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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate more objective laboratory methods that may help practicing pathologists to discern malignancy in human adrenocortical neoplasms, we have examined cellular DNA content by flow cytometry and immunohistochemical distribution of c-myc, vimentin, proliferating cell nuclear antigen (PCNA), and epidermal growth factor receptor (EGFR) in 15 cases of human adrenocortical neoplasms (nine carcinomas and six adenomas). All of these examinations were performed on routinely processed surgical pathology specimens. All carcinoma cases met Weiss's histologic criteria. Seven of eight adrenocortical carcinomas demonstrated aneuploid DNA content, while all adenomas were diploid by flow cytometry. c-myc oncoprotein was observed both in cytoplasms and nuclei in all carcinomas but only in nuclei in adenomas. Vimentin was present in all carcinoma cases examined but was also observed in three of six cases of adenoma. There were no clinical or histologic differences between vimentin-positive and vimentin-negative adenomas. Immunoreactivity of PCNA and EGFR was observed in all the cases examined. There were no significant differences in distribution or patterns of immunoreactivity between adrenocortical carcinoma and adenoma. Therefore, we conclude that only DNA ploidy examined by flow cytometry and immunolocalization patterns of c-myc oncoprotein expression have any practical value in the pathologic evaluation of adrenocortical neoplasms. Careful morphologic and/or clinical studies are still considered to be the best available methods in discerning malignancy in resected human adrenocortical neoplasms.
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PMID:Discerning malignancy in human adrenocortical neoplasms: utility of DNA flow cytometry and immunohistochemistry. 135 77

Sections of normal colon (n = 14), hyperplastic polyps (n = 31) ulcerative colitis (n = 97) and tubular adenomas (n = 40) were examined by immunohistochemistry for the expression of the c-myc proto-oncogene product in order to assess its potential diagnostic value in predicting the malignant potential of these lesions. We compared the degree of epithelial abnormality in these colorectal specimens with the extent of immunoperoxidase staining for c-myc oncoprotein, we found that high c-myc protein expression correlated with the degree of epithelial alteration in ulcerative colitis and tubular adenoma groups. Weakly positive staining was found in 10 out of 14 normal colon samples and 28 out of 31 hyperplastic polyps. High tissue expression of c-myc protein, when combined with histologic dysplasia, may prove to be an additional factor in the evaluation of malignant potential in ulcerative colitis specimens and adenomas.
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PMID:High c-myc protein expression in benign colorectal lesions correlates with the degree of dysplasia. 156 65

Ras gene family (c-Ha, Ki, N ras) and c-myc proto-oncogenes were analyzed in seven colonic and three gastric adenomatous polyps obtained from a patient with Turcot's syndrome. The rearrangement and amplification as well as overexpression of c-Ha ras gene in one colonic adenomatous polyp were determined. The amplified c-Ha ras gene in this polyp revealed larger fragments of BamHI, PstI and SacI than those in the normal colonic mucosa from the same patient. But, such abnormalities were not observed in other polyps. No abnormalities of c-Ki ras, c-N ras or c-myc gene were observed in any polyps. These results suggest that the alternations of c-Ha ras gene in this patient may not be responsible for the adenomatous change, but may be related to the transition from adenoma to carcinoma of the colon.
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PMID:Rearrangement, amplification and overexpression of c-Ha Ras gene in premalignant lesion of Turcot's syndrome. 170 48

The inherited cancer-inducing disease familial polyposis coli (FPC) provides an excellent model not only for studying tumor progression in colorectal cancer but also for elucidating molecular mechanisms in general oncogenesis. This paper reviewed recent remarkable progresses of molecular mechanisms in colorectal tumorigenesis. This is concerned with the various kinds of genetic alterations that accumulate in the development from normal mucosa to adenoma, and then to adenocarcinoma in comparison with FPC and sporadic cases. This review included also information on the localization of FPC major gene. These observations indicate that in cases of colorectal tumorigenesis several genetic alterations may be involved, including activation of K-ras gene, deregulated expression of c-myc gene or c-fos gene and inactivation of tumor suppressor genes such as p53 and DCC genes, as well as the loss of heterozygosity. The observation suggest that adenomas will have undergone several gene or chromosome mutations before reaching to the fully malignant state. Therefore, DNA diagnosis for colorectal tumors in the clinical level may contribute to more accurate prognosis and better results for further therapy.
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PMID:[Diagnosis of colorectal cancer from DNA level]. 184 82

The distribution of the c-myc oncogene product p62 was examined by immunohistochemistry using the monoclonal antibody Mycl-9E10 in a series of 50 colorectal resections for carcinoma. The specimens were specially handled to ensure rapid fixation in formalin, and a significant improvement was shown in the quality and localization of staining compared with routinely handled specimens. Non-neoplastic mucosa showed the presence of nuclear staining of epithelial cells in 93 per cent of the samples, whilst all carcinomas showed cytoplasmic staining and infrequent nuclear staining. Adenomas showed an intermediate pattern, with significantly more frequent cytoplasmic distribution than non-neoplastic mucosa, but less than carcinomas. The results show that whilst fixation conditions are important in the immunolocalization of the c-myc protein product, there may be a consistent difference between non-neoplastic mucosa and carcinoma in the manner of association of p62 with the nucleus.
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PMID:Immunohistochemical demonstration of altered intracellular localization of the C-Myc oncogene product in human colorectal neoplasms. 219 34

Structural alterations of protooncogene sequences may be involved in the pathogenesis of human neoplasms. We screened 54 thyroid tumors (36 benign and 18 malignant) for gene rearrangements of the protooncogenes c-myc, c-myb, c-fos, c-erb-B1, c-erb-B2, c-erb-A, N-ras, K-ras, and H-ras. Only mutations of H-ras were observed. None of the 15 colloid adenomas examined had detectable H-ras rearrangements. Of the remaining tumors, we observed mutations of H-ras in 4 benign and 4 malignant neoplasms. Gene amplification was found in 5 tumors. An aggressive recurrent papillary carcinoma had a marked amplification of one of the H-ras alleles. The amplified allele was truncated, in that the 3' variable tandem repeat was not a part of the amplification unit, and contained a codon 12 point mutation leading to a valine for glycine substitution. We also observed the association of low copy gene amplification with a codon 12 valine for glycine mutation in a follicular adenoma. Two tumors contained H-ras EcoRI polymorphisms not present in the DNA of normal thyroid from the same individuals, and one follicular carcinoma showed loss of an H-ras allele. Ras protooncogenes may become transforming by quantitative mutations, leading to increased expression, or qualitative mechanisms, through activating point mutations. Both of these appear to coexist in thyroid neoplasms, and it may be that a combination of both mechanisms is capable of inducing a more complete spectrum of neoplastic phenotypes.
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PMID:H-ras protooncogene mutations in human thyroid neoplasms. 219 80

Abnormalities in oncogenes, which are broadly classified into viral and cellular oncogenes, and suppressor genes appear critical for the development of colon cancer. Cellular oncogenes contribute to malignant transformation when they become activated by point mutation, translocation, amplification, or loss of regulator sequences. The properties of the oncoproteins, the proteins encoded by oncogenes which are essential for carcinogenesis, are unclear. Suppressor genes normally suppress the tumorigenic phenotype by keeping the growth of cells in check; it is their inactivation that contributes to malignant transformation. Development of colon cancer appears to take place by stepwise accumulation of multiple genetic alterations during the progression from normal colon to adenoma and carcinoma. Activation of ras, an early event in this sequence, is found in 50% of colon cancers; overexpression of c-myc is found in approximately 80%. Inactivation of suppressor genes, which occurs during later stages, is noted in greater than 70% of tumors. A current model of colonic tumorigenesis is presented.
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PMID:Oncogenes and suppressor genes: their involvement in colon cancer. 222 91

The authors investigated the effects of 17 beta-estradiol (E) and thyroid-stimulating hormone (TSH) on tgb (coding for thyroglobulin), c-myc RNA levels, and [3H]thymidine (thy) incorporation in suspension cultures of normal, adenomatous and carcinomatous human thyroid follicles. The cultured follicles showed decreased tgb RNA and enhanced c-myc RNA levels. In the culture of normal and adenomatous samples E caused a significant increase of [3H]thy incorporation and tgb RNA levels, with no effect on c-myc RNA levels. No effect of E was observed in the carcinomatous thyroid culture. TSH induced a significant increase of [3H]thy incorporation and c-myc expression only in adenoma cultures and a significant increase of tgb RNA levels in both normal and adenomatous samples. TSH had no effect on the carcinoma. The results show that E, like TSH, stimulates in vitro the expression of the tgb gene in differentiated cells, without stimulating the expression of the c-myc proto-oncogene, suggesting a possible action of E on normal thyroid function and perhaps growth, even if not associated with increased c-myc expression.
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PMID:In vitro effects of estrogen on tgb and c-myc gene expression in normal and neoplastic human thyroids. 247 35

The expression of 8 oncogenes and the structures of 19 oncogenes were analyzed in 15 adenocarcinomas (12 primary and 3 metastatic), 18 adenomatous polyps, and 18 normal colonic mucosae derived from 19 patients with familial polyposis coli. The expression of c-myc gene was most elevated in carcinoma, and moderately elevated in adenoma, compared with corresponding normal colonic mucosa. In contrast, the expression of c-fos gene was markedly decreased in all samples of adenoma and carcinoma, compared with that of normal colonic mucosa. These characteristic expression patterns of c-myc and c-fos genes were revealed not only in familial polyposis coli but also in cases of nonhereditary colon carcinoma. Structures of the 19 oncogenes were not modified in either adenoma or carcinoma, except for amplification of the c-myc gene detected in one carcinoma, but not in adenoma, from the same patient. Analyses of the amplified c-myc gene suggest that gene duplication may relate to the mechanism of gene amplification. Thus, the enhanced expression of c-myc gene in adenoma and carcinoma may reflect the proliferative activity, while the c-fos gene may be a prerequisite to stabilize the state of terminal differentiation of colonic epithelial cells.
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PMID:Differential expression of c-myc gene and c-fos gene in premalignant and malignant tissues from patients with familial polyposis coli. 284 40

Tumour specimens from 23 patients with thyroid carcinoma, 22 patients with thyroid adenoma, 3 with Graves' disease, and tissues from 8 normal thyroid glands were analyzed by Southern blot hybridization for the physical state of c-myc and c-fos proto-oncogenes. In 4 patients, both the primary tumour and lymph node metastases were analyzed. No amplification or rearrangement of the two proto-oncogenes was detected. Total RNAs were also analyzed. Elevated levels of the 2.4 kb c-myc RNA and of the 2.2 kb c-fos RNA were found in 13/23 (57%) and 14/23 (61%) of the cancer patients, respectively. High levels of c-myc transcripts were more frequently found in thyroid carcinomas with unfavourable prognosis. Concomitant elevated levels of both c-myc and c-fos RNAs were found in 8 cancers. High levels of c-myc RNA were also found in 1 out of 22 specimens of adenoma, in 1 specimen of Graves' disease and in 2 normal thyroid glands. High levels of c-fos RNA were found in 20 of the 22 adenoma samples and in 2 out of 8 normal thyroid tissues. These data indicate that the overexpression of c-myc and c-fos genes is independent of an alteration of the loci. The high levels of c-fos found in adenoma may be associated with the differentiation state of these tumours.
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PMID:Structure and expression of c-myc and c-fos proto-oncogenes in thyroid carcinomas. 334 48


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