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)

In this study, we analyzed 105 paired sporadic primary breast tumor and normal tissue samples for loss of heterozygosity (LOH) on chromosome 17, using 12 polymorphic markers. We have identified partial or interstitial LOH in five separate regions of chromosome 17. Two of the deleted regions lie on the short arm of the chromosome, the first (region I, D17S5) in the telomeric part, distal to TP53 and the second spanning the TP53 gene (region II). Three of the five deleted regions lie on the long arm of chromosome 17: region III, on the proximal long arm between D17S250 and THRA1; region IV, between D17S776 and D17S579, including the BRCA1 gene, and region V, located distal to D17S733. No statistically significant correlations were observed between clinicopathological characteristics or steroid hormone receptor status and deletion of either region I or II. However, patients whose tumors had LOH for region I showed relapse or death more frequently than patients with tumors informative for this region but without LOH (p = 0.002). Statistically significant correlations between LOH at each of the three deleted regions of 17q and a high mitotic index were observed (region III, p = 0.005; region IV, p = 0.02, and region V, p = 0.004). In addition, LOH at region IV showed a significant association with paucity of estrogen receptors (p = 0.01). Our results show a complex pattern of LOH on chromosome 17 in breast cancer and a correlation of these events with different clinical parameters. This pattern suggests that particular subsets of allele loss may contribute specifically to different clinically defined subsets of sporadic breast tumors.
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PMID:Five distinct deleted regions on chromosome 17 defining different subsets of human primary breast tumors. 747 29

Breast tumors are thought to originate, grow, and metastasize in an environment which includes steroid hormone receptors, their cognate steroid ligands, and many gene products which are regulated by steroid hormone receptor-ligand complexes. In this paper we describe highly sensitive and quantitative immunofluorometric procedures for measuring three proteins that are candidate prognostic indicators in breast cancer, namely, the p53 tumor suppressor gene product, carcinoembryonic antigen (CEA), and prostate specific antigen (PSA). These proteins were quantified in over 950 cytosolic tumor extracts along with estrogen and progesterone receptors (ER, PR). Association analysis between all five biochemical parameters revealed strong negative associations between p53 and receptors and strong positive associations between CEA and receptors. Negative associations between p53 and CEA and between CEA and PSA were also found. These associations, not quantitatively studied in previous reports, are related to each other using a hypothetical model. The observed associations may further contribute to the understanding of the biology of breast tumors.
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PMID:Quantitative analysis of mutant p53 protein in breast tumor cytosols and study of its association with other biochemical prognostic indicators in breast cancer. 752 72

Prostate-specific antigen (PSA) is a glycoprotein produced by the epithelial cells of the prostate. PSA is currently used in clinical practice to facilitate diagnosis and monitoring of prostate carcinoma. The prostate is an organ that possesses androgen, estrogen, and progesterone receptors, and in this respect is similar to the breast. We postulated that breast tumors might also have the ability to produce PSA. We performed these studies on a collection of 525 tumor specimens collected for routine biochemical determination of estrogen and progesterone receptors. Using a highly sensitive immunofluorometric procedure, we measured the p53 tumor suppressor gene product and PSA. Twenty nine percent of the breast tumor extracts contained detectable levels of PSA immunoreactivity (> 0.05 microgram/L). The immunoreactive PSA content was associated with estrogen and/or progesterone receptor-positive tumors (P < 0.002). No association was found between PSA immunoreactivity and levels of the p53 tumor suppressor gene product (P = 0.37). High performance liquid chromatography and Western blot analysis revealed that the PSA immunoreactivity in the tumor had a molecular weight of 30 kDa, similar to that of seminal PSA. Immunoreactive PSA-positive tumors were associated with younger women (P = 0.012) and earlier disease stage (P = 0.064). We postulate that PSA immunoreactivity may be an additional marker of steroid hormone receptor-ligand action.
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PMID:Detection of prostate-specific antigen immunoreactivity in breast tumors. 753 68

In the present study we evaluated the prognostic significance and correlation between ploidy status, lymph node status, estrogen-progesterone receptor status and the expression of Erb-B2 and p53 protein in 77 primary breast carcinomas. Quantitation of DNA ploidy was determined on Feulgen-stained touch imprints with an image analyzer, whereas localization of the immunohistochemical reaction of Erb-B2 and p53 protein was evaluated in paraffin-embedded tumor specimens with microscopy. The DNA histogram was diploid in 17 cases, poly/tetraploid in 24 and aneuploid in 36. We observed no correlation between ploidy status and hormone receptor content or lymph node status. The expression of Erb-B2 protein was observed exclusively in the membrane and in the cytoplasm of neoplastic cells and was uniformly distributed. Overexpression was observed in 89.2% of cases. Aneuploid tumors intensively expressed the oncogene in 20.3% of cases. A statistically significant correlation was observed between lymph node metastasis and Erb-B2 overexpression. The expression of p53 protein was expressed as nuclear staining in 17.6% of the cases, with variable intensity, mainly in ductal histotypes. Among these, 62% were aneuploid. Lymph node status and steroid receptor status did not correlate significantly with p53. From these data we conclude that DNA ploidy and Erb-B2 and p53 expression correlate with cell proliferation and differentiation and therefore may identify breast carcinoma patients with more aggressive disease.
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PMID:Correlation between ploidy status, Erb-B2 and p53 immunohistochemical expression in primary breast carcinoma. 754 49

In a retrospective study, 204 formalin-fixed and paraffin-embedded biopsies of primary breast carcinomas were tested immunohistochemically for the expression of p53 protein (PAb 1801). 38% of the carcinomas were positive with respect to p53. The expression of p53 correlated significantly with the loss of tumor differentiation (P = 0.013), but not with menopausal status, patients' age, tumor size, axillary lymph node involvement or hormone receptor status. The influence of p53 expression on prognosis was evaluated in 197 patients (T1-4 N0-2 M0, median observation time 72 months). Detection of p53 protein was associated with a significantly longer disease-free survival in node-positive women (P = 0.03). However, p53 protein did not prove to be a prognostic factor in node-negative patients. The results demonstrate the prognostic value of p53 expression in breast cancer which appears to be limited to patients with node-positive tumors.
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PMID:P53 protein in 204 patients with primary breast carcinoma--immunohistochemical detection and clinical value as a prognostic factor. 757 6

Several oncogenes and tumour-suppressor genes have been identified that may have an important role in the development of human breast carcinoma. Furthermore, some of these gene alterations may be linked to the development of invasion and subsequent metastasis. Alterations in the expression of ras p21, p53 and c-erbB-2 have all been linked to tumours with rapid cellular proliferation, but the evidence that they are of prognostic importance in patients with breast cancer is conflicting. This study explores the relationship between expression of these oncoproteins and clinical outcome in 92 patients with either locally advanced or metastatic breast cancer treated with primary endocrine therapy. Specimens of the primary carcinoma were available for analysis of hormone receptor, Ki67 labelling index, epidermal growth factor receptor (EGFR), c-erbB-2, p53 and ras p21. Clinical response was measured according to UICC criteria after 6 months of treatment and all patients were followed for time to progression and overall survival. As shown previously, oestrogen receptor (ER) negativity, high Ki67 labelling index and EGFR overexpression were associated with a shorter time to progression and overall survival. However, no statistically significant relationship existed between expression of ras p21, p53 or c-erbB-2 and response to treatment, time to progression or overall survival. We conclude that staining for these three oncoproteins has no role in therapeutic decision-making in patients with advanced breast cancer. The negative finding implies that while abnormal expression of these genes may have an important role in the development of breast cancer, the variations in growth characteristics of advanced breast cancer may be influenced by other factors.
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PMID:Expression of ras p21, p53 and c-erbB-2 in advanced breast cancer and response to first line hormonal therapy. 757 79

We studied 51 paired samples of tissue sections and cytosol extracts from patients with breast cancer. A very high affinity monoclonal antibody to human p53 protein, DO-1, and polyclonal serum CM-1 to p53 protein were used for two site ELISA assays and CM-1 was used for immunohistochemistry to detect p53 protein accumulation in breast cancer samples. Eighteen carcinomas were positive for p53 by tissue staining and ELISA assay. Nineteen tumours were negative by ELISA and immunohistochemistry, and 14 cases with low levels of positive staining by immunohistochemistry were negative by the ELISA assay. A statistically significant correlation has been found between the degree of staining and the amount of p53 protein measured by ELISA (Pearson's correlation coefficient r = 0.59, P < 0.00001). Our ELISA assay offers an alternative approach to evaluating the p53 status of breast biopsy material, using cytosol extracts routinely prepared for steroid hormone receptor assays. This assay should also be of general application to other situations where the level of p53 protein needs to be determined.
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PMID:Comparison between p53 staining in tissue sections and p53 proteins levels measured by an ELISA technique. 768 17

The profiles of functional (proliferative rate and cell distribution in the cell cycle) and phenotypic (nuclear DNA content and hormone receptor status) biological markers and the expression of P53 and Bcl-2 proteins were prospectively evaluated in breast cancers before and after different regimens of primary chemotherapy. Overall, changes induced on the 2 proliferation indices (3H-thymidine labelling index, 3H-dT LI, and flow-cytometric S-phase fraction, FCM-S) mainly consisted of a decrease for rapidly proliferating tumours and an increase or no change for slowly proliferating tumours. However, when considered as a function of treatment type, changes of 3H-dT LI and FCM-S were superimposable in rapidly proliferating tumours, regardless of the type of treatment, and in slowly proliferating tumours only after anthracycline-including regimens. Conversely, following CMF, FCM-S was increased in 90% of the cases and 3H-dT LI in only 50%. Our data imply that the 2 proliferation indices could reflect different phenomena: an actual variation of proliferative activity by 3H-dT LI and an accumulation of cells in the S-phase by FCM-S. In addition, a higher accumulation of cells in G2-M phases could be detected by FCM after anthracycline-including regimens than after CMF. The fraction of P53-positive cells was reduced by primary chemotherapy in about 50% of P53-positive tumours, whereas Bcl-2 expression was only marginally affected. DNA ploidy and hormone receptor status did not change in about 75% of cases, regardless of the chemotherapeutic regimen.
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PMID:Changes in biological markers after primary chemotherapy for breast cancers. 772 38

Breast cancer tissue was examined for overexpression of HER-2/neu and p53 oncogene proteins. Samples from 105 breast cancer patients were investigated by Western-blot analysis and their relationship to other established markers and clinical outcome was examined. In 21.0% of the cases HER-2/neu was overexpressed, and in 46.7% the p53 protein level was increased. Expression of these two oncogene products was closely correlated. Overexpression of both oncogenes was associated with larger tumour size and negative hormone receptor. The percentage of HER-2/neu and p53 overexpression was higher in node-positive patients, although statistical evaluation was not significant. While overexpression of HER-2/neu as well as p53 in node-positive patients was associated insignificantly with shorter disease-free survival, a significant difference could be documented when the disease-free survival of patients with overexpression of both oncogene proteins was compared to that of patients with no overexpression.
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PMID:Coexpression of HER-2/neu and p53 is associated with a shorter disease-free survival in node-positive breast cancer patients. 779

We have developed 2 new quantitative methods for measuring anti-p53 antibodies in human serum. Using these methods we analyzed 1,392 sera from patients with various malignancies and 230 sera from individuals without malignancy. Highest prevalence of anti-p53 antibodies was associated with ovarian and colon cancers (15%), followed by lung (8%) and breast (5%) cancers. Prevalence in other malignancies was lower (< 4%). In hospitalized patients and apparently healthy individuals, prevalence was very low (< 2 and 1% respectively). Extremely high antibody concentrations (> 10(5) U/L) were found in 5 ovarian, 2 breast, 1 lung and 1 colon cancers. Sequential analysis of 6 positive samples has shown that the p53 antibody test may have potential for patient monitoring. The p53 antibody-positive sera from breast cancer patients were associated with tumors that were steroid hormone receptor-negative (p < 0.002). We propose that the measurement of p53 antibodies is a relatively specific serological test for cancer, which can be performed with easily automatable and quantitative methodologies and may be further exploited for patient monitoring, prognosis, diagnosis and probably screening for selected cancers.
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PMID:Prevalence of serum antibodies against the p53 tumor suppressor gene protein in various cancers. 805 43


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