcisternal approaches to tumors in a suprasellar localization or lying along the pituitary stalk. The advantages of minimally invasive surgical techniques such as intrasellar endoscopic surgery are discussed. Adapted surgical techniques for second transnasal surgery indicated for recurrent tumors are described. Guidelines are given for peroperative tumor identification with macroscopic assessment or histological control with frozen section biopsies. Different techniques for tumor removal are discussed from selective microadenomectomy to enlarged pituitary resection and total hypophysectomy. Methods for preoperative guidance of total tumor removal are proposed including histological or biological assessment of normal adjacent pituitary tissue. the strategy of surgical intrasellar exploration and tumor resection is outlined using a set of algorithms. The first is devoted to positive preoperative documentation of the tumor. The second is proposed for the surgical scenario where there is no preoperative MRI evidence of the tumor. Special strategies are discussed for ectopic adenoma or multiple tumors. Revision surgical management after surgical failure or tumor recurrence is described. Special guidelines for surgical treatment of large clinically silent corticotroph macroadenomas are given with emphasis on the high risk of recurrence in comparison with other silent pituitary tumors such as gonadotroph or immunonegative adenomas.
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PMID:[Technical aspects and surgical strategy for removal of corticotroph pituitary adenoma]. 1205 25

The pituitary contains estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR). In accordance with immunocytochemistry, it is agreed that sex hormone receptors reside into the nucleus. All three receptors are found predominantly in gonadotrophs and lactotrophs, and less frequently in other cell types. ER plays a major role in prolactin (PRL) production and lactotroph proliferation, and protracted estrogen administration induces lactotroph hyperplasia and adenoma in rodents. Most research on PR and AR is focused on their role in the fine-tuning of gonadotropin secretion during estrous cycle. Contrary to the effect in nontumorous pituitary, estrogens can inhibit the proliferation of transplantable rat pituitary tumors and of cell lines derived from them. In humans, despite the presence of ER in all types of adenohypophysial tumors, the role of estrogen in tumor cell proliferation is still unclear. Few results indicate that tumor growth is stimulated by estrogen, and inhibited by progesterone and androgen. Novel data reveal that steroid hormones can act directly on plasma membrane or via other receptors, and interact with growth factors, oncogenes, and other transcription factors. The mechanisms by which steroid hormones control cell proliferation remain a major challenge for future research.
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PMID:Pituitary Sex Steroid Receptors: Localization and Function. 1211 30


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