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)

The loss of HLA antigens by neoplastic cells is considered important for tumor growth and metastasis, since it may allow tumors to escape immune surveillance. We studied the expression of HLA class I and II antigens in the colons of 10 patients with familial adenomatous polyposis (FAP), a condition which leads inevitably to colorectal cancer. Expression of HLA class antigens was studied by immunohistochemistry in (a) adenomas from patients with FAP, (b) histologically normal mucosa distant from the adenomas, and (c) histologically normal colonic mucosa from normal subjects. The expression of HLA class I and II antigens was decreased in histologically normal mucosa from FAP patients compared to normal controls. Adenomas showed a similar but quantitatively more pronounced reduction (or loss) of HLA antigen expression. The reduction of HLA expression in adenomas was comparable to that observed in sporadic colon carcinomas. This generalized suppression of HLA gene expression in the colon of FAP patients, which precedes the onset of overt histological manifestations of neoplasia, may be an important early event in colon carcinogenesis.
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PMID:Loss of colonic HLA antigens in familial adenomatous polyposis. 131 51

Many hepatic adenomas have been demonstrated to have a clear relationship with oral contraceptive use, and it is presumed that there may be hormone receptors within the cytoplasm or nucleus of adenoma cells that mediate tumor growth in response to hormonal stimulation. Only a small number of examples of benign hepatic tumors have been analyzed for the presence of estrogen and progesterone receptors, and there has been a lack of consensus with regard to the findings. All previous studies have determined receptor levels by biochemical methods. In a retrospective study, we employed specific monoclonal antibodies against estrogen and progesterone receptors in 10 benign paraffin-embedded hepatic lesions: five examples of hepatic adenoma and five examples of focal nodular hyperplasia. All patients were female, except for one male with adenoma and one male with focal nodular hyperplasia. No patient had received tamoxifen citrate or any other form of hormonal therapy for their hepatic lesion. Positive controls included benign and malignant breast tissue. No positive staining was seen in hepatic adenoma, focal nodular hyperplasia, or normal adjacent liver parenchyma. Intense positive staining was seen in all positive control tissues. This negative result with the use of specific monoclonal antibodies in an established immunohistochemical method for analysis of estrogen and progesterone receptors does not exclude the presence of these receptors in benign hepatic lesions, but does suggest that, if present, they occur in much smaller amounts than in benign and malignant breast tissue. The presence of hormone receptors in benign hepatic tumors deserves further study.
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PMID:Expression of steroid hormone receptors in benign hepatic tumors. An immunocytochemical study. 133 49

A retrolenticular fibrovascular membrane occurred in the setting of a ciliary body mass in a 10-year-old black girl who had been successfully treated for a rhabdomyosarcoma of the lung. The results of a transscleral biopsy of the mass demonstrated it to be a pigmented adenoma of the ciliary body. A lensectomy and membranectomy were performed to aid in the follow-up and rehabilitation of the eye. At 9 months after surgery, the patient had 20/25 vision with no evidence of tumor growth. This case demonstrates an unusual cause of cyclitic membrane formation and suggests that transscleral biopsy may be a useful adjunct in the management of selected ciliary body masses.
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PMID:Ciliary body adenoma in a 10-year-old girl who had a rhabdomyosarcoma. 843 Nov 46

We have investigated the structure of dopamine (DA) D2 receptors present in an estrone-induced, prolactin (PRL)-secreting, DA-sensitive adenoma and in two PRL-secreting and DA-insensitive transplantable tumors 7315a and MtTW15, in order to identify better the anomalies present in DA-resistant lactotrophs. D2 receptors were found in both a high- and a low-affinity state in adenomatous lactotrophs as shown by displacement studies with the agonist N-propylnorapomorphine (NPA), but only in the low-affinity state in the two DA-resistant tumors. Treatment with the alkylating agent N-ethylmaleimide induced a disappearance of the high-affinity state of the D2 receptor in the adenoma and a reduction in receptor concentration, but did not have any effect on the affinity of receptors present in DA-resistant tumors. Moreover, target size analysis and radiation inactivation studies of D2 receptors, using membranes preincubated with NPA and [3H]spiperone as ligand or using [3H]NPA as ligand on membranes preparations, have shown the presence of distinct structural differences between adenomatous and tumoral D2 receptors and between the two tumoral receptors themselves; these results suggest that the normal functional unit of the D2 receptor is a dimer associated with a guanine nucleotide-binding protein (G protein) subunit and that tumoral D2 receptors may exist in various polymeric forms unassociated with G proteins. The anomalies found to be present in tumoral D2 receptor complexes may be responsible for the insensitivity of these tumors to dopaminergic agonists' inhibitory activity on PRL release and tumor growth.
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PMID:Structural differences between dopamine D2 receptors present in a rat pituitary adenoma and in transplantable rat pituitary tumors 7315a and MtTW15. 196 89

Mouse lung tumors were induced transplacentally in offspring by treating C3H/HeNCrMTV- and Swiss Webster [Tac:(SW)fBR] mice during different periods of gestation with a single i.p. injection of N-nitrosoethylurea (ENU) at 0.5 mmol or 0.74 mmol/kg. Quantitative and qualitative evaluation of the lung tumors in the offspring at ages ranging from 1 week to 52 weeks was carried out by light microscopic study of hematoxylin and eosin-stained (H&E) serial and step sections. By nitroblue tetrazolium enzyme histochemistry, 3-hydroxybutyrate dehydrogenase (seen predominantly in Clara cells) was localized in frozen tissue sections. By avidin-biotin peroxidase complex immunohistochemistry, various specific cellular and nuclear markers were investigated on paraffin sections (antisera against surfactant apoprotein, Clara cell antigen, lysozyme, and 5-bromo-2' deoxyuridine). Normal lung and lung tumors were also studied by electron microscopy. A histological method was developed to assess all lesions present in the entire lung. It was shown that solid and papillary tumor types arose individually and that mixed solid/papillary forms represented a progression of the benign solid adenoma to the malignant papillary carcinoma. Immunocytochemical localization of DNA synthesis with 5-bromo-2' deoxyuridine gave the highest labeling indices at early stages of tumor growth. As the size of the papillary tumors increased, fewer nuclei were labeled/mm2 of tumor section. Lack of both specific Clara cell antigen and 3-hydroxybutyrate dehydrogenase and the absence of typical nonosmiophilic Clara cell granules indicated a cell of origin other than Clara cells. Evidence for alveolar type II cell origin of both solid and papillary neoplasms in spontaneous and induced tumors was found in the expression of surfactant apoprotein, the presence of mature lamellar bodies (solid tumors) or small lamellar bodies, and immature stages of lamellar bodies (papillary tumors). Lysozyme was present in mature alveolar type II cells and solid tumors but absent in fetal lung and papillary neoplasms. Tumors induced on gestation day 14 or day 16 had all developed by 2 weeks of age and generally did not increase in multiplicity with age, whereas those induced on day 18 showed a protracted development with regard to frequency, growth (size), and progression. The multiplicity of mouse lung tumors induced at different stages of fetal development paralleled the number of alveolar type II precursor cells (i.e., followed a bell-shaped pattern peaking on day 16 of gestation).
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PMID:Origin of spontaneous and transplacentally induced mouse lung tumors from alveolar type II cells. 205 24

In A/J strain mice, the carcinogen urethan induces lung adenomas and adenocarcinomas that contain Ki-ras-activating mutations primarily in codon 61. These mutations affect the middle adenine in codon 61 resulting in the substitution of either arginine (AT----GC transition) or leucine (AT----TA transversion) for the wild-type glutamine. To analyze the expression of the wild-type and mutant Ki-ras mRNAs in primary mouse lung tumors and transformed mouse lung cell lines, we utilized reverse transcription of total mRNA and DNA amplification by the polymerase chain reaction. The wild-type allele of codon 61 was expressed in all normal lung and primary tumor samples and in all transformed cell lines, except one. Significantly, the leucine-substituted allele was expressed primarily in very small lung adenomas, whereas the arginine-substituted allele was expressed in large lung adenocarcinomas and transformed lung cell lines. The relative amounts of expression of the mutant versus wild-type Ki-ras alleles and the total Ki-ras mRNA expression was similar in both lung adenomas and adenocarcinomas. Further, the arginine mutant allele was present in adenocarcinomas having either alveolar or papillary tumor morphologies. These results suggest that the specific activating Ki-ras mutation is more critical to either lung adenoma or adenocarcinoma development than is the tumor's cell of origin or the extent to which the mutant alleles are expressed. A distinct role of the specific activating Ki-ras mutations in affecting lung tumor growth or malignant potential is indicated.
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PMID:Specific Ki-ras codon 61 mutations may determine the development of urethan-induced mouse lung adenomas or adenocarcinomas. 224 61

Fecal intestinal flora in patients with colon adenoma showed significant decrease of Bifidobacterium. A tendency of decrease of Bifidobacterium and increase of Clostridium-other was shown in adenomas with higher degree atypia, but no definite tendency could be found concerning its size. Compared with the control group, patients with colon cancer showed significant increase of Clostridium-other and decrease tendency of Bifidobacterium which was not relevant to its percentage of total circum ference involved by the cancer. From the above findings, it is suggested that tumor growth or malignant transformation has relation to Bifidobacterium and Clostridium-other.
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PMID:[Fecal intestinal flora in patients with colon adenoma and colon cancer]. 238 24

The epidermal growth factor (EGF) and alpha-tumor growth factor are mitogenic proteins which bind to the EGF-receptor and may play a role in carcinogenesis or tumor progression. Our study investigated whether colorectal carcinomas and adenomas express altered levels of EGF-receptors or overproduce EGF-like activity by comparing histologically normal mucosa to carcinomas resected from the same patients. EGF-receptors were characterized by radioligand binding studies. Carcinomas contained unchanged or decreased levels of EGF-receptors in 13/16 and moderately increased levels in 3/16 patients as compared to normal mucosa. Adenomas obtained from 2 patients with familial polyposis coli and from a third patient with a coincident carcinoma had similar numbers of EGF-receptors as normal mucosa. EGF-like growth factors, in contrast, were significantly elevated in carcinoma extracts as compared to extracts from normal mucosa of the same patients. Adenomas did not contain elevated levels of EGF-like activity. We conclude that increased expression of EGF-receptors is infrequent in colonic adenocarcinomas. Increased production of EGF-like growth factors may frequently occur but seems to be associated with tumor progression rather than with premalignant lesions as represented by adenomas.
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PMID:Epidermal growth factor receptors and epidermal growth factor-like activity in colorectal mucosa, adenomas and carcinomas. 254 69

The most frequent benign liver tumors are hemangioma, focal nodular hyperplasia (FNH) and adenoma. It is essential for the diagnosis to differentiate these lesions from malignant tumors. While sonography, bolus-CT scan, chole-/bloodpool scintigraphy usually yield a safe diagnosis of hemangioma or FNH, adenomas do not show characteristic features. Operation is indicated for hemangioma of FNH only in case of tumor growth and/or symptoms. Operation for adenoma is as a rule indicated because of possible malignant transformation or uncertain differentiation from malignoma. Operative procedures include anatomical/atypical liver resection, ex situ resection or liver transplantation.
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PMID:[Surgery of benign liver tumors]. 257 58

Carcinomas of the gallbladder can be grossly divided into two types: carcinoma in adenoma (CIA) and carcinoma without adenoma (CWA). The histogenesis of both types of gallbladder carcinoma (CIA and CWA) was investigated in association with metaplastic changes in 35 early carcinomas larger than 5 mm in diameter and 16 microcarcinomas up to 5 mm in largest diameter. In five early CIAs and two micro-CIAs, the carcinoma was surrounded by the adenoma, and the areas of both carcinoma and adenoma mainly showed gastric-type metaplasia (GM). On the other hand, 90% of the other 30 early CWAs showed GM and/or intestinal-type metaplasia (IM) in the tumor, and all of them were surrounded by GM and/or IM. Seven of the other 14 micro-CWAs showed GM and/or IM in the tumor as well as in the surrounding mucosa, and had non-neoplastic metaplastic glands underneath the carcinoma tissue. The remaining seven micro-CWAs showed no or only mild metaplasia in the tumor and were surrounded by proper mucosa without metaplasia. From these data, it is concluded that carcinoma of CIA possibly arises from adenoma mainly with GM, and that CWA originates either from the upper part of the metaplastic mucosa or from the proper mucosa of the gallbladder. In addition, some CWA may undergo secondary metaplastic changes during tumor growth.
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PMID:Histogenesis of gallbladder carcinoma from investigation of early carcinoma and microcarcinoma. 274 3


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