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)

Familial multiple adenoma of pancreatic beta-cells is described for the first time. The occurrence of diabetes mellitus in different members of the family raises the possibility of a common genetic origin for the multiple islet-cell adenomas and the diabetic trait. The evidence suggests that this gene is autosomal and dominant, that it is not linked with the HLA antigens, and that is causes an abnormal sensitivity of the beta-cells, which become hyperplastic or hypofunctional.
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PMID:Familial islet-cell adenomatosis. 7 Jun 43

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

Class II HLA antigen expression was studied in 30 polyps from 3 patients who were diagnosed with familial polyposis coli. The highest levels of this expression were associated with the most severe grades of dysplasia (p less than 0.00001), the sequence of positivity being HLA-DR greater than DQ greater than DP. No association was observed between the expression of these antigens and the presence of a specific inflammatory leukocytic infiltrate. Our results imply that HLA class II molecule expression is somehow related to malignant transformation in familial polyposis coli in accordance with the adenoma-dysplastic adenoma-adenocarcinoma sequence. Thus these antigens may be useful markers to tumoral progression.
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PMID:Class II HLA antigen expression in familial polyposis coli is related to the degree of dysplasia. 216 Sep 11

HLA-DR and -ABC antigens on adenoma and cancer cells of the colon and rectum were investigated. Fifteen specimens of adenomas from 15 patients with sporadic colorectal adenoma, seven specimens of adenomas from seven patients with familial polyposis coli (FPC), and 10 specimens of cancers from 10 patients with colorectal cancer were obtained. Normal colonic mucosa far from the lesions, taken from 15 patients with sporadic adenoma or cancer, served as normal control mucosa. HLA antigens were identified using an immunoperoxidase staining method. Epithelia of all normal control mucosa (n = 15) expressed HLA-ABC antigens, but not HLA-DR antigens. HLA-DR antigens were expressed on 47% (7/15) of sporadic adenomas, 71% (5/7) of adenomas in FPC, and 100% (10/10) of cancers. The extent of HLA-DR expression on adenoma and cancer cells became broader with more severe dysplasia in adenoma, and increased undifferentiation in cancer. It also became broader with increasing mononuclear cell infiltration in both adenomas and cancers. HLA-DR antigens on adenoma and cancer cells appeared to be related to the neoplastic transformation of the epithelia, and to the mononuclear cell infiltration. Partial disappearance of HLA-ABC antigens on adenoma and cancer cells was observed in a few specimens of both adenomas and cancers.
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PMID:HLA antigens on colorectal adenoma and cancer cells. 238 60

Described herein are two brothers with 21-hydroxylase deficiency (21-OHD) associated with adrenal tumors, and these possible mechanisms are discussed. A 34-year-old male was admitted on Jan. 9, 1984 because of an enlarged and tender left breast. Physical examination revealed short stature (152 cm, 76.5 kg), gynecomastia and shortening of metacarpal bone. His testes were small (2.6 X 1.6 X 1.9 cm). Urinary excretion of 17-OHCS was within normal range (5.9 mg/day), but those of 17-KS, 17-KGS and pregnanetriol were markedly increased (44.4, 110 and 22.6 mg/day, respectively). Plasma concentrations of progesterone and ACTH and urinary excretions of estrone, estradiol and estriol were also increased. Urinary excretions of 17-KS were decreased to 11.7 mg/day and 17-KGS to 22.3 mg/day after the ingestion of 2 mg/day dexamethasone for two days. The computed tomography and a scintigraphy with 131I-Adosterol revealed a tumor in the left adrenal gland, and the adrenal arteriography revealed a neovascularity and a tumor stain in the tumor. These data indicated that the patient was suffering from both 21-OHD and the left adrenal tumor. At this point, adenoma or adenocarcinoma of the adrenal gland was suspected. The left adrenal tumor (85 g) was resected on April 10, 1984, and the pathological diagnosis was adrenal adenoma. The patient's endocrinological abnormalities, however, did not improve after the operation. Urinary excretions of 17-KS and KGS were increased to 57.9 and 108.5 mg/day, respectively, in the patient's elder brother, and 63.3 and 127.9 mg/day, respectively, in his younger brother, indicating that they also had 21-OHD. Interestingly, an adrenal tumor was diagnosed by abdominal computed tomography in the elder brother who had the same HLA typing as the present case. The three brothers had 21-OHD, and two of them had both 21-OHD and adrenal tumor. To our knowledge, this is the first report documenting the co-existence of adrenal tumors in brothers with 21-OHD. This suggests that adenoma can be one of the complications of 21-OHD, probably due to the chronic stimulation by ACTH, and that a possible linkage to HLA may exist in such cases.
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PMID:[21-hydroxylase deficiency associated with adrenal tumor: case report of two brothers]. 278 51

We have extended our study of an incomplete variant of multiple endocrine neoplasia Type I (MEN IBurin). In this syndrome, primary hyperparathyroidism and prolactin-secreting adenoma are common, with hormone-secreting pancreatic tumors being rarely seen. The recent localization of the prolactin structural gene to chromosome 6 made further investigation of linkage to HLA of particular interest. Results in 2 multigeneration families exclude close linkage to HLA. We cannot at this time draw any inference regarding linkage of MEN IBurin to the prolactin structural gene.
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PMID:Variant multiple endocrine neoplasia I (MEN IBurin): further studies and non-linkage to HLA. 285 81

A profile of dexamethasone-suppressible hyperaldosteronism (DSH), a variant of primary aldosteronism, is drawn by reviewing its pathophysiological and clinical aspects. Genetic studies show no HLA linkage and point to an autosomal dominant mode of inheritance, suggesting that the prevalence of this disease has been underestimated in the past. Hypertension, hypokalemia, suppressed renin, and high aldosterone values characterize DSH in the basal state, similar to the other forms of primary aldosteronism, i.e., aldosterone-producing adenoma (APA) or bilateral idiopathic adrenal hyperplasia (IAH). Biochemically DSH and APA can be differentiated from IAH since in both aldosterone does not respond to upright posture, to angiotensin II infusion, and to angiotensin-converting enzyme (ACE) captopril. In contrast, morphologically DSH is similar to IAH, since neither macroscopic nor histologic examinations of the adrenals give evidence of any unilateral abnormality. However, DSH is differentiated from APA and IAH by the hyperresponsiveness of aldosterone to acute ACTH administration as well as by the failure of aldosterone to escape from prolonged ACTH stimulation. The final diagnosis of DSH rests upon the prompt reversal of the features of mineralocorticoid excess by glucocorticoid therapy. In some cases hypertension is unresponsive to dexamethasone and needs alternative treatment. The main pathogenetic hypotheses point to a pituitary and/or an adrenal abnormality, but the intrinsic nature of the disease remains to be elucidated.
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PMID:Dexamethasone-suppressible hyperaldosteronism: pathophysiology, clinical aspects, and new insights into the pathogenesis. 303 79

Autopsy findings of a 34-year-old Japanese male with stomach cancer in a renal allograft are presented. The renal graft was given by his 53-year-old mother, who had the same HLA type as the patient and showed negative response in the Mixed Leukocyte Culture Reaction test. Stomach cancer occurred 4 years and 5 months after the renal graft, and infiltrated widely into the abdominal cavity, causing rectal stricture. In his original left kidney, a small renal adenoma was found. The tumor cells of the adenoma were composed of clear cells. In the adenoma, infiltration of stomach cancer was found. The renal allograft functioned very well until his death in spite of several rejection episodes. This is the seventh reported case in Japan in which a renal allotransplant was accompanied by malignancies.
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PMID:Coexistence of stomach cancer and renal adenoma in renal allograft. Clinical and autopsy findings and a review of previous cases in Japan. 390 34

An investigation was made of the differences between colorectal cancer and adenoma using HLA markers. Subjects included 60 cases of colorectal cancer, 43 of colorectal adenoma and 120 healthy Japanese controls. In comparison with the controls, Bw40 was increased (p < 0.02) and B5 was decreased (p < 0.005) in the colorectal adenoma cases, whereas in the colorectal cancer cases, Bw35 was increased (p < 0.005). B5 was significantly less frequent in the adenoma cases than in the cancer cases (p < 0.05). It is suggested that the susceptibility of BW35 to the causal factors of colorectal cancer is under genetic control.
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PMID:HLA antigens in colorectal cancers and adenomas. 741 7

We report the case of a 62-year-old woman who was admitted to our hospital with diabetic ketoacidosis. Her urinary C-peptide was 3.5 micrograms/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was suspected, and pancreaticoduodenectomy was performed. The pathology of this tumor was polycystic adenoma. We examined the surgical specimen from around the tumor histologically. The pancreatic islets had decreased in number. The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved. Marked lymphocytic infiltration was observed in the islets. The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. No NK cells were present in the islets. The present case, which was examined histologically in detail, is consistent with the previously proposed hypothesis that autoimmunity might play an important role in the pathogenesis of insulin-dependent diabetes mellitus.
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PMID:Type 1 (insulin-dependent) diabetic patient with remarkable infiltration of lymphocytes to the islets. 795 31


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