Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 110 cases of thyroid carcinomas were examined immunohistochemically to evaluate the overexpression of mutant forms of p53 protein in the light of their relationship with their histological subtypes. A polyclonal antibody, CM-1, was applied to the routine formalin-fixed, paraffin-embedded tissues for this survey. Overall, immunohistochemically detected p53 expression confined to the nucleus was identified in 22.7% of the thyroid carcinomas. A significant difference in the positivity of p53 among histological subtypes was noted; the positivity was 11.1% of the cases in well-differentiated papillary carcinoma, 14.3% in well-differentiated follicular carcinoma, 40.9% in poorly differentiated carcinoma, and 63.6% in undifferentiated carcinoma. No immunohistochemical positivity was found in adjacent non-neoplastic tissues or in benign lesions, including follicular adenoma, adenomatous goiter, and chronic thyroiditis. These results suggest that overexpression of p53 is not a responsible factor for the oncogenesis itself, but rather that it plays a crucial role in aggressive subtypes of thyroid carcinomas. Additionally, the distinct entity of poorly differentiated carcinoma, previously categorized in the well-differentiated carcinoma under the name of papillary or follicular carcinoma, was statistically confirmed.
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PMID:Overexpression of p53 as a possible prognostic factor in human thyroid carcinoma. 768 2

Bovine thyroglobulin gene upstream regulatory sequences were used as a tissue specific promoter in order to direct the expression of different genes specifically to the thyroid gland. Transgenic models of thyroid diseases have been generated, by directing the expression of specific oncogenes to the thyroid cell. In one of these models (TgAgT), the sv40 large T antigen promoted the development of an aggressive undifferentiated tumor mimicking the phenotype of the human anaplastic carcinoma. In the second model (TgA2aR), the expression of the adenosine A2 alpha receptor, acting as a constitutive activator of adenylyl cyclase, resulted in the development of a hyperfunctioning goiter, and in old animals to the formation of malignant foci. Transgenic lines expressing the E6 oncogenic (TgE6) from type 16 human papillomavirus appeared to be asymptomatic. In contrast, the thyroid cells of mice expressing E7 oncogene divide very rapidly, but remain differentiated, resulting in the development of huge colloid goiters. Signs of malignancy appear late in the development. The molecular properties of E6 and E7 oncogenes are to bind, and inactivatc, the tumor suppressor gene producers p53 (E6), or RB (E7). Our transgenic models indicate that the RB protein (and/or related proteins) are essential factors in the negative control of thyroid cell proliferation. On the contrary, inactivation of p53 seems to play a minor role, at least in the early steps of tumor formation. In the last model (Tg alpha 1B), the expression of a mutant of the alpha 1B adrenergic receptor reported to activate both CAMP and sigma P3-CA-cascades, resulted in growth stimulation, hyperfunction, cell degeneracy attributed to the overproduction of free radicals and malignancy.
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PMID:[Transgenic models of human thyroid pathologies: hyperfunctional adenoma, anaplastic cancer, differentiated cancer, hypothyroidism]. 900 25

Mutations in the p53 tumour-suppressor gene (exons 5-8) were investigated in 31 Belarussian childhood thyroid tumours (24 cases of papillary thyroid carcinoma, 3 benign tumours and 2 cases each of thyroiditis and goiter); 33 thyroid tumours from juveniles and adults without radiation exposures (25 carcinomas of various histological types, including 11 papillary carcinomas and 8 adenomas) and 6 tumours from adults (4 papillary carcinomas, 1 adenoma, 1 goiter) served as controls. The mutational spectrum of p53 differed greatly between the childhood thyroid carcinomas from Belarus and the control groups. In the control groups of 29 malignant thyroid tumours, 7 different mutations were detected on exons 5-8, none of which occurred among the 15 papillary carcinomas in this group. Five mutations were found in tissue samples of the 24 childhood papillary carcinomas, and they were all the same p53 point mutation (CGA --> CGG) on codon 213 of exon 6. To determine whether this mutation is simply a polymorphism or whether it is specific to the tumour cells, laser-assisted microdissection was applied to collect various areas of tumorous and non-tumorous cells (10-20 cells per sample) from each paraffin-embedded tissue section of 8 of the papillary thyroid carcinomas. Using PCR-SSCP and sequence analysis on these cells, the very same p53 mutation on codon 213 was detected in various microdissected tumour samples of 2 cases, but it was not found in any microdissected non-tumorous sample. The exclusive occurrence of this p53 mutation in selective microdissected samples of tumour cells, even as homozygous mutation in 1 case, reflects a distinct tumour heterogeneity within papillary childhood thyroid carcinomas.
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PMID:p53 mutations in childhood thyroid tumours from Belarus and in thyroid tumours without radiation history. 939 55

A rare case of a macrofollicular variant of papillary thyroid carcinoma occurring in an 18-year-old male is described. The extirpated tumor, 5.5 x 5.5 x 3.5 cm in size, was well demarcated and multinodular, and histopathologically showed a predominantly macrofollicular structure reminiscent of adenomatous goiter or macrofollicular adenoma. In the tumor tissue, however, there were several small foci of microfollicular or papillary structure with the nuclei characteristic of papillary carcinoma. Parts of the macrofollicular areas also showed similar nuclear characteristics with a transition to microfollicular or papillary areas. Incomplete capsular invasion and minimal vascular invasion were also present. Additional resected specimens contained small metastatic nodules in the residual left lobe and lymph nodes. Immunohistochemistry showed a small number of p53-positive tumor cells in the microfollicular or papillary areas. It is suggested that this tumor is a well-differentiated variant which should be distinguished from benign thyroid lesions, although there have been some cases of metastases which appear related to capsular and/or vascular invasion.
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PMID:Macrofollicular variant of papillary thyroid carcinoma. 970 60

A 52-year female presented with an enlarged thyroid mass and lump sensation in the throat. The cytologic examination showed class five and she was admitted to the hospital to undergo operation. Total thyroidectomy was done and the tumoral invasion of the trachea was removed. We performed tracheoplasty using a sternocleidomastoid muscle-clavicle myoosseous flap in a single stage operation. Histologic diagnosis revealed anaplastic thyroid carcinoma After upper mediastinal dissection had been performed, systemic chemotherapy using pirarubicin, cisplatin and etoposide was administered. In addition, she was treated with radiochemotherapy using pirarubicin, cisplatin and a total of 58 Gy was administered. No recurrence of the tumor has been noted since the above operation 2 years ago. Immunohistochemical studies of primary and metastatic tissues in this case revealed a positive expression of p53 protein in both.
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PMID:A case of anaplastic thyroid carcinoma surviving disease free for over 2 years. 1021 4

Thyroid malignancy has been induced by long-term endogenous thyrotropin (TSH) stimulation in experimental animals, leading to local and distant metastasis. It has been postulated that constant and prolonged endogenous TSH stimulation in dyshormonogenetic thyroid tissues could result in thyroid neoplasia. The possible role of growth factors and oncogenes in goitrogenesis and favoring neoplasia has also been mentioned. Overexpression of certain growth factors and/or their receptors, and of oncogenes implicated in growth promotion may play a significant role in the relatively frequent finding of thyroid malignancy in congenital goiters. In this study the expression of epidermal growth factor (EGF), epidermal growth factor receptor (EGF-R), transforming growth factor-beta (TGF-beta), c-myc, and p53 mRNAs was determined in 14 thyroid tissue samples: 6 from patients with thyroid peroxidase (TPO) gene mutations, 4 with thyroglobulin (Tg) gene defects and 4 normal thyroid tissues. EGF mRNA overexpression was seen in 7 of 10 dyshormonogenetic tissues (3.5 to 12.0 arbitrary optical densitometry units [AODU]) and considered significantly higher (p < 0.01) when compared to normal thyroid tissues (0.25 to 0.32 AODU). Moreover, overexpression of EGF-R mRNA was present in 6 of 10 dyshormonogenetic tissues (2.23 to 13.03 AODU) and considered significantly higher (p < 0.01) when compared to normal thyroid tissues (0.42 to 0.65 AODU). There was no difference in c-myc, p53, and TGF-beta mRNAs expression between dyshormonogenetic and normal tissues. The overexpression of EGF and EGF-R mRNAs found in dyshormonogenetic tissues may suggest that this growth factor may play a role in cellular proliferation and contribute to goiter formation.
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PMID:Overexpression of epidermal growth factor and epidermal growth factor-receptor mRNAs in dyshormonogenetic goiters. 1127 91

A sequence of genetic events characterized by deletion and expression of several oncogenes may lead progressively to tumorgenesis. The expression of certain oncogenes is believed to be related with thyroid carcinogenesis and tumor progression. We investigated immunohistochemically p53 tumor suppressor gene and c-fos oncogene expression in forty patients with thyroid cancer. Thyroid biopsies from twenty patients with benign thyroid diseases were also examined. The forty patients with thyroid cancer varied histologically; 24 with papillary carcinoma (60%), 12 with follicular carcinoma (30%), 3 with anaplastic carcinoma (7.5%) and one with medullary carcinoma (2.5%). The patients with benign thyroid diseases consisted of 10 with adenomatous goiter (50%), 7 with goiter (35%) and three with Hashimoto thyroiditis (15%). Individual p53 and c-fos expression was more prevalent in thyroid carcinomas compared to benign tumors (p=0.001 and p=0.04, respectively). A marked increase of p53 and c-fos coexpression was found (p=0.02) in patients with thyroid cancer and metastasis to the regional lymph nodes. Furthermore c-fos was overexpressed in only female thyroid cancer patients. In conclusion, p53 and c-fos are significantly overexpressed in thyroid cancer patients, indicating their role in the genetic mechanisms leading to thyroid tumorigenesis. This hypothesis is further supported by the observation that p53/c-fos coexpression was related with more advanced disease status.
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PMID:P53 and C-FOS overexpression in patients with thyroid cancer: an immunohistochemical study. 1268 75

The expression of P53 and P21WAF1 proteins was analyzed immunohistochemically in archival material derived from 12 cases of follicular thyroid carcinoma, 57 cases of follicular adenoma and 17 cases of nodular goiter. In the follicular carcinoma group 6 out of 12 cases (50%) were positive for P53 protein and 4 out of 12 cases (33.3%) were positive for P21WAF1 protein. In the follicular adenoma group, 18 out of 57 cases (31.6%) were positive for P53 and 16 out of 57 cases (28.1%) were positive for P21WAF1 protein. No positive cases of P53 or P21WAF1 proteins presence were found in the nodular goiter group. Positive correlation between the expression of P53 and P21WAF1 proteins was found for follicular carcinoma and adenoma groups (p = 0.034 and p = 0.002, respectively). The obtained results demonstrate that simultaneous immunohistochemical detection of P53 and P21WAF1 proteins expression may be useful in determining functional status of P53 protein, helping to interpret expression of P53 protein in thyroid follicular carcinoma cells.
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PMID:Analysis of P53 and P21WAF1 proteins expression in follicular thyroid tumors. 1575

Most previous studies on RET and p53 proteins have focused on thyroid papillary carcinoma. We investigated the role of RET and p53 protein expressions using immunohistochemistry on 52 cases of thyroid follicular adenomas and studied the follow-up records of these patients. The range of follow-up period was 3 to 14 years. The patients were between 15 and 71 years of age with a median age of 34.5 years. There were 46 females and 6 males. Except for 3 cases, all patients were Malays. The minimum volume of the tumour was 1000 mm3 and the maximum was 512,000 mm3 with a median of 270,000 mm3. Eleven (21.2%) cases showed RET expression. RET expression was not statistically significant when cross-tabulated against sex (p = 0.322), ethnicity (p = 0.518), age (p = 0.466) and symptom duration (p = 0.144). Six (11.5%) of 52 cases showed p53 immunopositivity. p53 expressions were also not significantly correlated to the clinical parameters above. There was no correlation between RET and p53 protein expressions. The only statistically significant finding was the association of tumour volume with duration of symptoms (p = 0.05). All patients are alive at the time of writing. 3 had recurrent goitre, 2 of these were diagnosed as colloid goitre while the third was a follicular lesion. One patient suffered from depression requiring anti-depressant treatment. In conclusion, unlike papillary carcinoma in which the roles of ret and p53 oncogenes are known, their roles in influencing the behaviour of follicular adenoma has not been ascertained.
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PMID:RET and p53 expression in thyroid follicular adenoma: a study of 52 cases with 14 years follow-up. 1719 91

Ovarian tumor composed only of Brenner tumor and struma ovarii is very rare; only 6 cases have been reported in the English literature, to the best of the author's knowledge. A 66-year-old woman underwent right oophorectomy because of torsion of right ovarian cyst. Macroscopically, the ovarian cyst was hemorrhagic and red. Cystic content was hemorrhagic fluid. Microscopically, the cyst walls were composed only of Brenner tumor (50% in area) and struma ovarii (50% in area). Hemorrhage and ischemic changes were seen. Other elements were not recognized. No malignant transformation was noted. These two elements were separately present, and no mergers between them were recognized. Immunohistochemically, the Brenner tumor element was positive for cytokeratins (AE1/3 and CAM5.2) and Ki67 (labeling=3%), but negative for thyroglobulin, TTF-1, p53, CA125, and vimentin. The struma ovarii element was positive for cytokeratins (AE1/3 and CAM5.2), thyroglobulin, TTF-1 and Ki67 (labeling=5%), but negative for p53, CA125 and vimentin. The findings suggests that there were cases of ovarian cyst composed only of Brenner tumor and struma ovarii, that such a case may be monodermal mature cystic teratoma or the Brenner tumor element was derived from surface epithelium in the preexisting struma ovarii, and that such a tumor manifest as cystic torsion.
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PMID:Ovarian cystic tumor composed of Brenner tumor and struma ovarii. 2255 85


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